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Narin Derin

Publications and source records attributed to Narin Derin.

10 recordsLinked to original sources

Effect of chronic restraint stress and alpha-lipoic acid on lipid peroxidation and antioxidant enzyme activities in rat peripheral organs.

OBJECTIVES: The aim of this study was to evaluate the effect of chronic restraint stress and alpha-lipoic acid (LA) administration on lipid peroxidation and antioxidant enzyme activities in rat peripheral organs. METHODS: Forty male wistar rats, aged 3 months were randomized to one of the following groups: control, restraint stress, LA treated and restraint stress+LA treated. Chronic restraint stress was applied for 21 days (1h/day) and LA (100 mg/kg/day) was administered intraperitoneally for the same period. RESULTS: Restraint stress had no statistically significant effect on lipid peroxidation, copper/zinc superoxide dismutase (Cu/Zn SOD), catalase (CAT) and glutathione peroxidase (GPx) activity in rat liver and heart, when compared to the control group. Lipid peroxidation, determined by measuring malondialdehyde (MDA) levels, was found to be increased in the kidney of restraint stress treated rats, compared to controls. Restraint stress-induced lipid peroxidation in the kidney was significantly decreased via LA treatment. Administration of LA also enhanced GPx and decreased Cu/Zn SOD activity in rat kidney, liver and heart, compared to the control group. CONCLUSIONS: The presented data shows that LA is a protective agent against restraint stress--the inducer of lipid peroxidation in the kidney. These findings also suggest that LA-induced changes in antioxidant enzyme activities in rat peripheral organs may contribute to their versatile effects observed in vivo.

Animals↗

Changes in visual evoked potentials, lipid peroxidation and antioxidant enzymes in rats exposed to restraint stress: effect of L-carnitine.

The purpose of our study was to investigate the effects of L-carnitine on lipid peroxidation, Visual Evoked Potentials (VEPs) and antioxidant enzyme activities such as superoxide dismutase and catalase in rats exposed to chronic restraint stress. Forty male Wistar rats, aged three months were used. They were equally divided into four groups: control (C), the group exposed to restraint stress (R), the group treated with L-carnitine(L) and the group exposed to stress and treated with L-carnitine (RL). Chronic restraint stress was applied for 21 days (1 h/day) and L-carnitine (50 mg/kg/day) was given by gavage to the L and RL groups for the same period. Brain and retina levels of thiobarbituric acid reactive substances (TBARS) were significantly increased in the R group and were not altered in the L group compared to the C group. Brain and retina TBARS levels were lower in the RL group than in the R group. Brain and retina superoxide dismutase and catalase activities were significantly decreased in the L and R groups compared to the C group. L-carnitine pretreatment had no significant effect on superoxide dismutase and catalase activity in the RL group. All latencies of VEP components were prolonged in the R and L groups with respect to the C group. L-carnitine increased the latencies of all VEP components in the L group whereas shortened them in the RL group compared to their control groups. L-carnitine may be a promising agent for the prevention of VEP and TBARS alterations caused by stress.

Analysis of Variance↗

The effect of sulfite and chronic restraint stress on brain lipid peroxidation and anti-oxidant enzyme activities.

Sulfites are used as anti-microbial and anti-oxidant agents in a variety of drugs, and function as a preservative in many food preparations. In addition to these effects, sulfites oxidize to sulfite radicals initiating lipid peroxidation. The objective of our study was to investigate the effect of restraint stress and sulfite on brain lipid peroxidation and anti-oxidant enzyme activities. Forty male Wistar rats, aged three months, were randomized to one of the following groups: control, restraint stress, sulfite-treated and restraint stress + sulfite-treated. Chronic restraint stress was applied for 21 days (1 h/day) and sodium metabisulfite (520 mg/kg per day) was given by gavage for the same period. Lipid peroxidation was measured using the thiobarbituric acid (TBA) fluorometric assay. TBA-reactive substances (TBARS) were found increased in all treatment groups when compared to the control group. Spectrophotometric measurement of copper/zinc superoxide dismutase (Cu/Zn SOD) and catalase (CAT) revealed decreased enzyme activities in rats exposed to restraint stress compared to control and sulfite-treated rats. GSH-Px activities were significantly decreased in the restraint stress and sulfite-treated rats compared with the control rats. GSH-Px activity measured in restraint stress + sulfite-treated rats was significantly lower than in the other groups. The presented data confirms the pro-oxidant activity of restraint stress and establishes that decreased anti-oxidant enzyme activities in restraint stress-treated rats enhances brain lipid peroxidation caused via the ingestion of sulfites.

Animals↗

The prooxidant effect of sodium metabisulfite in rat liver and kidney.

Sodium metabisulfite (Na2S2O5) is used as an antioxidant and antimicrobial agent in a variety of drugs and functions as a preservative in many food preparations. In addition to their antioxidant activity, sulfites oxidize to sulfite radicals (SO3-) initiating lipid peroxidation. This study was performed to elucidate the effect of subchronic Na2S2O5 (520 mg/kg/day) ingestion on hepatic and renal antioxidant enzyme activities and lipid peroxidation in albino rats. The antioxidant effect of l-carnitine was also tested in rats treated with Na2S2O5. Plasma uric acid levels were monitored in all rats included in the study. Malondialdehyde (MDA) levels significantly increased in Na2S2O5 treated rats vs. controls, with kidney values of 2.21+/-0.21 vs. 1.22+/-0.35 and liver values of 79.85+/-19.5 vs. 31.36+/-5.0 nmol/mg protein, respectively. Selenium-glutathione peroxidase (GPx) activity was significantly increased in Na2S2O5 treated rats vs. controls, with kidney values of 38.22+/-2.21 vs. 8.09+/-0.76 and liver values of 31.11+/-6.37 vs. 11.70+/-1.02 U/g protein, respectively. Sodium metabisulfite treatment increased plasma uric acid levels in rats that were included in the study. No protective effect of l-carnitine was observed against lipid peroxidation in both liver and kidneys of rats treated with Na2S2O5. The presented data confirm the prooxidant activity of sulfites and suggest that increased GPx activity and plasma uric acid levels may partially reduce the observed renal and hepatocellular oxidative damage caused via the ingestion of sulfites.

Animals↗

The effect of chronic restraint stress and sulfite on visual evoked potentials (VEPs): relation to lipid peroxidation.

Stress and sulfite can stimulate numerous pathways leading to an increased production of free radicals which generate a peroxidation cascade producing lipid peroxidation, protein oxidation, DNA damage and cell death, and contribute to the occurrence of pathologic conditions. The purpose of our study was to investigate the effects of stress and sulfite on visual evoked potentials (VEPs) and to examine the relationship between lipid peroxidation and VEP changes. Forty male wistar rats, aged three months were used. They were equally divided into four groups: control (C), the group exposed to restraint stress (R), the group treated with sulfite (S) and the group exposed to stress and treated with sulfite (RS). Chronic restraint stress was applied for 21 days (1h/day) and sodium metabisulfite (520 mg/kg/day) was given by gavage for the same period. All latencies of VEP components were prolonged in the R, S and RS groups with respect to the C group. Brain and retina TBARS levels were found to be increased in those groups compared to the C group. Our results strongly suggest that the latency prolongations of all VEP components may have resulted from the enhancement of lipid peroxidation. Correlation analysis between brain and retina TBARS levels and VEP latencies also support this conclusion. Our data in regard to latency prolongations of all VEP components in the stress group exposed to sulfite, reflected an additive effect of sulfite toxicity on VEP components. Therefore it could be suggested that chronic exposure to stress and sulfite together is associated with a considerable health risk.

Animals↗

Peritoneal macrophages function modulation by L-carnitine in aging rats.

BACKGROUND AND AIMS: The aging process is associated with a progressive decline in physiological functions involving immune response in most species. The aim of the present study was to determine the effect of L-carnitine on impaired macrophages function in aged rats. METHODS: Superoxide anion production, chemotaxis and phagocytic activity were studied in peritoneal macrophages obtained from young (2 months old) and aged (24 months old) rats. L-carnitine (50 mg/kg bw) or control vehicle was orally gavaged into young and aged rats for 30 consecutive days. RESULTS: The peritoneal macrophages of the aged rats exhibited an increase in superoxide anion generation and a decline in chemotaxis and phagocytic index by comparison with the young rats. Superoxide anion production in aged rats was significantly reduced by L-carnitine treatment, as accompanied by a significant enhancement of chemotactic activity, which was restored to control levels observed in young rats. The age-related reduction in phagocytic index was only slightly, but not significantly, restored by L-carnitine administration, however. CONCLUSION: The findings suggest that L-carnitine administration may be useful in reversing some age-related changes.

Aging↗

Effect of stress-induced lipid peroxidation on functions of rat peritoneal macrophages.

The aim of the present study was to investigate the effects of stress-induced lipid peroxidation on macrophages' functions. Animals were subjected to 4 h immobilization at 4 degrees C in restraining devices. The peritoneal macrophages obtained from rats exposed to cold and restraint stress exhibited an increase in lipid peroxidation and a decline of chemotaxis and phagocytosis compared with control rats. After supplementation with vitamin E, the increment in thiobarbituric acid reactive substances (TBARS) content as the oxidative stress marker and the decline of chemotaxis and phagocytosis in peritoneal macrophages observed during cold-restraint stress was significantly removed. No significant change in catalase activity of peritoneal macrophages was observed in groups exposed to cold-restraint stress and treated with vitamin E. These findings indicate that phagocytic and chemotactic capacities of peritoneal macrophages are decreased by cold-restraint stress and this effect of stress may be related to lipid peroxidation.

Animals↗

Effects of L-carnitine on neutrophil functions in aged rats.

Several age-related alterations occur at the cellular level in the immune system leading to a decrease in the immune response. The present study was designed to determine the effect of L-carnitine on impaired neutrophil functions of aged rats. For this reason, superoxide anion radical production, chemotaxis and phagocytic activity were studied in the neutrophils obtained from the peripheral blood of young and old rats. We orally gavaged L-carnitine (50 mg/kg b.w. per day) or control vehicle into young (2 months) and aged (24 months) rats for 30 consecutive days. The neutrophils of aged rats exhibited an increase in superoxide anion production and decline in phagocytosis and chemotaxis when compared with that in young rat neutrophils. Superoxide anion production in aged rats was significantly decreased by L-carnitine treatment which was accompanied with a significant enhancement of chemotactic and phagocytic activity being restored to control levels. These findings demonstrated that L-carnitine is capable of restoring the age-related changes of neutrophil functions.

Aging↗

Effects of L-carnitine on neutrophil-mediated ischemia-reperfusion injury in rat stomach.

Reactive oxygen metabolites play an important role in ischemia-reperfusion related gastric injury. Primary sources of reactive oxygen metabolites seem to be the xanthine/xanthine oxidase system and neutrophils accumulating within the reperfused tissue. Tissue myeloperoxidase activity is an important index of neutrophil accumulation. The purpose of the present study was to clarify the effect of L-carnitine on the accumulation of neutrophils and neutrophil-induced gastric mucosal damage in rats exposed to ischemia-reperfusion. Rats were randomly divided into three groups: sham-operated, ischemia-reperfusion and ischemia-reperfusion plus L-carnitine groups. Ischemia was induced by clamping the celiac artery for 30 min and then reperfusion was established for 60 min. Gastric injury was assessed by measuring myeloperoxidase activity in gastric tissue. The neutrophil accumulation and hemorrhagic lesions due to ischemia-reperfusion in gastric mucosa were ascertained in a histological study. L-Carnitine (100 mg kg(-1)) administrated intravenously 5 min before ischemia significantly reduced both the gastric injury and myeloperoxidase activity compared with the ischemia-reperfusion group. The results suggest that L-carnitine provides marked protection against ischemia-reperfusion-related gastric injury which could be due to its ability to reduce neutrophil accumulation in ischemic tissue.

Acute Disease↗

Effect of L-carnitine on carrageenan-induced inflammation in aged rats.

BACKGROUND: It is known that L-carnitine is a cofactor in the transport of fatty acids across the inner mitochondrial membrane for beta-oxidation. However, L-carnitine is an antioxidant compound widely used for the treatment of deficits in functions due to the aging process. OBJECTIVE: The purpose of the study was to investigate the effect of L-carnitine on carrageenan-induced inflammation in aged rats. METHODS: L-carnitine (50 mg/kg/day) or control vehicle was given by gavage for 30 consecutive days to young (2-month-old) and aged (24-month old) rats. 6 ml of air was injected subcutaneously into the dorsum of each rat, followed 2 days later by 4 ml of 2% carrageenan. After 2 days, the exudate was collected from the inflamed site of each rat. The quantity of collected exudate and the number of cells which have migrated to the inflamed site were determined. RESULTS: No differences were observed in quantity of exudate in all groups; a decrease in the number of exudate cells was established in aged rats. However, L-carnitine treatment significantly increased the number of exudate cells in both young and aged rats. The exudate cells from the aged rats exhibited a decline of both phagocytic and chemotactic activities as compared with those from the young rats, and the decreased functions were significantly enhanced by L-carnitine treatment. However, superoxide anion release was seen to be unchanged in exudate cells due to aging, and L-carnitine intake decreased the production of superoxide anion by these cells in young and aged rats. CONCLUSIONS: These findings demonstrate that L-carnitine is capable of restoring the age-related changes in the functions of inflammatory cells. Moreover, L-carnitine may play a protective role in the tissue destruction in inflammation by decreasing the superoxide anion production.

Aging↗