Home About us Contact
|
Home About us Contact | ||
|
|
||
Oxygen Free Radicals (oxygen + free_radical)
Selected AbstractsSumatriptan Scavenges Superoxide, Hydroxyl, and Nitric Oxide Radicals: In Vitro Electron Spin Resonance StudyHEADACHE, Issue 9 2002DMSc, Yukio Ikeda MD Background.,The molecular mechanisms of migraine have not yet been clarified. Oxygen free radicals have been implicated in the genesis of many pathological processes, including migraine. Sumatriptan succinate is known to be a very effective drug for acute relief of migraine attack. Objective.,To investigate the direct scavenging activities of sumatriptan for superoxide, hydroxyl, and nitric oxide (NO) radicals using electron spin resonance (ESR) spectroscopy. Methods.,Measurement of superoxide and hydroxyl radical scavenging activities was performed by ESR using 5,5-dimethyl-1-pyrroline- N -oxide as a spin trap. NO was generated from 1-hydroxy-2-oxo-3-(N -3-methyl-3-aminopropyl)-3-methyl-1-triazene and analyzed by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl produced from the reaction between 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide and NO. Results.,The ESR study demonstrated that sumatriptan scavenged superoxide, hydroxyl, and NO in a dose-dependent manner. Conclusion.,Sumatriptan has direct scavenging activity on free radicals and NO. Acute migraine drugs with antioxidant properties may provide heretofore unheralded benefits via this mechanism. [source] Measurement of free radicals and NO by chemiluminescence to identify the reperfusion injury in renal transplantationLUMINESCENCE: THE JOURNAL OF BIOLOGICAL AND CHEMICAL LUMINESCENCE, Issue 2 2002S. Oehlschläger Abstract Oxygen free radicals are generated during the reperfusion of ischaemic organs. Several experimental studies have demonstrated that the damage produced by reperfusion can be prevented by a scavenger of free radicals. Furthermore, a significantly improved 5 year graft survival rate after cadaveric renal transplantation has been reported in patients treated with scavengers of free radicals (Land et al., 1993). Therefore, a question remains to be answered: whether a routine monitoring of the radical-mediated reperfusion injury with renal transplantation is useful, and whether there is a necessity for a generalized protective treatment in transplant patients. In a prospective trial, we evaluated a group of eight patients during and after renal cadaveric transplantation (three men, five women), using the chemiluminometric measurement of serum free radicals and NO. The serum quantities of free radicals and NO were significantly increased after reperfusion of the transplant kidney (p,<,0.02). The mean time of noticeably increased levels of serum free radicals was 4.8,±,1.2,h after reperfusion. The results thus showed an increased liberation of free radicals in the peripheral blood of transplant recipients as possible evidence of free radicals-mediated reperfusion injury in renal transplantation. The generation of free radicals measured by chemiluminescence allow a controlled therapy to decrease the generation of free radicals with antioxidants during the early transplantation period e.g. in older recipients. Copyright © 2002 John Wiley & Sons, Ltd. [source] Effects of electromagnetic radiation from a cellular telephone on the oxidant and antioxidant levels in rabbitsCELL BIOCHEMISTRY AND FUNCTION, Issue 4 2002M. Kemal Irmak Abstract The number of reports on the effects induced by electromagnetic radiation (EMR) in various cellular systems is still increasing. Until now no satisfactory mechanism has been proposed to explain the biological effects of this radiation. Oxygen free radicals may play a role in mechanisms of adverse effects of EMR. This study was undertaken to investigate the influence of electromagnetic radiation of a digital GSM mobile telephone (900,MHz) on oxidant and antioxidant levels in rabbits. Adenosine deaminase, xanthine oxidase, catalase, myeloperoxidase, superoxide dismutase (SOD) and glutathione peroxidase activities as well as nitric oxide (NO) and malondialdehyde levels were measured in sera and brains of EMR-exposed and sham-exposed rabbits. Serum SOD activity increased, and serum NO levels decreased in EMR-exposed animals compared to the sham group. Other parameters were not changed in either group. This finding may indicate the possible role of increased oxidative stress in the pathophysiology of adverse effect of EMR. Decreased NO levels may also suggest a probable role of NO in the adverse effect. Copyright © 2002 John Wiley & Sons, Ltd. [source] Airway function in infants treated with inhaled nitric oxide for persistent pulmonary hypertensionPEDIATRIC PULMONOLOGY, Issue 3 2008Aparna U. Hoskote MD Abstract Rationale Inhaled nitric oxide (iNO), used for treatment of persistent pulmonary hypertension of newborn (PPHN), is an oxygen free radical with potential for lung injury. Deferring ECMO with iNO in these neonates could potentially have long-term detrimental effects on lung function. We studied respiratory morbidity (defined as occurrence of respiratory infections requiring treatment, episodes of wheezing, and/or need for ongoing medications following discharge) and airway function at 1 year postnatal age in term neonates treated with iNO but not ECMO for PPHN, and compared data from similar infants recruited to the UK ECMO Trial randomized to receive ECMO or conventional management (CM). Methods Maximal expiratory flow at FRC (V'maxFRC) was measured in infants treated with iNO for PPHN (oxygenation index ,25) at birth. Results V'maxFRC was measured in 23 infants and expressed as z -scores, to adjust for sex and body size and compared to data from 71 (46 ECMO, 25 CM) infants studied at a similar age in the ECMO Trial. Respiratory morbidity was low in iNO group. V'maxFRCz -score was lower than predicted in all groups (P,<,0.001), with no significant difference between those treated with iNO [mean (SD) z -score: ,1.65 (1.2)] and those treated with ECMO [,1.59 (1.2)] or CM [,2.1(1.0)]. Within iNO, ECMO and CM groups; 26%, 37% and 56%, respectively, had V'maxFRCz -scores below normal. Conclusions Respiratory outcome at 1 year in iNO treated neonates with moderately severe PPHN is encouraging, with no apparent increase in respiratory morbidity when compared to the general population. Sub-clinical reductions in airway function are evident at 1 year, suggesting that continuing efforts to minimize lung injury in the neonatal period are warranted to maximize lung health in later life. Pediatr Pulmonol. 2008; 43:224,235. © 2008 Wiley-Liss, Inc. [source] Comparative mutagenic effects of structurally similar flavonoids quercetin and taxifolin on tester strains Salmonella typhimurium TA102 and Escherichia coli WP-2 uvrAENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 6 2009Patrudu S. Makena Abstract Quercetin (QT) and Taxifolin (TF) are structurally similar plant polyphenols. Both have been reported to have therapeutic potential as anti-cancer drugs and antioxidants. Mutagenic effects of QT and TF were evaluated using Salmonella typhimurium TA102 and Escherichia coli WP-2 uvrA tester strains. Either in the presence or absence of S9 mix, QT was mutagenic to TA102 and WP2 uvrA. However, the mutagenicity of QT was significantly enhanced in the presence of S9 mix. Likewise, in the presence of Iron (Fe2+) and NADPH generating system (NGS) and absence of S9 mix, QT induced significantly high mutations in both TA102 and WP-2 uvrA. Mutagenicity of QT decreased in both strains in the presence of Iron (Fe2+) or NGS alone. TF was not mutagenic in the presence or absence of S9 mix in both TA102 and WP-2 uvrA 2, regardless of the presence of iron or NGS. Incorporation of antioxidants (ascorbate, superoxide dismutase (SOD), catalase (CAT)) and/or iron chelators (desferroxamine (DF) and ethylenediamine-tetraacetate (EDTA)) in the test systems markedly decreased QT-induced mutations in both tester strains. These results suggest that QT but not TF, could induce mutations in the presence or absence of rat liver S9 or Iron (Fe2+) and NGS in both tester strains by redox cycling and Fenton reactions to produce oxygen free radicals. Our results indicate that a minor structural variation between the two plant polyphenols could elicit a marked difference in their genotoxicities. These results provide a basis for further study into the potential use of QT in combination with iron supplements. Environ. Mol. Mutagen. 2009. © 2009 Wiley-Liss, Inc. [source] Complement and its implications in cardiac ischemia/reperfusion: strategies to inhibit complementFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 5 2001Tiphaine Monsinjon Although reperfusion of the ischemic myocardium is an absolute necessity to salvage tissue from eventual death, it is also associated with pathologic changes that represent either an acceleration of processes initiated during ischemia or new pathophysiological changes that were initiated after reperfusion. This so-called ,reperfusion injury' is accompanied by a marked inflammatory reaction, which contributes to tissue injury. In addition to the well known role of oxygen free radicals and white blood cells, activation of the complement system probably represents one of the major contributors of the inflammatory reaction upon reperfusion. The complement may be activated through three different pathways: the classical, the alternative, and the lectin pathway. During reperfusion, complement may be activated by exposure to intracellular components such as mitochondrial membranes or intermediate filaments. Two elements of the activated complement contribute directly or indirectly to damages: anaphylatoxins (C3a and C5a) and the membrane attack complex (MAC). C5a, the most potent chemotactic anaphylatoxin, may attract neutrophils to the site of inflammation, leading to superoxide production, while MAC is deposited over endothelial cells and smooth vessel cells, leading to cell injury. Experimental evidence suggests that tissue salvage may be achieved by inhibition of the complement pathway. As the complement is composed of a cascade of proteins, it provides numerous sites for pharmacological interventions during acute myocardial infarction. Although various strategies aimed at modulating the complement system have been tested, the ideal approach probably consists of maintaining the activity of C3 (a central protein of the complement cascade) and inhibiting the later events implicated in ischemia/reperfusion and also in targeting inhibition in a tissue-specific manner. [source] Molecular phylogenetic evidence for an extracellular Cu Zn superoxide dismutase gene in insectsINSECT MOLECULAR BIOLOGY, Issue 6 2004J. D. Parker Abstract Representatives of three ancient gene families of the antioxidant enzyme superoxide dismutase (SOD) can be found in most metazoans. In mammals and Caenorhabditis elegans, there is at least one gene each of the cytoplasmic, mitochondrial and extracellular lineages of SOD genes. The cytoplasmic SOD was one of the first enzymes to be implicated in ageing due to its protection against damaging oxygen free radicals. In contrast to other metazoans, insects were thought to lack a gene for the extracellular SOD. We have cloned and sequenced an SOD mRNA in the ant Lasius niger that appears to belong to this extracellular family. Subsequent searches and analyses of SOD gene sequences in insect databases revealed that insects do indeed express all three SOD genes including the extracellular form. We conclude that insects as well as other metazoans appear to have the full repertoire of the three families of SOD. [source] Overexpression of human copper/zinc-superoxide dismutase in transgenic animals attenuates the reduction of apurinic/apyrimidinic endonuclease expression in neurons after in vitro ischemia and after transient global cerebral ischemiaJOURNAL OF NEUROCHEMISTRY, Issue 2 2005Purnima Narasimhan Abstract Oxidative stress after ischemia/reperfusion has been shown to induce DNA damage and subsequent DNA repair activity. Apurinic/apyrimidinic endonuclease (APE) is a multifunctional protein in the DNA base excision repair pathway which repairs apurinic/apyrimidinic sites in DNA. We investigated the involvement of oxidative stress and expression of APE in neurons after oxygen,glucose deprivation and after global cerebral ischemia. Our results suggest that overexpression of human copper/zinc-superoxide dismutase reduced oxidative stress with a subsequent decrease in APE expression. Production of oxygen free radicals and inhibition of the base excision repair pathway may play pivotal roles in the cell death pathway after ischemia. [source] Melatonin stimulates glutathione peroxidase activity in human chorionJOURNAL OF PINEAL RESEARCH, Issue 4 2001Yuji Okatani In preeclampsia, placental production of lipid peroxides is abnormally increased, while placental glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities are decreased. Administration of melatonin, a powerful scavenger of oxygen free radicals, also may protect the placenta from free radical-induced damage by increasing the activity of antioxidant enzymes. To test this hypothesis we administered melatonin to pregnant women before they underwent voluntary interruption of pregnancy between 7 and 9 wk of gestation. Melatonin (6 mg) was administered orally at 12:00 hr, and samples of chorion and maternal blood were obtained at the time of the procedure, 1, 2 or 3 hr later. We measured the melatonin concentration in maternal serum and activities of GSH-Px and SOD and levels of melatonin in chorionic homogenates. Melatonin administration was reflected by markedly increased melatonin concentrations in maternal serum and in chorion, with peak levels achieved 1 hr after melatonin administration (serum, 46.87±10.87 nM/L; chorionic homogenate, 4.36±1.56 pmol/mg protein). Between 1 and 3 hr after melatonin administration, GSH-Px activity in chorionic homogenates increased significantly (P<0.001), with peak levels occurring at 3 hr (51.68±3.22 mU/mg protein per min, 137.3% of GSH-Px activity in untreated control subjects). No significant changes in chorionic SOD activity occurred during the 3-hr post-administration period. These results indicate that exogenous melatonin increases GSH-Px activity in the chorion and thereby may protect indirectly against free radical injury. Melatonin could be useful in treating preeclampsia and possibly other clinical states involving excessive free radical production, such as intrauterine fetal growth retardation and fetal hypoxia. [source] Melatonin increases activities of glutathione peroxidase and superoxide dismutase in fetal rat brainJOURNAL OF PINEAL RESEARCH, Issue 2 2000Yuji Okatani Melatonin is a powerful scavenger of oxygen free radicals. In humans, melatonin is rapidly transferred from the maternal to the fetal circulation. To investigate whether or not maternal melatonin administration can protect the fetal rat brain from radical-induced damage by increasing the activities of antioxidant enzymes, we administered melatonin to pregnant rats on day 20 of gestation. Melatonin (10 mg/kg) was injected intraperitoneally at daytime (14:00 hr) and, to remove the fetuses, a laparotomy was performed at 1, 2, or 3 hr after its administration. We measured the melatonin concentration in the maternal serum and in fetal brain homogenates and determined the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in fetal brain homogenates. Melatonin administration markedly increased melatonin concentrations in the maternal serum and fetal brain homogenates, with peak levels achieved 1 hr after melatonin administration (serum: 538.2±160.7 pM/mL; brain homogenates: 13.8±2.8 pM/mg protein). Between 1 and 3 hr after melatonin administration, GSH-Px activity in fetal brain homogenates increased significantly (P<0.01). Similarly, SOD activity increased significantly between 1 and 2 hr after melatonin administration (P<0.01). These results indicate that melatonin administration to the mother increases antioxidant enzyme activities in the fetal brain and may thereby provide indirect protection against free radical injury. Thus, melatonin may potentially be useful in the treatment of neurodegenerative conditions that may involve excessive free radical production, such as fetal hypoxia and preeclampsia. [source] Neopterin induces pro-atherothrombotic phenotype in human coronary endothelial cellsJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 10 2006P. CIRILLO Summary.,Background: Inflammation plays a pivotal role in atherothrombosis. Recent data indicate that serum levels of neopterin, a marker of inflammation and immune modulator secreted by monocytes/macrophages, are elevated in patients with acute coronary syndromes and seem to be a prognostic marker for major cardiovascular events. The aim of the present study was to determine whether neopterin might affect the thrombotic and atherosclerotic characteristics of human coronary artery endothelial cells (HCAECs). Methods and results: In HCAECs, neopterin induced TF-mRNA transcription as demonstrated by real time polymerase chain reaction and expression of functionally active tissue factor (TF) as demonstrated by procoagulant activity assay, and of cellular adhesion molecules (CAMs) as demonstrated by FACS analysis, in a dose-dependent fashion. These neopterin effects were prevented by lovastatin, a HMG-CoA reductase inhibitor. Neopterin-induced TF and CAMs expression was mediated by oxygen free radicals through the activation of the transcription factor, nuclear factor-kappa B (NF- ,B), as demonstrated by electrophoretic mobility shift assay and by suppression of CAMs and TF expression by superoxide dismutase and by NF- ,B inhibitor, pyrrolidine-dithio-carbamate ammonium. Conclusions: These data indicate that neopterin exerts direct effects on HCAECs by promoting CAMs and TF expression and support the hypothesis that neopterin, besides representing a marker of inflammation, might be an effector molecule able to induce a pro-atherothrombotic phenotype in cells of the coronary circulation. [source] Protective effects of glucagon-like peptide 2 on intestinal ischemia-reperfusion ratsMICROSURGERY, Issue 4 2008Wei Zhang Ph.D. Our objective was to evaluate the protective effects of glucagon-like peptide 2 (GLP-2) on intestinal ischemia/reperfusion (I/R) rats. Thirty-two rats were randomly assigned to four experimental groups, each of 8: Group A, sham rats underwent laparotomy only, without superior mesenteric artery (SMA) occlusion; Group B, I/R animals underwent laparotomy and occlusion of the SMA for 60 minutes followed by 120 minutes of reperfusion; Group C, I/R animals underwent intestinal I/R, and received pretreatment with GLP-2 for 3 days preoperatively; and Group D, I/R animals underwent intestinal I/R, received pretreatment with GLP-2 as above, and during the reperfusion phase were injected intravenously with GLP-2. After the reperfusion of intestinal ischemia, samples of intestinal mucosa, mesenteric lymph nodes (MLN) and blood were prepared for determination. In the pretreatment rats with GLP-2 (group C), Chiu's scores, bacterial colony counts, serum D -lactate, intestinal mucosal MDA and ET-1, and serum endotoxin, TNF-, and IL-6 were significantly reduced compared with intestinal I/R rats (group B). Administration of GLP-2 during the reperfusion phase following pretreatment (group D) showed further protective effects in comparison with the pretreatment rats (group C). We conclude that treatment with GLP-2 attenuates intestinal I/R injury, reduces bacterial translocation, inhibits the release of oxygen free radicals and ET-1, and may well inhibit the production of proinflammatory cytokines. © 2008 Wiley-Liss, Inc. Microsurgery, 2008. [source] Immunohistochemical study of the expression of cytokines and nitric oxide synthases in brains of patients with dementia with Lewy bodiesNEUROPATHOLOGY, Issue 1 2003Omi Katsuse Regional expression of cytokines (IL-1,, TNF-,), inducible nitric oxide synthase (iNOS) and neuronal NOS (nNOS) was immunohistochemically investigated in the brains of patients with dementia with Lewy bodies (DLB), compared with those of patients with Alzheimer's disease (AD) and non-demented elderly persons. It has been reported that inflammatory responses by cytokines and oxygen free radicals such as nitric oxide (NO) are associated with damaged neurons, degenerative neurites or amyloid deposits in AD brains. In the present study, overexpression of IL-1,, TNF-, and iNOS was demonstrated in the amygdala, hippocampus, entorhinal and insular cortices of DLB brains, which are pathologically the most vulnerable regions in DLB brains as well as AD brains. In addition, some Lewy body (LB)-bearing neurons were involved by the processes of IL-1,- and TNF-,-positive microglia, and most extracellular LB were associated with the processes of TNF-,- and iNOS-positive astroglia. Glial involvement was also found around neuritic plaques and extracellular neurofibrillary tangles. In contrast, the expression of nNOS was reduced in the amygdala of DLB brains showing severe Lewy pathology. These findings suggest that cytokines and NO are significantly implicated in neuronal damage and death including LB formation in DLB brains. [source] Pharmacological effects of fermented red pepperPHYTOTHERAPY RESEARCH, Issue 11 2004Y. M. Choi Abstract The pharmacological effects were investigated of fermented red pepper (HF-S), which consisted of 14.7% carbohydrate, 1.5% lipid, 4.9% protein, 0.3% ash, 78.2% moisture content, with 0.15% capsaicin and 0.06% dihydrocapsaicin. Oral administration of 0.25 mL HF-S for 3 weeks produced signi,cant changes of the perirenal fat pad weight compared with the HF-control group, suggesting a suppressive effect on lipid accumulation and a signi,cant decrease in the risk of arteriosclerosis. The HF-S (0.25 mL) group also showed a lower plasma TG, TC level and atherogenic index than that of the HF-control. In addition, the HF-S (0.25 mL) group showed a marked increase in the production of glutathione, which is the major endogenous antioxidant, and a decrease in the production of lipid peroxide as the product of chemical damage by oxygen free radicals. It is assumed that the effect of HF-S might relate to high glutathione production on the suppression of lipid peroxidation. HF-S stimulated not only the proliferation of macrophages (as high as the positive control, LPS at 1000 µg/mL) but also mitogenic activity (1.2-fold of LPS at 100 µg/mL). Copyright © 2004 John Wiley & Sons, Ltd. [source] Inhibitory effects of aromatic herbs on lipid peroxidation and protein oxidative modification of mice brain homogenate by copperin vitroPHYTOTHERAPY RESEARCH, Issue 6 2001Shizuo Toda Abstract Several aromatic herbs were inferred to have inhibitory effects on the generation of oxygen free radicals. It has been demonstrated that free radicals produced by copper produce lipid peroxidation and protein oxidative modification in the brain. The results presented here showed that several aromatic herbs, Caryophylli flos, Cinnamomi cortex, Foeniculi fructus and Zedoariae rhizoma, have inhibitory effects on lipid peroxidation or protein oxidative modification of mice brain homogenate produced by copper in vitro. Copyright © 2001 John Wiley & Sons, Ltd. [source] Effect of exercise training on endothelium-derived nitric oxide function in humansTHE JOURNAL OF PHYSIOLOGY, Issue 1 2004Daniel J. Green Vascular endothelial function is essential for maintenance of health of the vessel wall and for vasomotor control in both conduit and resistance vessels. These functions are due to the production of numerous autacoids, of which nitric oxide (NO) has been the most widely studied. Exercise training has been shown, in many animal and human studies, to augment endothelial, NO-dependent vasodilatation in both large and small vessels. The extent of the improvement in humans depends upon the muscle mass subjected to training; with forearm exercise, changes are restricted to the forearm vessels while lower body training can induce generalized benefit. Increased NO bioactivity with exercise training has been readily and consistently demonstrated in subjects with cardiovascular disease and risk factors, in whom antecedent endothelial dysfunction exists. These conditions may all be associated with increased oxygen free radicals which impact on NO synthase activity and with which NO reacts; repeated exercise and shear stress stimulation of NO bioactivity redresses this radical imbalance, hence leading to greater potential for autacoid bioavailability. Recent human studies also indicate that exercise training may improve endothelial function by up-regulating eNOS protein expression and phosphorylation. While improvement in NO vasodilator function has been less frequently found in healthy subjects, a higher level of training may lead to improvement. Regarding time course, studies indicate that short-term training increases NO bioactivity, which acts to homeostatically regulate the shear stress associated with exercise. Whilst the increase in NO bioactivity dissipates within weeks of training cessation, studies also indicate that if exercise is maintained, the short-term functional adaptation is succeeded by NO-dependent structural changes, leading to arterial remodelling and structural normalization of shear. Given the strong prognostic links between vascular structure, function and cardiovascular events, the implications of these findings are obvious, yet many unanswered questions remain, not only concerning the mechanisms responsible for NO bioactivity, the nature of the cellular effect and relevance of other autacoids, but also such practical questions as the optimal intensity, modality and volume of exercise training required in different populations. [source] Mechanisms of adenosine-induced cytotoxicity and their clinical and physiological implicationsBIOFACTORS, Issue 1-4 2006Sharmila P. Seetulsingh-Goorah Abstract Extracellular ATP (ATPo) and adenosine are cytotoxic to several cancer cell lines, suggesting their potential use for anticancer therapy. Adenosine causes cytotoxicity, either when added exogenously or when generated from ATPo hydrolysis, via mechanisms which are not mutually exclusive and which involve, adenosine receptor activation, pyrimidine starvation and/or increases in intracellular S-adenosylhomocysteine: S-adenosylmethionine ratio. Given that adenosine also appears to protect against cytotoxicity via mechanisms including immunity against damage by oxygen free radicals, an understanding of the contribution of adenosine to ATPo-induced cytotoxicity is thus crucial, when considering any potential therapeutic use for these compounds. However, such an understanding has been largely hindered by the fact that many studies have not focused enough on the possibility that both ATPo and adenosine may mediate cytotoxicity in the same system. Such studies can benefit from use a range of ATPo concentrations when assessing the contribution of adenosine to ATPo-induced cytotoxicity. Whilst future molecular and pharmacological studies are needed to establish the nature of the cytotoxic adenosine receptor, it is possible that more than just one adenosine receptor type is involved and that the cytotoxic receptor(s) type is more likely to have a low affinity for adenosine. Activation of the adenosine receptor(s) would thus lead to cytotoxicity only at relatively high adenosine concentrations, while lower adenosine concentrations mediate non-cytotoxic physiological effects. [source] Protective effect of L -carnitine on testicular ischaemia,reperfusion injury in rats,CELL BIOCHEMISTRY AND FUNCTION, Issue 6 2007Dikmen Dokmeci Abstract Testicular torsion is a urological emergency referred to as ,acute scrotum', because inappropriate treatment can lead to male subfertility and infertility. A possible cause of testicular damage is the ischaemia,reperfusion (I/R) injury attributed to oxygen free radicals. L -carnitine, a vitamin-like antioxidant, plays a pivotal role in the maturation of spermatozoa within the reproductive tract. The aim of the present paper was to determine the protective effect of L -carnitine on testicular I/R-induced injury. Thirty-two male rats were divided into 4 groups (n,=,8). Testicular torsion was created by rotating the right testis 720° in a clockwise direction. Group 1: sham-operated control; group 2: ischaemia; group 3: I/R; group 4: ischaemia,L -carnitine treatment,reperfusion group. L -carnitine (500,mg,kg,1, intraperitoneally) was administered before 30 min of detorsion in Group 4. After torsion (5,h) and detorsion (5,h), bilateral orchidectomy was performed. The malondialdehyde (MDA) level was evaluated in testes. Histopathologically, Johnsen's spermatogenesis criteria and mean seminiferous tubule diameter (MSTD) measurements were used. Testicular MDA levels were higher in the torsion group compared to the sham-control group (p,<,0.05). Detorsion (reperfusion) caused a further increase in MDA levels (p,<,0.05). Pretreatment with L -carnitine prevented a further increase in MDA levels (p,<,0.05). Histologically, torsion caused some separation among germinal cells in the seminiferous tubules, which became much more prominent in the I/R group but was attenuated with L -carnitine pretreatment. In conclusion, L -carnitine pretreatment may have a protective effect in experimental testicular torsion,detorsion model in rats by its well-known antioxidant potential. Copyright © 2006 John Wiley & Sons, Ltd. [source] MELATONIN PROTECTS AGAINST HYDROGEN PEROXIDE-INDUCED GASTRIC INJURY IN RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2009Ahmed M Mohamadin SUMMARY 1Melatonin (MT) is a pineal hormone that is also abundant in the gut and has a well known role in scavenging oxygen free radicals. The aim of the present study was to evaluate the potential protective effects of MT against H2O2 -induced gastric lesions in rats. 2An experimental model of gastric ulceration was established in rats using 15% H2O2. Melatonin (12.5, 25 or 50 mg/kg, intagastrically) was administered to rats 30 min before H2O2 challenge. 3Intragastric administration of H2O2 resulted in haemorrhagic lesions in the fundic area of the stomach. Furthermore, H2O2 induced gastric oxidative stress, as indicated by depletion of reduced glutathione (GSH), inhibition of glutathione peroxidase (GPx) activity and elevation of malonedialdehyde (MDA) levels. These effects were accompanied by decreased gastric tissue levels of prostaglandin (PG) E2 and nitric oxide (NO), as well as increased levels of tumour necrosis factor (TNF)-,. Administration of MT (12.5, 25 or 50 mg/kg) 30 min before H2O2 significantly attenuated the development of gastric lesions in a dose-dependent manner. The protective effects of MT were accompanied by significant inhibition of the H2O2 -induced reduction in gastric content of GSH and GPx activity and elevation in MDA levels. Furthermore, MT antagonized H2O2 -induced reduction of gastric PGE2 and NO levels and elevation of TNF-,. 4In conclusion, MT protects rat gastric mucosa against H2O2 -induced damage. The observed protective effects of MT can be attributed, at least in part, to its anti-oxidant properties, preservation of PGE2 and NO levels, as well as inhibition of TNF-, induction in gastric tissues. [source] | |||||||||||||