Home About us Contact
|
Home About us Contact | ||
|
|
||
Malondialdehyde
Kinds of Malondialdehyde Terms modified by Malondialdehyde Selected AbstractsMalondialdehyde modification of myelin oligodendrocyte glycoprotein leads to increased immunogenicity and encephalitogenicityEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 7 2007Maja Wĺllberg Abstract Self proteins may become autoantigenic through structural modification. We studied malondialdehydation of recombinant rat (rr) myelin oligodendrocyte glycoprotein (MOG), an autoantigen in multiple sclerosis. Malondialdehyde (MDA) modification changed protein weight and charge, the location of these adducts being mapped by Fourier transform ion cyclotron resonance. Molecular modelling revealed significant differences in the MDA-rrMOG three-dimensional structure. DBA/1 mice immunised with MDA-rrMOG developed greater proliferative responses and more severe experimental autoimmune encephalomyelitis than mice immunised with unmodified rrMOG. MDA-rrMOG was taken up more effectively by antigen-presenting cells (APC), at least partially through scavenger receptors. Exposure to MDA-rrMOG led to increased expression of IL-23, IL-12 and IL-12R, indicating a role not only for increased antigen uptake but also for activation of APC. We thus provide biochemical, structural, immunological and clinical data that suggest that the post-translationally modified form of this myelin autoantigen is a more relevant form of the molecule. [source] The 8-epimer of prostaglandin F2,, a marker of lipid peroxidation and oxidative stress, is decreased in the nipple aspirate fluid of women with breast cancerINTERNATIONAL JOURNAL OF CANCER, Issue 9 2007Ferdinando Mannello Abstract Breast cancer (BC), a worldwide disease with increasing incidence, develops from ductal/lobular epithelium. Nipple aspirate fluid (NAF), secreted from the breast ducts and lobules, can be analyzed to assess breast metabolic activity. Whether lipid peroxidation in the mammary gland promotes or prevents tumorigenesis is unclear. Malondialdehyde (MDA) and the 8-epimer of Prostaglandin F2, (8-iso-PGF2,), two lipid peroxidation markers, were studied in milk (n = 10), NAF (n = 140) and plasma (n = 35) samples. MDA was detected in all plasma, in 80% of milk samples and in 95% of NAF samples. MDA levels in NAF and plasma were significantly higher than in milk (p = 0.016 and p = 0.029, respectively). We found no significant difference between levels of MDA in NAF samples from BC patients compared to healthy controls. 8-iso-PGF2, was detectable in all samples. 8-iso-PGF2, median levels in NAF were significantly higher than in both milk and plasma (p < 0.0001). The highest 8-iso-PGF2, levels were found in NAF from healthy women, significantly higher than in women with BC (p < 0.0001). No significant differences were found in both markers after the age-adjustment. High levels of lipid peroxidation products in NAF suggest their in situ production in the nonlactating breast. Active lipid peroxidation may have a physiologic role in the normal mammary gland. Lower levels of 8-iso-PGF2, in NAF from BC patients suggest altered production of arachidonic acid metabolites during breast carcinogenesis. © 2006 Wiley-Liss, Inc. [source] Lipid peroxidation levels and total oxidant status in serum, saliva and gingival crevicular fluid in patients with chronic periodontitisJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 7 2007Ferda Alev Akal Abstract Objectives: Increased levels of reactive oxygen species lead to oxidative stress. Recent data suggest increased lipid peroxidation (LPO) levels and oxidative stress in periodontitis. Malondialdehyde (MDA), a significant LPO product, increases in oxidative stress. In this study, MDA levels and total oxidant status (TOS) in serum, saliva and gingival crevicular fluid (GCF) were investigated in patients with chronic periodontitis (CP). Materials and Methods: Thirty-six CP patients and 28 periodontally healthy controls were included in the study. Following clinical measurements and samplings, MDA and TOS levels were measured by high-performance liquid chromatography and a novel automatic colorimetric method, respectively. Results: While the saliva and GCF MDA levels, and serum, saliva and GCF TOS values were significantly higher in the CP group than the control group (p<0.05), no significant difference in serum MDA levels was found (p>0.05). Strong positive correlations were observed between periodontal parameters and MDA and TOS levels (p<0.05). Conclusions: The results revealed that LPO significantly increased locally in the periodontal pocket/oral environment, while TOS displayed both systemic and local increases in periodontitis. The findings suggest that increased LPO and TOS may play an important role in the pathology of periodontitis, and are closely related to the clinical periodontal status. [source] Potential implications of endogenous aldehydes in ,-amyloid misfolding, oligomerization and fibrillogenesisJOURNAL OF NEUROCHEMISTRY, Issue 5 2006Kun Chen Abstract Aldehydes are capable of inducing protein cross-linkage. An increase in aldehydes has been found in Alzheimer's disease. Formaldehyde and methylglyoxal are produced via deamination of, respectively, methylamine and aminoacetone catalyzed by semicarbazide-sensitive amine oxidase (SSAO, EC 1.4.3.6. The enzyme is located on the outer surface of the vasculature, where amyloidosis is often initiated. A high SSAO level has been identified as a risk factor for vascular disorders. Serum SSAO activity has been found to be increased in Alzheimer's patients. Malondialdehyde and 4-hydroxynonenal are derived from lipid peroxidation under oxidative stress, which is also associated with Alzheimer's disease. Aldehydes may potentially play roles in ,-amyloid aggregation related to the pathology of Alzheimer's disease. In the present study, thioflavin-T fluorometry, dynamic light scattering, circular dichroism spectroscopy and atomic force microscopy were employed to reveal the effect of endogenous aldehydes on ,-amyloid at different stages, i.e. ,-sheet formation, oligomerization and fibrillogenesis. Formaldehyde, methylglyoxal and malondialdehyde and, to a lesser extent, 4-hydroxynonenal are not only capable of enhancing the rate of formation of ,-amyloid ,-sheets, oligomers and protofibrils but also of increasing the size of the aggregates. The possible relevance to Alzheimer's disease of the effects of these aldehydes on ,-amyloid deposition is discussed. [source] Malondialdehyde, nitric oxide and adrenomedullin levels in patients with primary dysmenorrheaJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 6 2008Ebru Dikensoy Abstract Aim:, The aim of the study was to examine whether there was a relationship between primary dysmenorrhea and serum levels of malondialdehyde (MDA), nitric oxide (NO) and adrenomedullin (AM) in young women. Methods:, Sixty female subjects without serious medical problems, aged between 20 and 34, who had regular menses for at least six previous cycles, were involved. Blood samples were obtained from each patient on the first and the 21st days of her menstrual cycles. Pelvic examination and ultrasound were performed to determine any organic cause for dysmenorrhea in each patient. The subjects were divided into two groups. The study group consisted of 30 subjects with primary dysmenorrhea, and the control group consisted of 30 healthy subjects. Results:, No statistically significant difference was observed in comparison of the following variables between the groups: age, parity and body mass index. The serum levels of MDA, NO, and AM were significantly higher on the first day compared to those on the 21st day in the study group (P < 0.05). The serum levels of MDA, NO, and AM were significantly higher in the study group compared to the control group both on the first and the 21st days of the menstrual cycles (P < 0.05). Conclusion:, In conclusion, the results of this study showed that the serum levels of MDA, NO, and AM increase in subjects with primary dysmenorrhea, suggesting the possibility that lipid peroxidation and oxidative stress play a significant role in the etiopathogenesis of primary dysmenorrhea. [source] Melatonin reduces dimethylnitrosamine-induced liver fibrosis in ratsJOURNAL OF PINEAL RESEARCH, Issue 2 2004Veysel Tahan Abstract:, Increased deposition of the extracellular matrix components, particularly collagen, is a central phenomenon in liver fibrosis. Stellate cells, the central mediators in the pathogenesis of fibrosis are activated by free radicals, and synthesize collagen. Melatonin is a potent physiological scavenger of hydroxyl radicals. Melatonin has also been shown to be involved in the inhibitory regulation of collagen content in tissues. At present, no effective treatment of liver fibrosis is available for clinical use. We aimed to test the effects of melatonin on dimethylnitrosamine (DMN)-induced liver damage in rats. Wistar albino rats were injected with DMN intraperitoneally. Following a single dose of 40 mg/kg DMN, either saline (DMN) or 100 mg/kg daily melatonin was administered for 14 days. In other rats, physiologic saline or melatonin were injected for 14 days, following a single injection of saline as control. Hepatic fibrotic changes were evaluated biochemically by measuring tissue hydroxyproline levels and histopathogical examination. Malondialdehyde (MDA), an end product of lipid peroxidation, and glutathione (GSH) and superoxide dismutase (SOD) levels were evaluated in blood and tissue homogenates. DMN caused hepatic fibrotic changes, whereas melatonin suppressed these changes in five of 14 rats (P < 0.05). DMN administration resulted in increased hydroxyproline and MDA levels, and decreased GSH and SOD levels, whereas melatonin reversed these effects. When melatonin was administered alone, no significant changes in biochemical parameters were noted. In conclusion, the present study suggests that melatonin functions as a potent fibrosuppressant and antioxidant, and may be a therapeutic choice. [source] Immunohistochemical Characterization of Hepatic Malondialdehyde and 4-Hydroxynonenal Modified Proteins During Early Stages of Ethanol-Induced Liver InjuryALCOHOLISM, Issue 6 2003Brante P. Sampey Background: Chronic ethanol consumption is associated with hepatic lipid peroxidation and the deposition or retention of aldehyde-adducted proteins postulated to be involved in alcohol-induced liver injury. The purpose of this study was to characterize hepatocellular formation of aldehyde-protein adducts during early stages of alcohol-induced liver injury. Methods: Female Sprague Dawley® rats were subjected to the intragastric administration of a low-carbohydrate/high-fat total enteral nutrition diet or a total enteral nutrition diet containing ethanol for a period of 36 days. Indexes of hepatic responses to ethanol were evaluated in terms of changes in plasma alanine aminotransferase activity, hepatic histopathologic analysis, and induction of cytochrome P-4502E1 (CYP2E1). Immunohistochemical methods were used to detect hepatic proteins modified with malondialdehyde (MDA) or 4-hydroxynonenal (4-HNE) for subsequent quantitative image analysis. Results: After 36 days of treatment, rats receiving the alcohol-containing diet displayed hepatic histopathologies characterized by marked micro- and macrosteatosis associated with only minor inflammation and necrosis. Alcohol administration resulted in a 3-fold elevation of plasma alanine aminotransferase activity and 3-fold increases (p < 0.01) in hepatic CYP2E1 apoprotein and activity. Quantitative immunohistochemical analysis revealed significant (p < 0.01) 5-fold increases in MDA- and 4-HNE modified proteins in liver sections prepared from rats treated with alcohol. The MDA- or 4-HNE modified proteins were contained in hepatocytes displaying intact morphology and were colocalized primarily with microvesicular deposits of lipid. Aldehyde-modified proteins were not prevalent in parenchymal or nonparenchymal cells associated with foci of necrosis or inflammation. Conclusions: These results suggest that alcohol-induced lipid peroxidation is an early event during alcohol-mediated liver injury and may be a sensitizing event resulting in the production of bioactive aldehydes that have the potential to initiate or propagate ensuing proinflammatory or profibrogenic cellular events. [source] Effect of vitamin C on oxidative liver injury due to isoniazid in ratsPEDIATRICS INTERNATIONAL, Issue 1 2010Yakup Ergul Abstract Background:, The aim of the present study was to investigate the effect of different doses of vitamin C on oxidative liver injury due to isoniazid (INH) in rats. Methods:, Rats were divided into four subgroups, each containing 10 rats. Group 1 was the control group; group 2, INH 50 mg/kg per day; group 3, INH 50 mg/kg per day + low-dose vitamin C (100 mg/kg per day); group 4, INH 50 mg/kg per day + high-dose vitamin C (1000 mg/kg per day). INH and vitamin C were administered into their stomachs through an oral tube. After 21 days, measurements were made in both serum and homogenized liver tissues. The levels of glutathione (GSH), superoxide dismutase (SOD) and other biochemical variables were measured. Malondialdehyde (MDA), glutathione peroxidase (GSH-px) and vitamin C were measured using commercial kits. Results:, Aspartate amino transferase and alanine aminotransferase in group 2 were higher than those in groups 1, 3 and 4 (P < 0.008 for both). Serum and tissue levels of MDA in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). There was no difference in the SOD levels between the four groups (P= 0.095). Erythrocyte and tissue GSH in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). Interestingly, erythrocyte and tissue GSH in group 4 were lower than those in group 1 (P < 0.008 for both). Erythrocyte level of GSH-px in group 2 was higher than that in groups 1 and 3 (P < 0.008 for both). Conclusions:, INH-induced liver injury is associated with oxidative stress, and co-administration of low-dose vitamin C may reduce this damage effectively in a rat model. The antioxidant effect of high-dose vitamin C does not seem more potent compared to the low dose. [source] Effect of Two Different UVA Doses on the Rabbit Cornea and LensPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2009ejka, estmír The aim of the present paper was to examine the irradiation effect of two doses of UVA rays (365 nm) on the rabbit cornea and lens. Corneas of anesthetized adult albino rabbits were irradiated with UVA rays for 5 days (daily dose 1.01 J cm,2 in one group of rabbits and daily dose 2.02 J cm,2 in the second group of animals). The third day after the last irradiation, the rabbits were killed, and their eyes were employed for spectrophotometrical, biochemical and immunohistochemical investigations. Normal eyes served as controls. Absorption spectra of the whole corneal centers were recorded over the UV,VIS (visible) spectral range. Levels of antioxidant and prooxidant enzymes, nitric oxide synthases and nitric oxide (indirectly measured as nitrate concentration) were investigated in the cornea. Malondialdehyde, a byproduct of lipid peroxidation, was examined in the cornea and lens. The results show that the staining for endothelial nitric oxide synthase was more pronounced in corneas irradiated with the higher UVA dose. Otherwise, UVA rays at either dose did not significantly change corneal light absorption properties and did not cause statistically significant metabolic changes in the cornea or lens. In conclusion, UVA rays at the employed doses did not evoke harmful effects in the cornea or lens. [source] In Vivo Radioprotective Effects of Nigella sativa L Oil and Reduced Glutathione Against Irradiation-Induced Oxidative Injury and Number of Peripheral Blood Lymphocytes in RatsPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 6 2006Mustafa Cemek Radiotherapy is one of the most common therapies for treating human cancers. Several studies have indicated that irradiation induces reactive oxygen species (ROS), which play an important role in radiation damage of the cell. It has been shown that Nigella saliva L. (NS) and reduced glutathione (GSH) have both an antiperoxidative effect on different tissues and a scavenger effect on ROS. The purpose of this study was to determine the antioxidant and radio-protective roles of NS and GSH against irradiation-induced oxidative injury in an experimental model. The NS group was administrated NS (1 mL/kg body weight), the GSH group was injected GSH (150 mg/kg body weight) and the control group was given physiologic saline solution (1 mL/kg body weight) for 30 consecutive days before exposure to a single dose of 6 Gy of radiation. Animals were sacrificed after irradiation. Malondialdehyde, nitrate, nitrite (oxidative stress markers) and ascorbic acid, retinol, ,-carotene, GSH and ceruloplasmin (nonenzymatic antioxidant markers) levels and peripheral blood lymphocytes were measured in all groups. There were statistically significant differences between the groups for all parameters (P < 0.05). Whole-body irradiation caused a significant increase in blood malondialdehyde, nitrate and nitrite levels. The blood oxidative stress marker levels in irradiated rats that were pretreated with NS and GSH were significantly decreased; however, non-enzymatic antioxidant levels were significantly increased. Also, our results suggest that NS and GSH administration prior to irradiation prevent the number of alpha-naphthyl acetate esterase peripheral blood T lymphocytes from declining. These results clearly show that NS and GSH treatment significantly antagonize the effects of radiation. Therefore, NS and GSH may be a beneficial agent in protection against ionizing radiation-related tissue injury. [source] The effects of EGb 761 on lipid peroxide levels and superoxide dismutase activity in sunburnPHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 3 2002Mehtap Kilinc Ozkur Background/Purpose: Free oxygen radicals are involved in inflammatory skin reactions induced by ultraviolet B (UVB). In this study, the effect of a herbal antioxidant Ginkgo biloba extract (EGb 761) was investigated in UVB irradiated mice skin. Methods: The study was carried out on four groups of mice (n = 6 in each group). The first group was a control group (G1). The second group (G2) was only exposed to acute UVB irradiation. The third group (G3) received 100 mg/kg/day of EGb 761 orally for 5 days before UVB irradiation and the fourth group (G4) was given only a single dose of EGb 761 immediately after UVB irradiation. Eighteen hours after exposing to UVB, lipid peroxide levels, and superoxide dismutase (SOD) activities were studied and UVB damage was evaluated histopathologically according to ,sun-burn cell count'. Results: The SOD activities and Malondialdehyde (MDA) levels in G2, G3 and G4 were found to be decreased significantly when compared with G1 (P < 0.05). The SOD activities of G3 and G4 were higher when compared with G2 (P < 0.05). The number of sunburn cells (SBCs) was the highest in G2. Conclusions: Our results suggest that EGb 761 may have an important effect, both as a protective and therapeutic agent, in sunburn after UVB irradiation. [source] Betulinic acid protects against ischemia/reperfusion-induced renal damage and inhibits leukocyte apoptosisPHYTOTHERAPY RESEARCH, Issue 3 2010Emel Ek, lu-Demiralp Abstract The possible protective effect of betulinic acid on renal ischemia/reperfusion (I/R) injury was studied. Wistar Albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. Betulinic acid (250 mg/kg, i.p.) or saline was administered at 30 min prior to ischemia and immediately before the reperfusion. Creatinine, blood urea nitrogen (BUN), lactate dehydrogenase (LDH) and TNF-, as well as the oxidative burst of neutrophil and leukocyte apoptosis were assayed in blood samples. Malondialdehyde (MDA), glutathione (GSH) levels, Na+, K+ -ATPase and myeloperoxidase (MPO) activities were determined in kidney tissue which was also analysed microscopically. I/R caused significant increases in blood creatinine, BUN, LDH and TNF-,. In the kidney samples of the I/R group, MDA levels and MPO activity were increased significantly, however, GSH levels and Na+, K+ -ATPase activity were decreased. Betulinic acid ameliorated the oxidative burst response to both formyl-methionyl-leucyl-phenylalanine (fMLP) and phorbol 12-myristate 13-acetate (PMA) stimuli, normalized the apoptotic response and most of the biochemical indices as well as histopathological alterations induced by I/R. In conclusion, these data suggest that betulinic acid attenuates I/R-induced oxidant responses, improved microscopic damage and renal function by regulating the apoptotic function of leukocytes and inhibiting neutrophil infiltration. Copyright © 2009 John Wiley & Sons, Ltd. [source] Determination of patterns of biologically relevant aldehydes in exhaled breath condensate of healthy subjects by liquid chromatography/atmospheric chemical ionization tandem mass spectrometryRAPID COMMUNICATIONS IN MASS SPECTROMETRY, Issue 7 2003Roberta Andreoli A method for the simultaneous determination of several classes of aldehydes in exhaled breath condensate (EBC) was developed using liquid chromatography/atmospheric pressure chemical ionization tandem mass spectrometry (LC/APCI-MS/MS). EBC is a biological matrix obtained by a relatively new, simple and noninvasive technique and provides an indirect assessment of pulmonary status. The measurement of aldehydes in EBC represents a biomarker of the effect of oxidative stress caused by smoke, disease, or strong oxidants like ozone. Malondialdehyde (MDA), acrolein, ,,, -unsaturated hydroxylated aldehydes [namely 4-hydroxyhexenal (4-HHE) and 4-hydroxynonenal (4-HNE)], and saturated aldehydes (n -hexanal, n -heptanal and n -nonanal) were measured in EBC after derivatization with 2,4-dinitrophenylhydrazine (DNPH). Atmospheric pressure chemical ionization of the analytes was obtained in positive-ion mode for MDA, and in negative-ion mode for acrolein, 4-HHE, 4-HNE, and saturated aldehydes. DNPH derivatives were separated on a C18 column using variable proportions of 20,mM aqueous acetic acid and methanol. Linearity was established over 4,5 orders of magnitude and limits of detection were in the 0.3,1.0 nM range. Intra-day and inter-day precision were in the 1.3,9.9% range for all the compounds. MDA, acrolein and n -alkanals were detectable in all EBC samples, whereas the highly reactive 4-HHE and 4-HNE were found in only a few samples. Statistically significant higher concentrations of MDA, acrolein and n -hexanal were found in EBC from smokers. Copyright © 2003 John Wiley & Sons, Ltd. [source] Clinical evaluation of spermatogenic activity of processed Shilajit in oligospermiaANDROLOGIA, Issue 1 2010T. K. Biswas Summary The safety and spermatogenic activity of processed Shilajit (PS) were evaluated in oligospermic patients. Initially, 60 infertile male patients were assessed and those having total sperm counts below 20 million ml,1 semen were considered oligospermic and enrolled in the study (n = 35). PS capsule (100 mg) was administered twice daily after major meals for 90 days. Total semenogram and serum testosterone, luteinising hormone and follicle-stimulating hormone were estimated before and at the end of the treatment. Malondialdehyde (MDA), a marker for oxidative stress, content of semen and biochemical parameters for safety were also evaluated. Twenty-eight patients who completed the treatment showed significant (P < 0.001) improvement in spermia (+37.6%), total sperm count (+61.4%), motility (12.4,17.4% after different time intervals), normal sperm count (+18.9%) with concomitant decrease in pus and epithelial cell count compared with baseline value. Significant decrease of semen MDA content (,18.7%) was observed. Moreover, serum testosterone (+23.5%; P < 0.001) and FSH (+9.4%; P < 0.05) levels significantly increased. HPLC chromatogram revealed inclusion of PS constituents in semen. Unaltered hepatic and renal profiles of patients indicated that PS was safe at the given dose. The present findings provide further evidence of the spermatogenic nature of Shilajit, as attributed in Ayurvedic medicine, particularly when administered as PS. [source] Lipid peroxidation levels, total oxidant status and superoxide dismutase in serum, saliva and gingival crevicular fluid in chronic periodontitis patients before and after periodontal therapyAUSTRALIAN DENTAL JOURNAL, Issue 1 2010D Wei Abstract Background:, Recent data have demonstrated increased lipid peroxidation (LPO) levels and oxidative stress in periodontitis. Malondialdehyde (MDA) and superoxide dismutase (SOD) are both increased during oxidative stress. Furthermore, this study examined SOD concentration, total oxidative status (TOS) and MDA levels in periodontal patients and investigated the longitudinal effect of periodontal therapy on the index levels of chronic periodontitis (CP) patients. Methods:, Serum, saliva and gingival crevicular fluid (GCF) samples were obtained from 48 CP patients and 35 healthy control subjects prior to, as well as after 16 weeks following non-surgical post-periodontal therapy. MDA, TOS and SOD and clinical parameters were determined pre- and post-therapy. Results:, The levels of TOS and SOD values were significantly higher in the CP group than in the control group (p < 0.05), but only MDA in GCF. Post-periodontal therapy, serum, saliva and GCF TOS and SOD levels significantly decreased compared to basal levels (p < 0.05), but only MDA in GCF. Conclusions:, LPO was higher in the periodontal region, with TOS and SOD increasing both locally and peripherally. Non-surgical therapy can restore and control the subject antioxidant capacity by locally and systemically modifying the levels of MDA, TOS and SOD. [source] Cardioprotective Effects of Nigella sativa Oil on Cyclosporine A-Induced Cardiotoxicity in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 6 2008Uz Ebru However, it has been demonstrated that this drug produces side-effects in several organs, particularly in the kidney and in the heart. Nigella sativa oil has long been used in folk medicine for a wide range of illnesses. One of the potential properties of N. sativa oil is the ability of one or more of its constituents to reduce toxicity due to its antioxidant activities. The antioxidant effects of N. sativa oil have been examined using different hepatic and kidney toxicity in in vivo murine models. The aim of this study was to evaluate the effects of N. sativa oil in the antioxidant enzyme status and myocardium of cyclosporine-A-treated rats. This study included 24 male Wistar albino young healthy rats (8,12 weeks) weighing 150,200 g. The control group received sunflower oil (21 days, 2 ml/kg/day, orally) without any treatment. The second group received only N. sativa oil (21 days, 2 ml/kg, orally) (N. sativa oil group). The animals in the third group received only cyclosporine A (21 days, 25 mg/kg, orally) (cyclosporine A group). The animals in the fourth group were treated with cyclosporine A (21 days, 25 mg/kg, orally) and starting one day before cyclosporine A administration were treated with N. sativa oil (21 days, 2 ml/kg, orally) (cyclosporine A +N. sativa oil group). Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities in the heart tissues were significantly reduced in the cyclosporine A group compared to control values. Nigella sativa oil treatment caused an increase in the activities of SOD, CAT and GSH-Px compared to the control group. Malondialdehyde (MDA), nitric oxide and protein carbonyl (PC) levels were increased in the cyclosporine A-treated group in comparison with the control and N. sativa groups. Co-administration of N. sativa oil and cyclosporine A abrogated the cyclosporine A-induced MDA, N. sativa oil and PC increase compared to the cyclosporine A group. The results of our study show that pre-treatment with N. sativa oil reduced the subsequent cyclosporine A injury in rat heart, demonstrated by normalized cardiac histopathology, decrease in lipid peroxidation, improvement in antioxidant enzyme status and cellular protein oxidation. [source] Amelioration of Cyclosporine A-Induced Renal, Hepatic and Cardiac Damages by Ellagic Acid in Rats,BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2008Abdurrauf Yüce Cyclosporine A also causes a dose-related decrease in body functions in experimental animals and human beings. The generation of reactive oxygen species has been implicated in cyclosporine A-induced dysfunctions. The aim of this study was to determine the effects of ellagic acid on cyclosporine A-induced alterations in the kidney, liver and heart oxidant/antioxidant system. The control group was treated with placebo and subcutaneous injection of 0.5 ml isotonic saline + 0.5 ml slightly alkaline solution for 21 days. The cyclosporine A group received a subcutaneous injection of cyclosporine A (15 mg/kg) + 0.5 ml slightly alkaline solution for 21 days. The ellagic acid group was treated with a subcutaneous injection of 0.5 ml isotonic saline + ellagic acid (10 mg/kg) for 21 days. The cyclosporine A plus ellagic acid group received a subcutaneous injection of cyclosporine A + ellagic acid for 21 days. Ellagic acid and slightly alkaline solution were administered by gavage. The rats were killed at the end of the treatment period. Malondialdehyde (MDA) and reduced glutathione (GSH) levels, glutathione peroxidase (GSH-Px) and catalase (CAT) activities were determined in kidney, liver and heart tissues. While administration of cyclosporine A increased the MDA levels in kidney, liver and heart tissues, it decreased the GSH, GSH-Px and CAT in these samples when compared to the control group. However, the simultaneously administration of ellagic acid markedly normalized the cyclosporine A-induced liver and heart MDA levels, liver CAT activities and GSH-Px activities of all samples. Cyclosporine A caused marked damages in the histopathological status of kidney, liver and heart tissues, which were partially ameliorated by ellagic acid administration. In conclusion, ellagic acid may be used in combination with cyclosporine A in transplantation treatment to improve the cyclosporine A-induced oxidative stress parameters and other adverse effects. [source] Glycaemic control in relation to xanthine oxidase and antioxidant indices in Malaysian Type 2 diabetes patientsDIABETIC MEDICINE, Issue 10 2005U. R. Kuppusamy Abstract Aims Increased oxidative stress and oxidative damage are present in Type 2 diabetes mellitus (DM). The aim of this study was to assess the oxidative stress levels in the three major ethnic groups in Malaysia and to study the association between glycaemic control and oxidant,antioxidant levels in these patients. Methods Oxidative indices and glycaemic control were assessed in 650 Type 2 DM patients and 280 healthy age-matched controls by known established methods. Results Type 2 DM patients had significantly lower levels of antioxidant enzymes and non-enzymatic antioxidant (FRAP) and increased levels of HbA1c, fasting blood glucose (FBG), malondialdehyde (MDA) and xanthine oxidase (XO) when compared with control subjects. Markers of oxidative stress were more apparent in Indian patients compared with Malay and Chinese patients. Correlation analysis of oxidant,antioxidant parameters as a function of HbA1c in each ethnic group revealed a strong association of HbA1c with oxidative indices. Conclusions The present study provides evidence for the possible contribution of XO to oxidative stress and the pathophysiology of diabetes. HbA1c remains an important marker of glycaemic control for the management of Type 2 DM, but other confounding factors that predispose or lead to oxidative stress should also be taken into consideration. [source] Protective effect of CPUX1, a progesterone, on hydrogen peroxide-induced oxidative damage in PC12 cells,DRUG DEVELOPMENT RESEARCH, Issue 8 2008Bian-sheng Ji Abstract The protective effect of CPUX1, a novel progesterone analog, on hydrogen peroxide (H2O2)-induced oxidative damage was investigated in rat pheochromocytoma (PC12) cells. Following the exposure of PC12 cells to H2O2, there was a reduction in cell survival and activities of superoxide dismutase (SOD) and mitochondrial membrane potential (MMP) accompanied by increased levels of lactate dehydrogenase (LDH) release, malondialdehyde (MDA) production, and intracellular reactive oxygen species (ROS) and intracellular [Ca2+]i levels. Preincubation of cells with CPUX1 prior to H2O2 exposure attenuated all these changes mentioned and had a protective effect against H2O2 -induced toxicity in PC12 cells, indicating that the compound may have potential therapeutic benefit for CNS disorders influenced by oxidative damage. Drug Dev Res 69: 2008 ©2008 Wiley-Liss, Inc. [source] Bentazon triggers the promotion of oxidative damage in the Portuguese ricefield cyanobacterium Anabaena cylindrica: Response of the antioxidant systemENVIRONMENTAL TOXICOLOGY, Issue 5 2010Victor Galhano Abstract Rice fields are frequently exposed to environmental contamination by herbicides and cyanobacteria, as primary producers of these aquatic ecosystems, are adversely affected. Anabaena cylindrica is a cyanobacterium with a significantly widespread occurrence in Portuguese rice fields. This strain was studied throughout 72 h in laboratory conditions for its stress responses to sublethal concentrations (0.75,2 mM) of bentazon, a selective postemergence herbicide recommended for integrated weed management in rice, with special reference to oxidative stress, role of proline and intracellular antioxidant enzymes in herbicide-induced free radicals detoxification. Activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and glutathione S -transferase (GST) increased in a time- and herbicide dose-response manner and were higher than those in the control samples after 72 h. A time- and concentration-dependent increase of malondialdehyde (MDA) levels and the enhanced cell membrane leakage following bentazon exposure are indicative of lipid peroxidation, free radicals formation, and oxidative damage, while increased amounts of SOD, CAT, APX, GST, and proline indicated their involvement in free radical scavenging mechanisms. The appreciable decline in the reduced glutathione (GSH) pool after 72 h at higher bentazon concentrations could be explained by the reduction of the NADPH-dependent glutathione reductase (GR) activity. The obtained results suggested that the alterations of antioxidant systems in A. cylindrica might be useful biomarkers of bentazon exposure. As the toxic mechanism of bentazon is a complex phenomenon, this study also adds relevant findings to explain the oxidative stress pathways of bentazon promoting oxidative stress in cyanobacteria. © 2010 Wiley Periodicals, Inc. Environ Toxicol, 2010. [source] Malathion-induced oxidative stress in human erythrocytes and the protective effect of vitamins C and E in vitroENVIRONMENTAL TOXICOLOGY, Issue 3 2009Dilek Durak Abstract Malathion is an organophosphate (OP) pesticide that has been shown to induce oxidative stress in erythrocytes through the generation of free radicals and alteration of the cellular antioxidant defense system. We examined the effect of several different doses of malathion (25, 75, 200 ,M), or malathion in combination with vitamin C (VC; 10 ,M) or vitamin E (VE; 30 ,M), on the levels of malondialdehyde (MDA), and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in human erythrocytes in vitro. Erythrocytes were incubated under various treatment conditions (malathion alone, vitamins alone, or malathion plus vitamin) at 37°C for 60 min, and the levels of MDA, and SOD, CAT and GPx activities, were determined. Treatment with malathion alone increased the levels of MDA and decreased SOD, CAT, and GPx activities in erythrocytes (P < 0.05). There were no statistical differences among VC-treated, VE-treated, or VC + VE-treated erythrocyes, as compared with nontreated control cells. Treatment of cells with malathion + VC, malathion + VE, or a combination of all three agents prevented malathion-induced changes in antioxidant enzyme activity and lipid peroxidation. However, this effect was seen only at low concentrations of malathion (25 and 75 ,M), and the combination of VC + VE had a more protective effect than VC or VE alone. These results indicated that the presence of vitamins at concentrations that are similar to the levels found in plasma have no effect on malathion-induced toxicity in erythrocytes at a concentration of malathion (200 ,M) that is typically used in pesticides. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2009. [source] Oxidative stress, defense response, and early biomarkers for lead-contaminated soil in Vicia faba seedlings,ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 4 2008Cheng-Run Wang Abstract Chemical analyses and biological measurements were investigated in leaves of Vicia faba seedlings exposed to extraneous lead (Pb) at 0 to 2,000 mg/kg of soil for a month. The results showed that superoxide radical (O,,2) production, increased along with total Pb in leaves and available Pb in soil, resulted in enhancement of malondialdehyde and carbonyl groups. Antioxidant enzymes, including corresponding isoenzymes and heat shock protein 70 (hsp 70), were also enhanced to some extent. Significant changes were detected in the patterns and intensities of guaiacol peroxidase isoenzymes, while superoxide dismutase, catalase, and ascorbate peroxidase isoenzymes only changed intensities. Superoxide dismutase activities increased with the increase of extraneous Pb at 0 to 500 mg/kg of soil and tended to decline thereafter, which might be responsible for the decrease of hydrogen peroxide and accumulation of O,,2. Guaiacol peroxidase and ascorbate peroxidase enzymes were upregulated to become major scavengers of excess hydrogen peroxide on the condition of decreased catalase activities. Levels of hsp 70 were well correlated with Pb contents in leaves (r = 0.777), O,,2 accumulation (r = 0.985, p < 0.01), and carbonyl groups (r = 0.920, p < 0.01) under extraneous Pb at 0 to 250 mg/kg of soil, suggesting that hsp 70 induced by O,,2 was possibly involved in disposal of denatured proteins. The results showed that O,,2, hsp 70, and guaiacol peroxidase isoenzymes had the most sensitive responses in the seedlings and these parameters could be potential early biomarkers of soil Pb contamination. [source] Oxidative stress biomarkers in bivalves transplanted to the Guadalquivir estuary after Aznalcóllar spillENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 1 2003Antonio Romero-Ruiz Abstract Biological effects of metals were studied in clams (Scrobicularia plana) transplanted to Guadalquivir estuary (Spain) at several times after the spill of toxic metals from Aznalcóllar pyrite mine (southwest Spain) (April 1998) using biochemical biomarkers responsive to reactive oxygen species. Significant As, Cd, Fe, Mn, Ni, and Pb uptake was found in clams living for seven months at the estuary (from July 1999). Increased activity of antioxidant (catalase, glucose-6-phosphate, and 6-phosphogluconate dehydrogenase) and glutathione-related (glutathione reductase and glyoxalase I and II) enzymes was also found after short exposures; the levels of malondialdehyde and metallothionein increased also, particularly with long exposures. Clams living four weeks at the estuary (from March 2000) but not at a reference site also accumulated metals. The higher malondialdehyde and lower reduced-glutathione levels and the more oxidized glutathione status confirmed the oxidative stress of clams living at the estuary, while no marked increase of antioxidant activities was found this time. Lower metal availability along the second transplant could explain the limited responses in this shorter experiment. Although the status of Guadalquivir estuary has recovered since Aznalcóllar spill, continuous monitoring is needed to confirm its progress and to be alert to possible deterioration after heavy rains. [source] Anthracene photoinduced toxicity to plhc-1 cell line (Poeciliopsis lucida) and the role of lipid peroxidation in toxicityENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 11 2000Jonghoon Choi Abstract Many polycyclic aromatic hydrocarbons (PAHs) are acutely toxic to fish and other aquatic organisms in the presence of solar ultraviolet radiation (SUVR) of environmentally realistic intensities. In the present study, the photoinduced toxicity of a PAH (anthracene; ANT) to topminnow hepatoma cell line (PLHC-1) was assessed. After the toxicity was characterized, the role of lipid peroxidation in PAH photoinduced toxicity was examined by measuring lipid peroxidation products and by assessing the effect of lipid peroxidation antagonist (Trolox) treatment. In cytotoxicity tests using two assays (MTT, neutral red), the SUVR/ANT treatment elicited toxicity to PLHC-1 cells in a concentration- and SUVR (exposure duration and intensity)-dependent pattern. As found in previous organism-level studies, no significant cytotoxicity was observed in the cells exposed either to fluorescent light/ANT or to SUVR only. The SUVR/ANT treatment elicited the lipid peroxidation process and Trolox pretreatment significantly reduced SUVR/ANT-induced cell mortality. Microscopic observation showed that Trolox pretreatment relieved the SUVR/ANT-inflicted damage, such as cell shrinkage and membrane disruption. Together with a recent finding in our lab that increased production of superoxide anion and a lipid peroxidation product (malondialdehyde) was found in SUVR/ANT-treated fish microsomes, the present study suggests that reactive oxygen radical-induced lipid peroxidation is an important factor in PAH photoinduced toxicity to fish. [source] Evidence of oxidative stress in bluegill sunfish (Lepomis macrochirus) liver microsomes simultaneously exposed to solar ultraviolet radiation and anthraceneENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 7 2000Jonghoon Choi Abstract Many polycyclic aromatic hydrocarbons (PAHs) are acutely toxic to fish and other aquatic organisms in the presence of environmentally realistic intensities of solar ultraviolet radiation (SUVR). However, the biochemical mechanism of this toxicity is not well established. In this study, increased levels of both reactive oxygen species production and lipid peroxidation were hypothesized as a toxic mechanism. To test this hypothesis, the production of superoxide anion and of a lipid peroxidation product (malondialdehyde) was measured in bluegill sunfish (Lepomis machrochirus) liver microsomes. These microsomes were exposed to a representative phototoxic PAH (anthracene [ANT]) and to SUVR and normal laboratory fluorescent light (FLU) in four different combinations: FLU + no ANT, FLU + ANT, SUVR + no ANT, and SUVR + ANT. The highest mean levels of both superoxide anion and malondialdehyde production were observed in the SUVR + ANT group, and these levels were significantly different (p < 0.05) from those in all other treatment groups. We conclude that the photoinduced toxicity of ANT, and possibly of other phototoxic PAHs, manifests at least in part through lipid peroxidation after increased production of reactive oxygen species. [source] Elective coronary angioplasty with 60 s balloon inflation does not cause peroxidative injuryEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2002K. Cedro Abstract Background The aim of this study was to evaluate the ongoing controversial issue of whether ischemia/reperfusion during elective coronary angioplasty evokes myocardial peroxidative injury. Design We measured indicators of free radical damage to lipids (free malondialdehyde) and proteins (sulphydryl groups) in coronary sinus blood in 19 patients with stable angina who were undergoing elective angioplasty for isolated stenosis of the proximal left anterior descending coronary artery. Ischemia induced by 60 s balloon inflations was confirmed by lactate washout into coronary sinus after deflation, with immediate and 1 min samples. Peroxidative injury was assessed from washout of (a) malondialdehyde measured directly by high performance liquid chromatography and (b) reduced sulphydryl groups, inverse marker of protein oxidative stress. Results Mean lactate concentration immediately after each deflation increased by 120,150% of the initial value, confirming ischemia and showing that blood originated largely from the ischemic region. Lack of myocardial production of malondialdehyde was confirmed by (a) no arteriovenous differences in individual basal concentrations (aortic, range 0·33,12·03 nmol mL,1, mean 7·82; coronary sinus blood, range 0·52,15·82 nmol mL,1, mean 8·18), and (b) after deflations, mean concentrations were not significantly different from preocclusion value. There was no decrease in concentration of sulphydryl groups throughout angioplasty. Conclusion Elective coronary angioplasty with 60 s balloon inflations is a safe procedure that does not induce peroxidative myocardial injury as assessed by methods used in the present study. [source] N -acetylcysteine inhibits chromium hypersensitivity in coadjuvant chromium-sensitized albino guinea pigs by suppressing the effects of reactive oxygen speciesEXPERIMENTAL DERMATOLOGY, Issue 8 2010Bour-Jr Wang Please cite this paper as: N -acetylcysteine inhibits chromium hypersensitivity in coadjuvant chromium-sensitized albino guinea pigs by suppressing the effects of reactive oxygen species. Experimental Dermatology 2010; 19: e191,e200. Abstract Background:, Chromium hypersensitivity is an important issue in occupational skin disease. When hexavalent chromium enters the cell, it can be reduced to trivalent chromium, resulting in the formation of reactive oxygen species (ROS). ROS are considered to play an important role in the progression of allergic contact dermatitis. N -acetylcysteine (NAC) could increase glutathione levels in the skin and act as an antioxidant. Aims:, We attempted to demonstrate that NAC could inhibit chromium hypersensitivity in a coadjuvant chromium-sensitized albino guinea pig model by counteracting the formation of ROS. Methods:, We utilized a coadjuvant chromium-sensitized albino guinea pig model to evaluate both the severity of the skin reaction by intradermal and epicutaneous elicitation tests and the sensitization rate of chromium hypersensitivity in NAC-treated and NAC-untreated albino guinea pigs (GP). Furthermore, three ROS parameters, including H2O2, malondialdehyde (MDA) levels in the skin and the oxygen radical absorbance capacity (ORAC) in plasma, were analyzed in NAC-treated and NAC-untreated coadjuvant chromium-sensitized albino GP. Results:, The severity of the skin reaction in the intradermal and epicutaneous elicitation test significantly diminished when the albino GP were treated with a dose of 1200 mg/kg/day of NAC. This dose also significantly decreased the sensitization rate of chromium hypersensitivity. In addition, treatment with 1200 mg/kg/day of NAC significantly reduced the H2O2 and MDA levels in the skin and significantly increased the ORAC in the plasma of albino GP. Therefore, NAC could be a potential chemopreventative agent to prevent the progression of chromium hypersensitivity. [source] Energy metabolism and lipid peroxidation of human erythrocytes as a function of increased oxidative stressFEBS JOURNAL, Issue 3 2000Barbara Tavazzi To study the influence of oxidative stress on energy metabolism and lipid peroxidation in erythrocytes, cells were incubated with increasing concentrations (0.5,10 mm) of hydrogen peroxide for 1 h at 37 °C and the main substances of energy metabolism (ATP, AMP, GTP and IMP) and one index of lipid peroxidation (malondialdehyde) were determined by HPLC on cell extracts. Using the same incubation conditions, the activity of AMP-deaminase was also determined. Under nonhaemolysing conditions (at up to 4 mm H2O2), oxidative stress produced, starting from 1 mm H2O2, progressive ATP depletion and a net decrease in the intracellular sum of adenine nucleotides (ATP + ADP + AMP), which were not paralleled by AMP formation. Concomitantly, the IMP level increased by up to 20-fold with respect to the value determined in control erythrocytes, when cells were challenged with the highest nonhaemolysing H2O2 concentration (4 mm). Efflux of inosine, hypoxanthine, xanthine and uric acid towards the extracellular medium was observed. The metabolic imbalance of erythrocytes following oxidative stress was due to a dramatic and unexpected activation of AMP-deaminase (a twofold increase of activity with respect to controls) that was already evident at the lowest dose of H2O2 used; this enzymatic activity increased with increasing H2O2 in the medium, and reached its maximum at 4 mm H2O2 -treated erythrocytes (10-fold higher activity than controls). Generation of malondialdehyde was strictly related to the dose of H2O2, being detectable at the lowest H2O2 concentration and increasing without appreciable haemolysis up to 4 mm H2O2. Besides demonstrating a close relationship between lipid peroxidation and haemolysis, these data suggest that glycolytic enzymes are moderately affected by oxygen radical action and strongly indicate, in the change of AMP-deaminase activity, a highly sensitive enzymatic site responsible for a profound modification of erythrocyte energy metabolism during oxidative stress. [source] Hepatoprotective activity of picroliv, curcumin and ellagic acid compared to silymarin on paracetamol induced liver toxicity in miceFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2009C. Girish Abstract Oxidative stress is implicated as a common pathologic mechanism contributing to the initiation and progression of hepatic damage in a variety of liver disorders. Present study attempts to evaluate the hepatoprotective activity of picroliv, curcumin and ellagic acid in comparison to silymarin using paracetamol (PCM) induced acute liver damage. Hepatotoxicity was induced by administering a single oral dose of PCM (500 mg/kg) and was assessed by quantifying the serum enzyme activities, phenobarbitone induced sleeping time and histopathological analysis of liver tissues. The antioxidant parameters, malondialdehyde (MDA), reduced glutathione (GSH) and catalase of the liver tissue were also assessed. The herbal drugs were administered for 7 days by oral route at 50 and 100 mg/kg. PCM induced hepatic damage was manifested by a significant increase in the activities of marker enzymes (alanine transaminase, aspartate transaminase and alkaline phosphatase) in serum and MDA level in liver. There was also a significant decrease in activity of GSH and catalase levels. The histopathological examination on toxic models revealed centrizonal necrosis and fatty changes. Pretreatment of mice with picroliv, curcumin and ellagic acid reversed these altered parameters towards normal values, which were compared with silymarin. The normalization of phenobarbitone induced sleeping time suggests the restoration of liver cytochrome P450 enzymes. This study supports the use of these active phytochemicals against toxic liver injury, which may act by preventing the lipid peroxidation and augmenting the antioxidant defense system or regeneration of hepatocytes. These active phytochemicals may be developed as drugs for the treatment of liver diseases. [source] Possible involvement of GABAergic modulation in the protective effect of gabapentin against immobilization stress-induced behavior alterations and oxidative damage in miceFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2007Anil Kumar Abstract Introduction Acute stress may be experienced in response to an immediate physical, emotional or psychological stimulus. Stress has been known to affect several brain activities and promote long-term changes in multiple neural systems. In the present study, we investigated the possible involvement of GABAergic modulation in the protective effect of gabapentin in acute immobilization-induced behavioral alterations and oxidative damage in mice. Materials and methods Mice were immobilized for periods of 6 h. Animals were divided into different groups, consisting of six in each. Various GABAergic modulators were administered either alone or in their combinations, 30 min before subjecting the animals for immobilization stress. Various behavioral tests (mirror chamber, actophotometer) followed by oxidative parameters (malondialdehyde level, glutathione, catalase, nitrite and protein) were assessed in animals. Results Six hours acute immobilization stress caused significant locomotor impairment, anxiety-like behavior in mice. Biochemical analyses also revealed an increase malondialdehyde, nitrite level and depletion of glutathione and catalase activity in 6 h stressed brains. Pretreatment with gabapentin (50 and 100 mg/kg, i.p.) significantly improved ambulatory movements, anti-anxiety effect (decreased time latency to enter in mirror chamber, increased number of entries and duration in mirror chamber) and antioxidative activity in stressed mice (P < 0.05). Further, picrotoxin (1.0 mg/kg) blocked and muscimol (0.05 mg/kg) potentiated the protective action of gabapentin (50 mg/kg). Results of both behavior as well as biochemical alterations in combination studies were significant as compared to their effect per se (P < 0.05). Conclusion Results of present study suggest GABAergic modulation might be involved in the protective effect of gabapentin against immobilization-induced behavior alteration and oxidative damage in mice. [source] | ||||||||||||||||||||||||||||||||||||||||