Biomedical subjects
Publications and source records attributed to Sundaram Kumaran.
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The mitochondrial respiratory chain is a powerful source of reactive oxygen species (ROS), considered as the pathogenic agent of many diseases and aging. L-Carnitine (4-N-trimethylammonium-3-hydroxybutric acid) plays an important role in transport of fatty acid from cytoplasm to mitochondria for energy production. Previous studies in our laboratory reported L-carnitine as a free radical scavenger in aged rats. In the present study we focused the effect of L-carnitine on the activities of electron transport chain in young and aged rats. The activities of electron transport chain complexes were found to be significantly decreased in aged rats when compared to young control rats. Supplementation of carnitine to young and aged rats for 14 and 21 days improved the electron transport chain complexes levels in aged rats when compared with young rats in duration dependent manner. No significant changes were observed in young rats. Our result suggested that L-carnitine improved the activities of electron transport chain enzymes there by improving the energy status in aged rats.
Arsenic exists ubiquitously in our environment and various forms of arsenic circulate in air, water, soil and living organisms. Since arsenic compounds have shown to exert their toxicity chiefly by generating reactive oxygen species, we have evaluated the effect of antioxidants ascorbic acid and alpha-tocopherol on lipid peroxidation, antioxidants and mitochondrial enzymes in liver and kidney of arsenic exposed rats. A significant increase in the level of lipid peroxidation and decrease in the levels of antioxidants and in the activities of mitochondrial enzymes were observed in arsenic intoxicated rats. Co-administration of arsenic treated rats with ascorbic acid and alpha-tocopherol showed significant reduction in the level of lipid peroxidation and elevation in the levels of ascorbic acid, alpha-tocopherol, glutathione and total sulfhydryls and in the activities of isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, NADH-dehydrogenase and cytochrome c oxidase. From our results, we conclude that ascorbic acid and alpha-tocopherol alleviate arsenic- induced alterations in mitochondria.
OBJECTIVE: Levocarnitine is important in beta-oxidation of fatty acids. We evaluated the role of levocarnitine in the skeletal muscle mitochondrial antioxidant system of aged rats. METHODS: Male albino Wistar rats were used in this study. The animals were divided into two groups: young rats (group I) and aged rats (group II). These rats were further subdivided into three groups: one control group (groups Ia and IIa) and two experimental groups (groups Ib, IIb and Ic, IIc) for supplementation with levocarnitine for 14 and 21 days, respectively. After the experimental period, the animals were killed by cervical decapitation; blood and skeletal muscle were isolated for further analysis. RESULTS: Levels of antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase, and non-enzymatic antioxidants such as reduced glutathione, ascorbic acid (vitamin C) and tocopherol (vitamin E) were found to be decreased in the blood and skeletal muscle mitochondria of aged rats. Supplementation with levocarnitine in aged rats improved the antioxidant status in a dose-dependent manner. CONCLUSIONS: These findings demonstrated that levocarnitine enhances the activity of the mitochondrial antioxidant system and decreases the incidence of free radical-induced lipid peroxidation in aged rats.
Free radicals have been implicated in the development of many acute and chronic diseases and in conditions involving brain or neurological tissue. The primary genetic material is subjected to damage by endogenous and exogenous agents, which may lead to instability and transcriptional infidelity. In the present study, we evaluated the protective effect of DL-alpha-lipoic acid, a metabolic antioxidant on lipid peroxidation, protein carbonyl content in various brain regions of aged rats when compared to brain regions of young rats. DL-alpha-lipoic acid was administered intraperitoneally (100mg/kg body weight/day) to experimental rats. Nucleic acid and protein content were low whereas thiobarbituric acid reactive substances and protein carbonyl content (markers of free radical damage) were high in cortex, striatum, hippocampus and hypothalamus followed by cerebellum of aged rat brain. Lipoate administration for 14 days in aged rats increased the levels of nucleic acid and protein and reduced lipid peroxidation and protein oxidation. These results demonstrate that lipoic acid is a potent antioxidant for neuronal cells against age associated oxidative damage.