Effects of nicotine and vitamin E on glucose 6-phosphate dehydrogenase activity in some rat tissues in vivo and in vitro.

Effects of nicotine, and nicotine + vitamin E on glucose 6-phosphate dehydrogenase (G-6PD) activity in rat muscle, heart, lungs, testicle, kidney, stomach, brain and liver were investigated in vivo and in vitro on partially purified homogenates. Supplementation period was 3 weeks (n = 8 rats per group): nicotine [0.5 mg/kg/day, intraperitoneal (ip)]; nicotine + vitamin E [75 mg/kg/day, intragastric (ig)]; and control group (receiving only vehicle). The results showed that nicotine (0.5 mg/kg, ip) inhibited G-6PD activity in the lungs, testicle, kidney, stomach and brain by 12.5% (p < 0.001), 48% (p < 0.001), 20.8% (p < 0.001), 13% (p < 0.001) and 23.35% (p < 0.001) respectively, and nicotine had no effects on the muscle, heart and liver G6PD activity. Also, nicotine + vitamin E inhibited G-6PD activity in the testicle, brain, and liver by 32.5% (p < 0.001), 21.5% (p < 0.001), and 16.5% (p < 0.001) respectively, and nicotine + vitamin E activated the muscle, and stomach G-6PD activity by 36% (p < 0.05), and 20% (p < 0.001) respectively. In addition, nicotine + vitamin E did not have any effects on the heart, lungs, and kidney G-6PD activity. In addition, in vitro studies were also carried out to elucidate the effects of nicotine and vitamin E on G-6PD activity, which correlated well with in vivo experimental results in lungs, testicles, kidney, stomach, brain and liver tissues. These results show that vitamin E administration generally restores the inactivation of G-6PD activity due to nicotine administration in various rat tissues in vivo, and also in vitro.

Sex-related differences in tuberculin reaction, free and total testosterone concentrations in patients with autoimmune disorders and controls.

Earlier studies reported the associations among testosterone hormone, autoimmunity, and left-handedness. In the present study, sex differences in tuberculin reaction, a measure of cell-mediated hypersensitivity, serum free and total testosterone levels in controls and patients with autoimmune diseases were studied. There was a sex difference in right and left tuberculin reactions in controls, but not in patients. Both right and left tuberculin reactions were smaller in male and female patients than male and female controls. Free and total testosterone levels were higher in male controls than in male patients. Total testosterone levels were higher in female controls than in female patients. These results suggest that autoimmune diseases may be associated with a decrease in the blood testosterone concentrations.

Endurance training attenuates exercise-induced oxidative stress in erythrocytes in rat.

The aim of this study was to investigate whether endurance training reduces exercise-induced oxidative stress in erythrocytes. Male rats (n=54) were divided into trained (n=28) and untrained (n=26) groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h x day(-1), 5 days a week for 8 weeks, reaching the speed of 2.1 km x h(-1) at the fourth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km x h(-1) at the 95th min, 10% uphill, and was continued until exhaustion. Acute exhaustive exercise increased the erythrocyte malondialdehyde level in sedentary but not in trained rats compared with the corresponding sedentary rest and trained rest groups, respectively. While acute exhaustive exercise decreased the erythrocyte superoxide dismutase activity in sedentary rats, it increased the activity of this enzyme in trained rats. On the other hand, acute exhaustive exercise increased the erythrocyte glutathione peroxidase activity in sedentary rats; however, it did not affect this enzyme activity in trained rats. Erythrocyte glutathione peroxidase activity was higher in trained groups compared with untrained sedentary group. Neither acute exhaustive exercise nor treadmill training affected the erythrocyte total glutathione level. Treadmill training increased the endurance time in trained rats compared with sedentary rats. The results of this study suggest that endurance training may be useful to prevent acute exhaustive exercise-induced oxidative stress in erythrocytes by up-regulating some of the antioxidant enzyme activities and may have implications in exercising humans.

Vitamin E but not Hippophea rhamnoides L. prevented nicotine-induced oxidative stress in rat brain.

Oxidant effects of nicotine in the central nervous system is not clear. The aim of this study was to investigate whether nicotine induces oxidative stress in rat brain, and if it does, to test the effects of Hippophea rhamnoides L. extract (HRe-1) and also vitamin E as a positive control. The groups were: nicotine [0.5 mg/kg/day, intraperitoneal (i.p.)]; nicotine+vitamin E [75 mg/kg/day, intragastric (i.g.)]; nicotine+HRe-1 (250 mg/kg/day, i.g.); and control group (receiving only vehicles). There were eight rats per group and supplementation period was 3 weeks. Malondialdehyde (MDA) level was increased by nicotine in brain tissue, which was prevented by vitamin E whereas not affected by HRe-1. Brain tissue glutathione S-transferase activities of nicotine administered and HRe-1 supplemented groups were lower than control and vitamin E supplemented groups, while glutathione peroxidase (GSH-Px) activities of vitamin E and HRe-1 supplemented groups were lower than the nicotine administered group. Superoxide dismutase activity was not affected by any of the treatments. Total glutathione level was higher in the vitamin E supplemented group compared with control and nicotine administered groups. Vitamin E might have easily diffused to rat brain as a lipid soluble antioxidant, however, the plant extract, HRe-1, would not have sufficiently diffused to the brain to exert its antioxidant effect.

Beneficial effects of Hippophae rhamnoides L. on nicotine induced oxidative stress in rat blood compared with vitamin E.

The aim of this study was to determine the effects of Hippophae rhamnoides L. extract (HRe-1) and also vitamin E as a positive control on nicotine-induced oxidative stress in rat blood, specifically alterations in erythrocyte malondialdehyde (MDA) level, activities of some erythrocyte antioxidant enzymes, and plasma vitamin E and A levels. The groups were: nicotine (0.5 mg/kg/d, intraperitoneal, i.p.); nicotine+vitamin E (75 mg/kg/d, intragastric, i.g.); nicotine+HRe-1 (1 ml/kg/d, i.g.); and control group (receiving only vehicles). There were 8 rats per group and the supplementation period was 3 weeks. Nicotine-induced increase in erythrocyte MDA level was prevented by both HRe-1 and vitamin E. Nicotine-induced decrease in erythrocyte superoxide dismutase (SOD) activity was prevented by HRe-1, but not vitamin E. HRe-1 increased the erythrocyte glutathione peroxidase (GSH-Px) activity compared with nicotine and the vitamin E groups. Catalase activity was not affected. Vitamin E supplementation increased plasma vitamin E level. Plasma vitamin A level was higher in both vitamin E and HRe-1 supplemented groups compared with nicotine and control groups. The results suggest that HRe-1 extract can be used as a dietary supplement, especially by people who smoke, in order to prevent nicotine-induced oxidative stress.