The effect of L-carnitine on lipid peroxidation and enzymatic antioxidants, such as superoxide dismutase, catalase, and glutathione peroxidase, was evaluated in brain regions of young and old rats. In all brain regions except the hypothalamus, lipid peroxidation was higher for old rats than for young control rats. The activity of superoxide dismutase, glutathione peroxidase, and catalase was lower in the striatum, cerebral cortex, and hippocampus, but no difference was observed in the hypothalamus and cerebellum. L-Carnitine administration (intraperitoneally) prevented thiobarbituric acid-reactive substance formation in the cerebral cortex, cerebellum, hypothalamus, hippocampus, and striatum of 24-month-old rats. Administration of L-carnitine reversed the age-associated changes in a duration-dependent manner. Results suggest that the neuroprotective effect on the brains in old rats was achieved by the elevation of antioxidants with L-carnitine.
Age-associated deficiency of vitamin C contributes to the impaired humoral immune response, which in turn plays a role in the increased risk of illness in old age. Healthy volunteers were given vitamin C supplementation. Neutrophil phagocytic function, complement C3 concen¬ tration, and immunoglobulin status were measured at 30, 60, and 90 days. Neutrophil phago¬ cytic function and levels of serum IgG and IgM and leukocytic ascorbate were considerably lower in the aged humans, but these decreases were attenuated by vitamin C supplementa¬ tion. The level of IgA was not affected by aging. Improved neutrophil phagocytic function and humoral immune response were associated with increased vitamin C status in the aged population and might well contribute to the decreased risk of disease in the aged.
In this study we investigated the oxidative stress, antioxidants and inflammatory molecules in patients of acute myocardial infarction (AMI) with diabetes (n=50) and non-diabetes (n=50). Fifty healthy subjects were taken as control. The levels of plasma TBARS and ceruloplasmin levels were significantly high in diabetic and non-diabetic AMI patients as compared with control. On the other hand, the activities of both enzymatic and non-enzymatic antioxidants were significantly decreased in diabetic and non-diabetic AMI patients as compared with control. Inflammatory markers showed significant rise in diabetic patients as compared with controls. Our results show increased inflammation and oxidative stress in patients with AMI, and magnitude of imbalance is greater in diabetic AMI patients, possibly because of greater inflammation in diabetic patients.
The aim of the study was to investigate the levels of lipid peroxidation, and both plasma and erythrocyte antioxidant states in patients with rheumatoid arthritis. The population consisted of 60 subjects divided into two groups, 30 subjects had evidence of rheumatoid arthritis and age and sex matched healthy subjects were studied as controls. The level of plasma and erythrocyte thiobarbituric acid reactive substances (TBARS) was markedly increased in both the rheumatoid arthritis patients when compared to control subjects. The activities of plasma and erythrocyte antioxidants were significantly decreased in rheumatoid arthritis. C reactive protein, rheumatoid factor and antistreptolysin-O were significantly higher in rheumatoid arthritis patients than in healthy subjects. In conclusion, on the basis of enhanced lipid peroxidation in rheumatoid arthritis patients with concomitant failure of both the plasma, and erythrocyte antioxidants defense mechanism. These results are consistent with the underlying hypothesis that there is an imbalance between reactive oxygen species production and the antioxidant defense system in inflammatory rheumatoid arthritis disease.
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