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Antioxidant Effects (antioxidant + effects)

Distribution by Scientific Domains

Medical Sciences	41%
Chemistry	33%
Life Sciences	25%

Selected Abstracts

Evaluation of Antioxidant Effects of Raisin Paste in Cooked Ground Beef, Pork, and Chicken

JOURNAL OF FOOD SCIENCE, Issue 4 2006
M.N. Vasavada
ABSTRACT:, The objective of this study was to evaluate the possible antioxidant activity of raisin paste added to raw ground beef, pork, or chicken before cooking to 163 °C. Samples were held at 2 °C for up to 14 d. TBA values were measured using a distillation method, to avoid yellow color interference found in "wet" TBA methods. Sample meat flavor intensity, rancid flavor intensity, and raisin flavor intensity were evaluated by a trained panel (n = 6). Addition of raisin paste lowered (p < 0.05) TBA values and decreased panel scores for rancid flavor scores of all meat samples in a concentration-dependent manner. Highest antioxidant effects were obtained with a minimum of 1.5%, 2.0%, or 2.0% raisin paste in cooked ground beef, pork, or chicken, respectively. There was a high correlation (0.93, 0.94, 0.94) between TBA values and sensory rancid flavor scores in beef, pork, and chicken samples respectively. Addition of a reducing sugar (glucose) was nearly as effective as raisins for maintenance of low TBA values and rancid flavor scores, probably due to antioxidant effects of Maillard browning products. There was no detectable raisin flavor in cooked ground beef samples with added raisins. However, all meats with added glucose had a higher raisin flavor intensity score than controls, indicating that panelists associated sweetness with raisin flavor. Maillard browning (sample darkening) was evident after cooking of ground chicken with either raisins or glucose. [source]

The alpha-amino group of l -arginine mediates its antioxidant effect

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2001
S. Wallner
Antioxidant effects may constitute part of the possible antiatherogenic effects of the amino acid l -arginine. These antioxidant properties were further characterized in a model of lipoprotein oxidation. Oxidation of lipoproteins in unfractionated human serum was continuously monitored by a fluorescent probe. The antioxidant effects of l -arginine, N -,-acetyl-arginine and vitamin E in combination with l -arginine were measured after initiation of free radical generation with either copper or 2,2,-azobis(2-amidinopropane) hydrochloride (AAPH). The half-time of the fast propagation rate for copper-induced lipoprotein oxidation increased after incubation with l -arginine in a dose-dependent manner (P < 0·01). N -,-acetyl-arginine did not show such effects. Vitamin E and l -arginine show different effects on copper-induced oxidation, the former increasing only lag-time, the latter increasing only propagation rate, and do not have reciprocal effects. In contrast to copper-induced oxidation, l -arginine increased the lag-time of AAPH-induced lipoprotein oxidation (P < 0·01), with no effect on the propagation rate at physiological concentrations. Again, N -,-acetyl-arginine did not show any antioxidant effects. Our experiments provide further evidence that mechanisms other than serving as a substrate for the NO-synthase could be involved in the antiatherosclerotic effect of l -arginine. In addition, our experiments clearly show, that the antioxidant effect of l -arginine is due to a chemical moiety different from that serving as the substrate for NO biosynthesis. [source]

Serum paraoxonase activity before and after treatment of thyrotoxicosis

CLINICAL ENDOCRINOLOGY, Issue 1 2004
Farbod Raiszadeh
Summary objective, Antioxidant effects of paraoxonase, a high density lipoprotein (HDL)-associated enzyme that inhibits low density lipoprotein cholesterol (LDL-C) oxidation in human serum, have been reported. Patients with thyroid dysfunction are more susceptible to oxidative stress, and may show enhanced LDL-C oxidation. The purpose of this study was to evaluate serum paraoxonase activity in patients with hyperthyroidism before and after treatment with methimazole (MMI). design and patients, Twenty-four hyperthyroid patients (15 women and nine men, aged 43·0 ± 12·9 years) and 23 age- and sex-matched healthy controls were studied. Serum paraoxonase activity, lipid, lipoprotein and apolipoprotein levels were measured in fasting samples. Patients were treated with MMI 20,30 mg daily for the first month, and 5,10 mg daily thereafter, and re-evaluated after 6,9 months of treatment. results, Significantly lower serum paraoxonase activity was present in hyperthyroid patients before treatment compared with the controls (43·4 ± 21·9 vs. 72·6 ± 41·2 U/ml, P < 0·005). After a mean follow-up of 7·3 months, 15 patients became euthyroid (treated) and nine were still hyperthyroid. After follow-up, serum paraoxonase activity had increased to 62·2 ± 37·4 U/ml in those who became euthyroid (P < 0·05 compared with baseline). In patients who were still hyperthyroid serum paraoxonase was unchanged from baseline, at 43·2 ± 23·2 U/ml. conclusion, Serum paraoxonase is reduced in patients with hyperthyroidism and reverts to normal after euthyroidism is attained. Reduced serum paraoxonase activity in thyrotoxicosis might predispose lipids to oxidation. [source]

Metformin decreases platelet superoxide anion production in diabetic patients

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2002
P. Gargiulo
Abstract Background Patients with type 2 diabetes mellitus are usually treated with oral antidiabetic agents but it is still not known whether these drugs have antioxidant effects in humans. Methods We studied 60 patients with type 2 diabetes mellitus, divided into three groups on the basis of hypoglycaemic treatment (Group A: metformin, Group B: glibenclamide, Group C: diet). All patients were followed for at least 1 year. The three subgroups had similar clinical characteristics. Twenty healthy subjects, of comparable sex and age, were enrolled as controls. In each subject, platelet production of superoxide anion (O2,) elicited by collagen, was determined by lucigenin assay. Results Patients with diabetes had higher platelet O2, production than controls; no correlation was observed between blood glucose and platelet O2, production. Group A patients had platelet O2, production similar to that of healthy subjects but lower than Group B and Group C patients. Conclusion The present findings suggest an in vivo antioxidant activity of metformin and warrant prospective studies to further explore this hypothesis. Copyright © 2002 John Wiley & Sons, Ltd. [source]

Structure,activity relationships of isoeugenol-based chlorophenylpiperazine derivatives on serotonergic/adrenergic receptor, platelet aggregation, and lipid peroxidation

DRUG DEVELOPMENT RESEARCH, Issue 5 2010
Kuo-Ping Shen
Abstract Three isoeugenol-based eugenosedin chlorphenylpiperazine derivatives, Eu-A, Eu-B, and Eu-C, were synthesized and tested for their serotonergic, adrenergic antagonist, antioxidant, and anti-aggregation activities. In radioligand binding assays, all three agents displayed significant binding affinities on ,1, ,2, ,1, 5-HT1B, and 5-HT2A receptors. In human platelet, they inhibited epinephrine and 5-HT-induced aggregation, and in human platelet with ,2 and 5-HT2A receptors they had a competitive binding effect. Eu-B and Eu-C were more potent than Eu-A. All compounds had antioxidant effects derived from aryloxypropanolamine. Eu- A, Eu-B, or Eu-C (1, 3, 5,mg/kg iv) given to normotensive Wistar rats produced a dose-dependent decrease in mean arterial blood pressure and heart rate and when injected into the cisternum, Eu-A, Eu-B, or Eu-C (0.3, 0.03,µmol) increased blood pressure within 15,min. Pretreatment with any of the three agents inhibited clonidine (38,pmol)-induced hypotension. In vitro experiments, Eu-A, Eu-B, or Eu-C (1, 10, and 100,µM) competitively antagonized norepinephrine-, clonidine-, and 5-HT (10,8,10,4,M)-induced vasocontraction in isolated rat aorta, and competitively antagonized isoproterenol (10,8,10,4,M)-induced positive inotropic effects in a concentration-dependent manner in the isolated rat left atrium. In isolated rabbit ear arteries sensitized with 16,mM K+, all three agents antagonized 5-nonyloxytryptamine- and 5-HT-induced vasocontractions. These findings show that Eu-A, Eu-B, and Eu-C possess functional ,1, ,2, ,1, 5-HT1B, and 5-HT2A receptor blocking activities. In conclusion, the changes in the position of chloride at phenylpiperazine influenced the serotonergic receptor, adrenoceptor antagonistic activities, but not anti-aggregation and antioxidant activities. Drug Dev Res 71:1,9, 2010. © 2010 Wiley-Liss, Inc. [source]

Influence of lipophilicity and stereochemistry at the C7 position on the cardioprotective and antioxidant effect of ginkgolides during rat heart ischemia and reperfusion,

DRUG DEVELOPMENT RESEARCH, Issue 3 2005
Ludovic Billottet
Abstract The extent to which the cardioprotective effect of ginkgolides is related to their lipophilicity rather than to their anti-platelet activating factor (PAF) effect was addressed in isolated rat hearts submitted to ischemia and reperfusion. A new derivative of ginkgolide C (1), the 7-,- O -(4-methylphenyl) ginkgolide C (4) was synthesized and compared to 7- O -(4-methylphenyl) ginkgolide C (2) that had the same absolute configuration at C7 as 1 for its lipophilicity, anti-PAF activity, and cardioprotective and antioxidant effects. Using reversed-phase high-performance liquid chromatography HPLC, 4 and 2 were found to be significantly more lipophilic (i.e., log kw of 3.42±0.05 and 3.64±0.07, respectively) than 1 (1.15±0.03) and the strong PAF inhibitor ginkgolide B (GkB; 1.65±0.03). The anti-PAF activities (IC50 values in ,M) were 8.2, 17.1, and 2.2 for 4, 1, and GkB, respectively, while 2 was inactive. In preischemic and/or reperfused hearts perfused with ginkgolides at 0.7 ,M: (i) 2 and 4 were more efficient in improving postischemic hemodynamic and metabolic recovery than 1, (ii) a key-step in cardioprotection occurred during ischemia where 2 and 4 limited myocardial ATP depletion and contracture development, (iii) a strong anti-lipoperoxidant effect was observed with 2 and 4, but not 1. In vivo administration of 2 to rats (4 mg/kg/day for 20 days) was more effective than that of 1 regarding ischemic heart protection, suggesting a positive role for lipophilicity. It was concluded that a high lipophilicity is not an absolute prerequisite for a strong anti-PAF effect for ginkgolides, whereas it appears essential for cardioprotection. Drug Dev. Res. 64:157,171, 2005. © 2005 Wiley-Liss, Inc. [source]

The alpha-amino group of l -arginine mediates its antioxidant effect

Detoxification and antioxidant effects of curcumin in rats experimentally exposed to mercury

JOURNAL OF APPLIED TOXICOLOGY, Issue 5 2010
Rakhi Agarwal
Abstract Curcumin, a safe nutritional component and a highly promising natural antioxidant with a wide spectrum of biological functions, has been examined in several metal toxicity studies, but its role in protection against mercury toxicity has not been investigated. Therefore, the detoxification and antioxidant effects of curcumin were examined to determine its prophylactic/therapeutic role in rats experimentally exposed to mercury (in the from of mercuric chloride-HgCl2, 12,µmol,kg,1 b.w. single intraperitoneal injection). Curcumin treatment (80,mg,kg,1 b.w. daily for 3 days, orally) was found to have a protective effect on mercury-induced oxidative stress parameters, namely, lipid peroxidation and glutathione levels and superoxide dismutase, glutathione peroxidase and catalase activities in the liver, kidney and brain. Curcumin treatment was also effective for reversing mercury-induced serum biochemical changes, which are the markers of liver and kidney injury. Mercury concentration in the tissues was also decreased by the pre/post-treatment with curcumin. However, histopathological alterations in the liver and kidney were not reversed by curcumin treatment. Mercury exposure resulted in the induction of metallothionein (MT) mRNA expressions in the liver and kidney. Metallothionein mRNA expression levels were found to decrease after the pre-treatment with curcumin, whereas post-treatment with curcumin further increased MT mRNA expression levels. Our findings suggest that curcumin pretreatment has a protective effect and that curcumin can be used as a therapeutic agent in mercury intoxication. The study indicates that curcumin, an effective antioxidant, may have a protective effect through its routine dietary intake against mercury exposure. [source]

Protective effects of quercetin on ultraviolet A light-induced oxidative stress in the blood of rat

JOURNAL OF APPLIED TOXICOLOGY, Issue 5 2002
Ahmet Kahraman
Abstract The oxidative effects of ultraviolet A (UVA) light (320,400 nm) and the antioxidant effects of quercetin were examined in rat blood. For this purpose, rats were divided into three groups: control, ultraviolet (UV) and ultraviolet + quercetin (UV + Q). The UV and UV + Q groups were irradiated for 4 h a day with UVA light (1.25 mW cm2) during periods of 3, 6 and 9 days. Quercetin (50 mg kg,1 body wt.) was administered intraperitoneally in the UV + Q group rats before irradiation periods. Blood was taken 3, 6 and 9 days post-treatment. Plasma malondialdehyde (MDA) levels significantly increased after 9 days of daily exposure to UVA. Whole blood glutathione (GSH) levels significantly declined after 3,9 days of irradiation. Glutathione peroxidase activity on days 6 and 9 and glutathione reductase activities on days 3, 6 and 9 post-irradiation were diminished significantly. Superoxide dismutase and catalase activities decreased significantly 3,9 days post-irradiation. The administration of quercetin before the 9-day period of irradiation significantly reduced the increase in plasma MDA value. Whole blood GSH levels significantly decreased with the administration of quercetin on all days. Quercetin significantly increased antioxidant enzymes diminished by UVA irradiation. Exposure of rats to UVA light leads to oxidative stress, reflected by increased MDA and reduced antioxidant enzyme levels. The administration of quercetin appears to be a useful approach to reduce the damage produced by UVA radiation. Copyright © 2002 John Wiley & Sons, Ltd. [source]

Antilipoperoxidative and antioxidant effects of S-allyl cysteine sulfoxide on isoproterenol-induced myocardial infarction in wistar rats

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 4 2006
T. Sangeetha
Abstract Our study evaluates the preventive effect of S-allyl cysteine sulfoxide (SACS) on lipid peroxidative products and enzymic and nonenzymic antioxidants in isoproterenol (ISO) induced myocardial infarction in rats. The male Wistar rats were rendered myocardial infarction by ISO (150 mg kg,1, once a day for two days). The concentrations of thiobarbituric acid reactive substances and lipid hydroperoxides were increased in hearts from ISO-treated rats, whereas the content of enzymic and nonenzymic antioxidants were declined in rats administered ISO. Oral pretreatment with SACS (40 mg kg,1 and 80 mg kg,1 daily for a period of 35 days) significantly (p < 0.05) decreased the lipid peroxidative products and significantly (p < 0.05) increased antioxidants in ISO-induced rats. Oral administration of SACS (40 mg kg,1 and 80 mg kg,1) did not show any significant effect in normal rats. Thus, the present study shows that SACS exhibits antilipoperoxidative and antioxidant effects in experimental myocardial infarction. © 2006 Wiley Periodicals, Inc. J Biochem Mol Toxicol 20:167,173, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20132 [source]

Different protective actions of losartan and tempol on the renal inflammatory response to acute sodium overload

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2010
María I. Rosón
The aim of this work was to study the role of local intrarenal angiotensin II (Ang II) and the oxidative stress in the up-regulation of pro-inflammatory cytokines expression observed in rats submitted to an acute sodium overload. Sprague,Dawley rats were infused for 2,h with isotonic saline solution (Control group) and with hypertonic saline solution alone (Na group), plus the AT1 receptor antagonist losartan (10,mg,kg,1 in bolus) (Na,Los group), or plus the superoxide dismutase mimetic tempol (0.5,mg,min,1,kg,1) (Na,Temp group). Mean arterial pressure, glomerular filtration rate, and fractional sodium excretion (FENa) were measured. Ang II, NF-,B, hypoxia inducible factor-1, (HIF-1,), transforming growth factor ,1 (TGF-,1), smooth muscle actin (,-SMA), endothelial nitric oxide synthase (eNOS), and RANTES renal expression was evaluated by immunohistochemistry. Ang II, NF-,B, and TGF-,1 and RANTES early inflammatory markers were overexpressed in Na group, accompanied by enhanced HIF-1, immunostaining, lower eNOS expression, and unmodified ,-SMA. Losartan and tempol increased FENa in sodium overload group. Although losartan reduced Ang II and NF-,B staining and increased eNOS expression, it did not restore HIF-1, expression and did not prevent inflammation. Conversely, tempol increased eNOS and natriuresis, restored HIF-1, expression, and prevented inflammation. Early inflammatory markers observed in rats with acute sodium overload is associated with the imbalance between HIF-1, and eNOS expression. While both losartan and tempol increased natriuresis and eNOS expression, only tempol was effective in restoring HIF-1, expression and down-regulating TGF-,1 and RANTES expression. The protective role of tempol, but not of losartan, in the inflammatory response may be associated with its greater antioxidant effects. J. Cell. Physiol. 224:41,48, 2010 © 2010 Wiley-Liss, Inc. [source]

Effects of a Brazilian herbal compound as a cosmetic eyecare for periorbital hyperchromia ("dark circles")

JOURNAL OF COSMETIC DERMATOLOGY, Issue 2 2009
Samara Eberlin PhD
Summary Background, Evidence suggests that periorbital hyperchromia (dark circles) occurs mainly as a consequence of postinflammatory hemodynamic congestion producing a typical bruising aspect on the lower eyelids. Aims, To evaluate the clinical effects of Pfaffia paniculata/Ptychopetalum olacoides B./Lilium candidum L.-associated compound (PPLAC) on periorbital hyperchromia and to study in vitro its underlying anti-inflammatory and antioxidant mechanisms. Methods, Twenty-one volunteers presenting with periorbital hyperchromia received a serum sample containing 5.0% PPLAC, which was applied topically in the periorbital area twice a day for 28 days. Skin color was measured using variations in the individual typological angle (,ITA0) and skin luminance (,L*) calculated in the area around the eyes and in the adjacent area. Colorimetric readings were taken at the onset and end of the 28-day treatment. Volunteers were also asked to fill out a questionnaire concerning the improvement in "dark circles." The anti-inflammatory and antioxidant effects of PPLAC were measured by quantification of prostaglandin E2, leukotriene B4, histamine, and superoxide dismutase levels using an in vitro model of human skin culture. Results, Topical application of PPLAC led to a significant improvement in skin luminance and tone in the periorbital area, which was demonstrated by increased values of ITA0 and L* in about 90% of volunteers. In addition, subjects reported reduced intensity and improved appearance of "dark circles." A dose-dependent decreased production of inflammatory mediators, concomitant to increased antioxidant enzyme levels, was observed in our in vitro studies, under basal and lipopolysaccharide-stimulated conditions. Conclusions, Although the precise mechanisms related to PPLAC remain to be clarified, our results indicate that the reduction in the inflammatory process as well as the antioxidant protection against deleterious elements may be considered as an integral approach to preserve the integrity of vascular endothelium, preventing the hemodynamic congestion that culminates in the formation of "dark circles" around the eyes. [source]

A 90-D Toxicity Study of,Monascus -Fermented Products Including High Citrinin Level

JOURNAL OF FOOD SCIENCE, Issue 5 2010
Chun-Hsien Lee
Abstract:,Monascus,is one of the traditional fermentation fungi and has been used in many kinds of food for thousands of years. Although,Monascus -fermented red mold rice performs cholesterol-lowering effects, blood pressure-lowing effects, and antioxidant effects, another metabolite, nephrotoxic and hepatotoxic citrinin, causes the concerns for safety. Various citrinin concentrations (1, 2, 10, 20, and 200 ppm) in the red mold rice are, respectively, estimated for safe use in animal tests. According to the results of serum biochemistry assays of liver and kidney in each group, citrinin did not reveal any nephrotoxicity and hepatotoxicity. Furthermore, the results of histopathological slices of liver and kidney in each group did not show any significant differences from control histopathological findings. As a result, we presume that citrinin concentrations in,Monascus -fermented products within 200 ppm will not affect the functions of liver and kidney or cause any nephrotoxicity and hepatotoxicity. According to safety factor, it is proposed that 2 ppm citrinin in,Monascus -fermented products may be a safe concentration. [source]

Evaluation of Garam Masala Spices and Phosphates as Antioxidants in Cooked Ground Beef

JOURNAL OF FOOD SCIENCE, Issue 5 2006
Mihir N. Vasavada
ABSTRACT:, This study determined antioxidant effects and sensory attributes of individual ingredients (black pepper, caraway, cardamom, chili powder, cinnamon, cloves, coriander, cumin, fennel, ginger, nutmeg, salt, star anise) of an Indian spice blend (garam masala) in cooked ground beef. Thiobarbituric acid (TBA) values were measured as an indicator of rancidity for cooked samples on 1-, 8-, or 15-d refrigerated storage. Cooked samples were evaluated by a trained panel (n= 13) for the intensity of rancid odor/flavor, beef flavor, and spice flavor and correlated with TBA values of same day samples. We also investigated possible additive effects between spice antioxidants and iron binding (type II) antioxidants on lipid oxidation by measuring TBA values. All spices had antioxidant effects on cooked ground beef, compared to controls. Among spices, cloves were the most effective in controlling lipid oxidation, with TBA values of 0.75, after 15-d refrigerated storage. All spices at their recommended levels lowered rancid odor and flavor in cooked ground beef, compared to controls. As expected, most spices also imparted distinctive flavors to cooked ground beef. There was a positive correlation (0.77) between TBA values on 15-d refrigerated storage and rancid odor/flavor. Type II antioxidants (iron-binding phosphate compounds) were more effective than individual type I antioxidants (spices and butylated hydroxytoluene; BHT) for maintenance of low TBA values in cooked ground beef during storage. Additive effects were observed with rosemary + milk mineral or sodium tripolyphosphate (STP) compared to rosemary alone. [source]

Evaluation of Antioxidant Effects of Raisin Paste in Cooked Ground Beef, Pork, and Chicken

Necrostatin-1 protects against glutamate-induced glutathione depletion and caspase-independent cell death in HT-22 cells

JOURNAL OF NEUROCHEMISTRY, Issue 5 2007
Xingshun Xu
Abstract Glutamate, a major excitatory neurotransmitter in the CNS, plays a critical role in neurological disorders such as stroke and Parkinson's disease. Recent studies have suggested that glutamate excess can result in a form of cell death called glutamate-induced oxytosis. In this study, we explore the protective effects of necrostatin-1 (Nec-1), an inhibitor of necroptosis, on glutamate-induced oxytosis. We show that Nec-1 inhibits glutamate-induced oxytosis in HT-22 cells through a mechanism that involves an increase in cellular glutathione (GSH) levels as well as a reduction in reactive oxygen species production. However, Nec-1 had no protective effect on free radical-induced cell death caused by hydrogen peroxide or menadione, which suggests that Nec-1 has no antioxidant effects. Interestingly, the protective effect of Nec-1 was still observed when cellular GSH was depleted by buthionine sulfoximine, a specific and irreversible inhibitor of glutamylcysteine synthetase. Our study further demonstrates that Nec-1 significantly blocks the nuclear translocation of apoptosis-inducing factor (a marker of caspase-independent programmed cell death) and inhibits the integration of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (a pro-death member of the Bcl-2 family) into the mitochondrial membrane. Taken together, these results demonstrate for the first time that Nec-1 prevents glutamate-induced oxytosis in HT-22 cells through GSH related as well as apoptosis-inducing factor and Bcl-2/adenovirus E1B 19 kDa-interacting protein 3-related pathways. [source]

Differential effects of the mitochondrial uncoupling agent, 2,4-dinitrophenol, or the nitroxide antioxidant, Tempol, on synaptic or nonsynaptic mitochondria after spinal cord injury

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2009
Samir P. Patel
Abstract We recently documented the progressive nature of mitochondrial dysfunction over 24 hr after contusion spinal cord injury (SCI), but the underlying mechanism has not been elucidated. We investigated the effects of targeting two distinct possible mechanisms of mitochondrial dysfunction by using the mitochondrial uncoupler 2,4-dinitrophenol (2,4-DNP) or the nitroxide antioxidant Tempol after contusion SCI in rats. A novel aspect of this study was that all assessments were made in both synaptosomal (neuronal)- and nonsynaptosomal (glial and neuronal soma)-derived mitochondria 24 hr after injury. Mitochondrial uncouplers target Ca2+ cycling and subsequent reactive oxygen species production in mitochondria after injury. When 2,4-DNP was injected 15 and 30 min after injury, mitochondrial function was preserved in both populations compared with vehicle-treated rats, whereas 1 hr postinjury treatment was ineffective. Conversely, targeting peroxynitrite with Tempol failed to maintain normal bioenergetics in synaptic mitochondria, but was effective in nonsynaptic mitochondria when administered 15 min after injury. When administered at 15 and 30 min after injury, increased hydroxynonenal, 3-NT, and protein carbonyl levels were significantly reduced by 2,4-DNP, whereas Tempol only reduced 3-NT and protein carbonyls after SCI. Despite such antioxidant effects, only 2,4-DNP was effective in preventing mitochondrial dysfunction, indicating that mitochondrial Ca2+ overload may be the key mechanism involved in acute mitochondrial damage after SCI. Collectively, our observations demonstrate the significant role that mitochondrial dysfunction plays in SCI neuropathology. Moreover, they indicate that combinatorial therapeutic approaches targeting different populations of mitochondria holds great potential in fostering neuroprotection after acute SCI. © 2008 Wiley-Liss, Inc. [source]

Estrogen attenuated markers of inflammation and decreased lesion volume in acute spinal cord injury in rats

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2005
Eric Anthony Sribnick
Abstract Spinal cord injury (SCI) is a devastating neurologic injury with functional deficits for which the only currently recommended pharmacotherapy is high-dose methylprednisolone, which has limited efficacy. Estrogen is a multiactive steroid that has shown antiinflammatory and antioxidant effects, and estrogen may modulate intracellular Ca2+ and attenuate apoptosis. For this study, male rats were divided into three groups. Sham group animals received a laminectomy at T12. Injured rats received both laminectomy and 40 g · cm force SCI. Estrogen-group rats received 4 mg/kg 17,-estradiol (estrogen) at 15 min and 24 hr post-injury, and vehicle-group rats received equal volumes of dimethyl sulfoxide (vehicle). Animals were sacrificed at 48 hr post-injury, and 1-cm-long segments of the lesion, rostral penumbra, and caudal penumbra were excised. Inflammation was assessed by examining tissue edema, infiltration of macrophages/microglia, and levels of cytosolic and nuclear NF,B and inhibitor of kappa B (I,B,). Myelin integrity was examined using Luxol fast blue staining. When compared to sham, vehicle-treated animals revealed increased tissue edema, increased infiltration of inflammatory cells, decreased cytosolic levels of NF,B and I,B,, increased levels of nuclear NF,B, and increased myelin loss. Treatment of SCI rats with estrogen reduced edema and decreased inflammation and myelin loss in the lesion and penumbral areas, suggesting its potential as a therapeutic agent. Further work needs to be done, however, to elucidate the neuroprotective mechanism of estrogen. © 2005 Wiley-Liss, Inc. [source]

Hepatoprotective and antioxidant effects of gallic acid in paracetamol-induced liver damage in mice

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 5 2010
Mahaboob Khan Rasool
Abstract Objectives The aim of this research paper was to investigate the hepatoprotective and antioxidant effects of gallic acid in paracetamol-induced liver damage in mice. Methods In the present study, the hepatoprotective and antioxidant effects of gallic acid were evaluated against paracetamol-induced hepatotoxicity in mice and compared with the silymarin, a standard hepatoprotective drug. The mice received a single dose of paracetamol (900 mg/kg body weight i.p.). Gallic acid (100 mg/kg body weight i.p.) and silymarin (25 mg/kg body weight i.p.) were administered 30 min after the injection of paracetamol. After 4 h, liver marker enzymes (aspartate transaminase, alanine transaminase and alkaline phosphatase) and inflammatory mediator tumour necrosis factor-alpha (TNF-,) were estimated in serum, while the lipid peroxidation and antioxidant status (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione- S -transferase and glutathione) were determined in liver homogenate of the control and experimental mice. Key findings Increased activities of liver marker enzymes and elevated TNF-, and lipid peroxidation levels were observed in mice exposed to paracetamol (P < 0.05), whereas the antioxidant status was found to be depleted (P < 0.05) when compared with the control group. However gallic acid treatment (100 mg/kg body weight i.p.) significantly reverses (P < 0.05) the above changes by its antioxidant action compared to the control group as observed in the paracetamol-challenged mice. Conclusions The results clearly demonstrate that gallic acid possesses promising hepatoprotective effects. [source]

Astaxanthin, a dietary carotenoid, protects retinal cells against oxidative stress in-vitro and in mice in-vivo

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 10 2008
Yoshimi Nakajima
We have investigated whether astaxanthin exerted neuroprotective effects in retinal ganglion cells in-vitro and in-vivo. In-vitro, retinal damage was induced by 24-h hydrogen peroxide (H2O2) exposure or serum deprivation, and cell viability was measured using a WST assay. In cultured retinal ganglion cells (RGC-5, a rat ganglion cell-line transformed using E1A virus), astaxanthin inhibited the neurotoxicity induced by H2O2 or serum deprivation, and reduced the intracellular oxidation induced by various reactive oxygen species (ROS). Furthermore, astaxanthin decreased the radical generation induced by serum deprivation in RGC-5. In mice in-vivo, astaxanthin (100 mg kg,1, p.o., four times) reduced the retinal damage (a decrease in retinal ganglion cells and in thickness of inner plexiform layer) induced by intravitreal N -methyl- d -aspartate (NMDA) injection. Furthermore, astaxanthin reduced the expressions of 4-hydroxy-2-nonenal (4-HNE)-modified protein (indicator of lipid peroxidation) and 8-hydroxy-deoxyguanosine (8-OHdG; indicator of oxidative DNA damage). These findings indicated that astaxanthin had neuroprotective effects against retinal damage in-vitro and in-vivo, and that its protective effects may have been partly mediated via its antioxidant effects. [source]

Histamine-3 receptor antagonists reduce superoxide anion generation and lipid peroxidation in rat brain homogenates

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 6 2005
H. E. Badenhorst
Using a cyanide model to induce neurotoxic effects in rat brain homogenates, we examined the neuroprotective properties of three H3 antagonists, namely clobenpropit, thioperamide and impentamine, and compared them to aspirin, a known neuroprotective agent. Superoxide anion levels and malondialdehyde concentration were assessed using the nitroblue tetrazolium and lipid peroxidation assays. Clobenpropit and thioperamide significantly reduced superoxide anion generation and lipid peroxidation. Impentamine reduced lipid peroxidation at all concentrations used, but only reduced superoxide anion generation at a concentration of 1 mM. In the lipid peroxidation assay, all the drugs compared favourably to aspirin. This study demonstrates the potential of these agents to be neuroprotective by exerting antioxidant effects. [source]

Potential roles of melatonin and chronotherapy among the new trends in hypertension treatment

JOURNAL OF PINEAL RESEARCH, Issue 2 2009
Fedor Simko
Abstract:, The number of well-controlled hypertensives is unacceptably low worldwide. Respecting the circadian variation of blood pressure, nontraditional antihypertensives, and treatment in early stages of hypertension are potential ways to improve hypertension therapy. First, prominent variations in circadian rhythm are characteristic for blood pressure. The revolutionary MAPEC (Ambulatory Blood Pressure Monitoring and Cardiovascular Events) study, in 3000 adult hypertensives investigates, whether chronotherapy influences the cardiovascular prognosis beyond blood pressure reduction per se. Second, melatonin, statins and aliskiren are hopeful drugs for hypertension treatment. Melatonin, through its scavenging and antioxidant effects, preservation of NO availability, sympatholytic effect or specific melatonin receptor activation exerts antihypertensive and anti-remodeling effects and may be useful especially in patients with nondipping nighttime blood pressure pattern or with nocturnal hypertension and in hypertensives with left ventricular hypertrophy (LVH). Owing to its multifunctional physiological actions, this indolamine may offer cardiovascular protection far beyond its hemodynamic benefit. Statins exert several pleiotropic effects through inhibition of small guanosine triphosphate-binding proteins such as Ras and Rho. Remarkably, statins reduce blood pressure in hypertensive patients and more importantly they attenuate LVH. Addition of statins should be considered for high-risk hypertensives, for hypertensives with LVH, and possibly for high-risk prehypertensive patients. The direct renin inhibitor, aliskiren, inhibits catalytic activity of renin molecules in circulation and in the kidney, thus lowering angiotensin II levels. Furthermore, aliskiren by modifying the prorenin conformation may prevent prorenin activation. At present, aliskiren should be considered in hypertensive patients not sufficiently controlled or intolerant to other inhibitors of renin,angiotensin system. Third, TROPHY (Trial of Preventing Hypertension) is the first pharmacological intervention for prehypertensive patients revealing that treatment with angiotensin II type 1 receptor blocker attenuates hypertension development and thus decreases the risk of cardiovascular events. [source]

Melatonin attenuates ifosfamide-induced Fanconi syndrome in rats

JOURNAL OF PINEAL RESEARCH, Issue 1 2004
Goksel Sener
Abstract:, Regarding the mechanisms of ifosfamide (IFO)-induced nephrotoxicity and hemorrhagic cystitis, several hypotheses have been put forward, among which oxidative stress and depletion of glutathione (GSH) are suggested. This investigation elucidates the role of free radicals in IFO-induced toxicity and the protection by melatonin. Wistar albino rats were injected intraperitoneally with saline (0.9% NaCl; control-C group), melatonin (Mel group; 10 mg/kg daily for 5 days) or ifosfamide (50 mg/kg daily for 5 days; IFO group) or IFO + Mel. On the 5th day (120 hr) after the first IFO dose, animals were killed by decapitation and trunk blood was collected. Kidney and bladder tissues were obtained for biochemical and histological analysis. Urine was collected 24 hr before the rats were killed. The results demonstrated that IFO induced a Fanconi syndrome (FS) characterized by wasting of sodium, phosphate, and glucose, along with increased serum creatinine and urea. Melatonin markedly ameliorated the severity of renal dysfunction induced by IFO with a significant decrease in urinary sodium, phosphate, and glucose and increased creatinine excretion. Moreover, melatonin significantly improved the IFO-induced GSH depletion, malondialdehayde accumulation and neutrophil infiltration in both renal and bladder tissues. In the kidney, Na+,K+ -ATPase activity which was significantly reduced by IFO, was increased with melatonin treatment. Increased collagen contents of the kidney and bladder tissues by IFO treatment were reversed back to the control levels with melatonin. Our results suggest that IFO causes oxidative damage in renal and bladder tissues and melatonin, via its antioxidant effects, protects these tissues. These data suggest that melatonin may be of therapeutic use in preventing acquired FS due to IFO toxicity. [source]

Neuroprotection by melatonin from glutamate-induced excitotoxicity during development of the cerebellum in the chick embryo

JOURNAL OF PINEAL RESEARCH, Issue 2 2000
Auxiliadora Espinar
This work investigated the ability of melatonin to prevent cell damage in the cerebellar cortex of chick embryo caused by glutamate administration. Cell injury was evaluated estimating, at ultrastructural level, the phenomenon of cell death and the synaptogenesis of the Purkinje cells and the cerebellar glomerular synaptic complex. Administration of glutamate during cerebellar development of the chick provokes excitotoxic neuronal degeneration characterized by a phenomenon of neuronal cell death that exhibits essentially the features of a death pattern described as necrosis and the deletion of synaptogenic processes. Our results show that melatonin has a neuroprotective effect against glutamate-induced excitotoxicity. This effect is morphologically revealed by the lack of neural cell death in the embryos treated with melatonin prior to glutamate injection and also by the degree of a synaptogenesis similar to that exhibited by the control group. Likewise, we corroborate the absence of teratological effects of melatonin on chick cerebellar development. Although the possible mechanisms involved in the neuroprotective effect of melatonin are discussed, i.e., direct antioxidant effects, up-regulating endogenous antioxidant defenses, and inhibiting nitric oxide formation activated by glutamate, further studies are required to establish the actual mechanism involved in the neuroprotective effect of melatonin. [source]

Storage affects the phenolic profiles and antioxidant activities of cherries (Prunus avium L) on human low-density lipoproteins

JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 9 2004
Berta Gonçalves
Abstract Four sweet cherry cultivars (cvs), Burlat, Saco, Summit and Van, were analysed at harvest and after storage at 2 and 15 °C for 30 and 6 days respectively. Phenolic profiles in methanolic extracts of freeze-dried samples of the fresh and differently stored cherries were quantified by high-performance liquid chromatography. Hydroxycinnamates dominated in all samples and represented 60,74% by weight of the phenols in the fresh and stored samples of the cvs Saco, Summit and Van, and 45% by weight of the phenols in the cv Burlat samples, which were richer in anthocyanins. The relative and total levels of hydroxycinnamates, anthocyanins, flavonols and flavan-3-ols varied among cultivars and during storage. Storage at 15 °C increased the phenol levels, particularly the cyanidin-3-rutinoside concentration. Cold storage induced decreased total phenol levels in the cvs Summit and Van but increased total phenol levels in the cvs Burlat and Saco. Phenolic cherry extracts inhibited low-density lipoprotein oxidation in vitro in a dose-dependent manner. Extracts of freshly harvested cherries exhibited significantly higher antioxidant activities than extracts of stored samples. The cv Summit samples had the highest antioxidant activity. Differences in the antioxidant effects of the cherry samples were positively correlated with their levels of p -coumaroylquinic acid (p < 0.1) but negatively correlated with their cyanidin-3-rutinoside levels (p < 0.05). Copyright © 2004 Society of Chemical Industry [source]

Hypocholesterolaemic and antioxidant effects of Glycyrrhiza glabra (Linn) in rats

MOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 11 2006
Nishant P. Visavadiya
Abstract The hypocholesterolaemic and antioxidant effects of Glycyrrhiza glabra (GG) root powder were examined in hypercholesterolaemic male albino rats. A 4-week administration of GG root powder (5 and 10 gm% in diet) to hypercholesterolaemic rats resulted in significant reduction in plasma, hepatic total lipids, cholesterol, triglycerides and plasma low-density lipoprotein and VLDL-cholesterol accompanied by significant increases in HDL-cholesterol levels. Furthermore, significant increases in fecal cholesterol, neutral sterols and bile acid excretion along with an increase in hepatic HMG-CoA reductase activity and bile acid production were observed in these animals. The root powder administration to hypercholesterolaemic rats also decreased hepatic lipid peroxidation with a concomitant increase in superoxide dismutase (SOD) and catalase activities and total ascorbic acid content. Thus, the hypocholesterolaemic and antioxidant effects of GG root appeared to be mediated via (i) accelerated cholesterol, neutral sterol and bile acid elimination through fecal matter with an increased hepatic bile acid production and (ii) improving the activities of hepatic SOD, catalase and increasing the ascorbic acid content. The normo-cholesterolaemic animals when fed with GG root powder at 10 gm% level, registered a significant decline in plasma lipid profiles and an increase in HDL-cholesterol content. The antioxidant status of these animals also was improved upon treatment. [source]

Antigenotoxic effect of extract from Cynara cardunculus L.

PHYTOTHERAPY RESEARCH, Issue 1 2008
E. Miadokova
Abstract The extract of artichoke Cynara cardunculus L. (CCE) was investigated for its potential antigenotoxic and antioxidant effects using four experimental model systems. In the Saccharomyces cerevisiae mutagenicity/antimutagenicity assay, CCE significantly reduced the frequency of 4-nitroquinoline- N -oxide-induced revertants at the ilv1 locus and mitotic gene convertants at the trp5 locus in the diploid Saccharomyces cerevisiae tester strain D7. In the simultaneous toxicity and clastogenicity/anticlastogenicity assay, it exerted an anticlastogenic effect against N-nitroso- N,-methylurea-induced clastogenicity in the plant species Vicia sativa L. On the contrary, despite CCE not being mutagenic itself, in the preincubation Ames assay with metabolic activation, it significantly increased the mutagenic effect of 2-aminofluorene in the bacterial strain Salmonella typhimurium TA98. In the 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging assay, CCE exhibited considerable antioxidant activity. The SC50 value representing 0.0054% CCE corresponds to an antioxidant activity of 216.8 µm ascorbic acid which was used as a reference compound. Although the mechanism of CCE action still remains to be elucidated, different possible mechanisms are probably involved in the CCE antigenotoxic effects. It could be concluded that CCE is of particular interest as a suitable candidate for an effective chemopreventive agent. Copyright © 2007 John Wiley & Sons, Ltd. [source]

Hepatoprotective and antioxidant effects of Alnus japonica extracts on acetaminophen-induced hepatotoxicity in rats

PHYTOTHERAPY RESEARCH, Issue 12 2004
Sang Tae Kim
Abstract The stem bark of the Betulaceae plant Alnus japonica, which is indigenous to Korea, has been used as a popular folk medicine for hepatitis and cancer. In this study, the antioxidant activity of the crude extract and the hepatoprotective activities on acetaminophen (AAP)-induced toxicity in the rat liver were evaluated. We investigated the effect of the methanol (AJM) and solvent fracton of the stem bark of Alnus japonica (AJ) on AAP-induced hepatotoxicity in rats. In rat hepatocyte culture, pretreatment with AJM (50, 100, 150 and 200 µg[sol ]ml) significantly decreased the cytotoxicity of AAP in a dose-dependent manner. The pretreated with EtOAc and BuOH fraction led to an increase in free radical scavenging activity and a decrease in inhibition of lipid peroxidation, both superoxide dismutase and catalase prevent the hepatotoxicity by AAP in the treatment of A. japonica fraction. We conclude that AJ is an important antioxidant in AAP-induced live hepatotoxicity and that extract of AJM plays a hepatoprotective effects in the against AAP-induced cytotoxicity in cultured rat hepatocytes in vitro. Pending more evaluation for safety and efficacy, AJ can potentially be used in mitigating AAP-induced hepatotoxicity. Copyright © 2004 John Wiley & Sons, Ltd. [source]

Carbocisteine inhibits oxidant-induced apoptosis in cultured human airway epithelial cells

RESPIROLOGY, Issue 7 2009
Motoki YOSHIDA
ABSTRACT Background and objective: Increased oxidant levels have been associated with exacerbations of COPD, and L-carbocisteine, a mucolytic agent, reduces the frequency of exacerbations. The mechanisms underlying the inhibitory effects of L-carbocisteine on oxidant-induced COPD exacerbations were examined in an in vitro study of human airway epithelial cells. Methods: In order to examine the antioxidant effects of L-carbocisteine, human tracheal epithelial cells were treated with L-carbocisteine and exposed to hydrogen peroxide (H2O2). Cell apoptosis was assessed using a cell death detection ELISA, and the pathways leading to cell apoptosis were examined by measurement of caspase-3 and caspase-9 by western blot analysis with fluorescent detection. Results: The proportion of apoptotic cells in human tracheal epithelium was increased in a concentration- and time-dependent manner, following exposure to H2O2. Treatment with L-carbocisteine reduced the proportion of apoptotic cells. In contrast, H2O2 did not increase the concentration of LDH in supernatants of epithelial cells. Exposure to H2O2 activated caspase-3 and caspase-9, and L-carbocisteine inhibited the H2O2 -induced activation of these caspases. L-carbocisteine activated Akt phosphorylation, which modulates caspase activation, and the inhibitors of Akt, LY294002 and wortmannin, significantly reversed the inhibitory effects of L-carbocisteine on H2O2 -induced cell apoptosis. Conclusions: These findings suggest that in human airway epithelium, L-carbocisteine may inhibit cell damage induced by H2O2 through the activation of Akt phosphorylation. L-carbocisteine may have antioxidant effects, as well as mucolytic activity, in inflamed airways. [source]

Biological effects of a nano red elemental selenium

BIOFACTORS, Issue 1 2001
Jin-Song Zhang
A novel selenium form, nano red elemental selenium (Nano-Se) was prepared by adding bovine serum albumin to the redox system of selenite and glutathione. Nano-Se has a 7-fold lower acute toxicity than sodium selenite in mice (LD50 113 and 15 mg Se/kg body weight respectively). In Se-deficient rat, both Nano-Se and selenite can increase tissue selenium and GPx activity. The biological activities of Nano-Se and selenite were compared in terms of cell proliferation, enzyme induction and protection against free racial-mediated damage in human hepatoma HepG2 cells. Nano-Se and selenite are similarly cell growth inhibited and stimulated synthesis of glutathione peroxidase (GPx), phospholipid hydroperoxide glutathione peroxidase (PHGPx) and thioredoxin reductase (TR). When HepG2 cells were co-treated with selenium and glutathione, Nano-Se showed less pro-oxidative effects than selenite, as measured by cell growth. These results demonstrate that Nano-Se has a similar bioavailability in the rat and antioxidant effects on cells. [source]