Background: Results from observational studies suggest that the oxidative stress and hyperlipidemic status, which prevails in hypertension, plays an important role in causation of secondary complications. So the aim of the present study is to evaluate the beneficial effect of tomatoes, which are a rich source of lycopene, a relatively new carotenoid known to play an important role in human health and disease. Methods: In this study lipid peroxidation rate was measured by estimating malondialdehyde (MDA) and the activity of plasma enzymes involved in antioxidant activities like superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione reductase (GR), reduced glutathione (GSH), and serum lipid profile which includes total cholesterol and triglycerides were estimated in a grade I hypertensive group (n = 40) and an age-matched control group (n = 50). Results: Significantly lower plasma antioxidant enzyme activity, very high lipid peroxidation rate and very high serum total cholesterol, triglycerides in the grade I hypertensive group was observed when compared to the control group (p < 0.001). Sixty days of tomato supplementation in the hypertensive group (n = 30) showed a significant improvement in the levels of serum enzymes involved in antioxidant activities and decreased lipid peroxidation rate (F value highly significant), but there were no significant changes in lipid profile (F value insignificant). Conclusion: These findings suggest that tomato lycopene may have considerable natural therapeutic potential as an antioxidant but may not be used as a hypolipidemic agent in hypertension.

No abstract

We have derived cells from the Chinese hamster V79 cell line by conditioning them with repeated low doses of hydrogen peroxide (H(2)O(2)). This mimics the physiological condition where cells are repeatedly exposed to low levels of oxidants. In an attempt to characterize such cells, we have exposed both conditioned cells (V79(C)) and the parental V79 cells (V79(P)) to different types of cytotoxic agents and compared their sensitivity to cell killing. The V79(C) cells were found to be stably resistant to killing by agents that produced toxicity through oxidative stress, e.g. H(2)O(2) and cisplatin. It was also found that the lipid peroxidation produced by these agents were considerably lower in the V79(C) cells. Thus, the difference in sensitivity could be due to lesser extent of damage to these cells. V79(C) cells had greater antioxidant defense through higher GSH content and greater activity of enzymes such as Cu-Zn superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), which provided protection from damage. Enzyme activities were also assayed at different times after treatment with various cytotoxic agents; there was a relatively large increase in SOD activity which perhaps plays a key role in determining the resistance of the V79(C) cells to killing.

Introduction. In view of the noteworthy role of adipocytokines in the onset of insulin resistance and diabetes in gene-knockout-rat-model-cell-line studies we aimed to study the influence of genetic predisposition for diabetes on adipocytokine levels and their role in building insulin-resistance-like environment well before the onset of diabetes; thus a hypothesis can be drawn on their role in developing diabetes in high risk population. Methods. Ages between 18 and 22 years were selected and divided into three groups. Group I (n = 81): control group with no family history of diabetes. Group II (n = 157): with one of their parents with history of type 2 diabetes. Group III (n = 47): with both parents having history of type 2 diabetes. In all the groups we estimated fasting plasma glucose, insulin and adipocytokines like adiponectin, leptin, TNF-α, and IL-6. Results. Of all adipocytokines we observed significantly lower levels of adiponectin (8.7 ± 1 μg/mL in group III and 9.5 ± 1.3 μg/mL group II) when compared to control (11.0 ± 1.2 μg/mL; P < 0.01) and it has strong correlation with family history of diabetes with Pearson's coefficient of −0.502. Linear regression analysis showed significant negative association with HOMA-IR (P < 0.01) and logistic regression analysis showed highest association with parental diabetes (P < 0.01; OR .260, 95% CI .260–.468). Conclusion. Genetic predisposition for diabetes may influence adiponectin gene expression leading to decrease in its plasma concentration, which might play a key role in developing diabetes in near future.

Aims: In view of significant role of osteocalcin and adiponectin in the onset of insulin resistance and diabetes in rat model and cell line studies we aimed to study the influence of family history for diabetes on osteocalcin and adiponectin levels and their role in initiating the changes in diabetic markers in healthy adult springs of diabetic parents, thus a hypothesis can be drawn on their role in developing diabetes in high risk population. Methodology: Age between 18 to 22 years was selected and divided into three groups. Group I: control group consists (n=81) with no family history of diabetes. Group II: (n=147) with one of their parents with history of type 2 diabetes. Group III: (n=47) with both parents having history of type 2 diabetes. In all the groups we estimated fasting plasma glucose, lipid profile, insulin and adiponectin and osteocalcin. Results: We observed significant lower levels of adiponectin 8.7 ± 1µg/ml in group-III