Oxidative stress and hypogonadism are linked to the increased incidence of cardiovascular disease in males. The objective of this research was to delineate whether drinking cranberry juice for 4 months affects antioxidant capacity and lipid profile in orchidectomized rats. Thirty-two 1-year-old male rats were randomized to two groups: a sham-control group (n = 8) and an orchidectomized group (n = 24). The orchidectomized group was divided into three groups of eight and assigned to one of the following treatments: orchidectomy, orchidectomy plus 27% cranberry juice, and orchidectomy plus 45% cranberry juice. At 120 days after initiation of the study, all rats were killed, blood was collected, and plasma was harvested for total antioxidant status, malondialdehyde, nitrate + nitrite, and superoxide dismutase (SOD) activity in liver, and concentrations of cholesterol and triglyceride in liver and in plasma. Orchidectomy depressed (P < .05) plasma antioxidant capacity and SOD activity, elevated (P < .05) nitrate + nitrite and malondialdehyde in plasma, and increased (P < .05) triglyceride and cholesterol values in liver and in plasma. Cranberry juice increased (P < .05) plasma antioxidant capacity and SOD activity and reduced (P < .05) nitrate + nitrite and malondialdehyde concentrations. Drinking cranberry juice did not affect cholesterol concentrations in liver and in plasma. Triglyceride concentration in plasma of orchidectomized rats that were drinking cranberry juice increased (P < .05), but its concentration in liver decreased (P < .05) to the level of shams. The protective effect of cranberry juice from oxidative damage may be mediated by a decrease in nitrate + nitrite and dose-dependent decrease in peroxidation.

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Vitamin E is known to improve antioxidant status and to prevent lipoprotein oxidation. However, the effect of vitamin E on other cardiovascular risk factors, including C-reactive protein (CRP) and lipid profile status, in orchiectomized rats is unknown. In the present study, 32 1-year-old male rats were randomized into two groups: a sham-control group (n = 8) and an orchiectomized group (n = 24). The orchiectomized group was divided into three groups of eight and assigned to one of the following treatments: orchiectomy (ORX), ORX + vitamin E mixture (65.6 mg/kg) diet, or ORX + vitamin E mixture (656 mg/kg) diet. For 120 days all four groups consumed a basal AIN-93M diet, while the vitamin E groups ate diets containing an additional vitamin E mixture. Four months after the study began, all the rats were killed, the blood was collected, and the plasma was assayed for antioxidant status, CRP, lipid profile, and indices of peroxidation. ORX decreased (P < .05) the plasma antioxidant status, superoxide dismutase (SOD) activity, and CRP level and increased (P < .05) the plasma malondialdeyde, nitrite, and lipid profile compared with that of the sham-control group. In contrast to the ORX group, supplementation with vitamin E mixture increased (P < .05) plasma antioxidant status and dose-dependently increased (P < .05) SOD activity, while the vitamin E decreased (P < .05) plasma malondialdeyde and nitrite. The vitamin E mixture had no effect on CRP or on lipid profiles when compared to the orchiectomized rats. In conclusion, vitamin E appears to reduce oxidative stress without modulating lipid profile or inflammatory response.

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