Hippophae rhamnoides attenuates nicotine-induced oxidative stress in rat liver.

The effects of vitamin E and Hippophae rhamnoides L. (Elaeagnaceae) extract (HRe-1) on nicotine-induced oxidative stress in rat liver were investigated. Four groups, eight rats each, were used in this study, and the supplementation period was 3 weeks. The groups were: nicotine (0.5 mg/kg/day, intraperitoneal (i.p.)); nicotine plus vitamin E (75 mg/kg/day, intragastric (i.g.)); nicotine plus HRe-1 (250 mg/kg/day, i.g.); and the control group. The malondialdehyde and nitric oxide levels, glutathione peroxidase, glutathione S-transferase, glutathione reductase, superoxide dismutase, and total and non-enzymatic superoxide scavenger activities were measured spectrophotometrically in supernatants of the tissue homogenates. Nicotine increased the malondialdehyde level in liver tissue compared with control. This nicotine-induced increase in lipid peroxidation was prevented by both vitamin E and HRe-1. Superoxide dismutase activity was higher in the nicotine plus vitamin E-supplemented group compared with nicotine and control groups. Glutathione reductase activity was higher in the nicotine group compared with the control group. However, glutathione peroxidase activity in the control group was higher than the levels in the nicotine, and the nicotine plus HRe-1 supplemented groups. The nitric oxide level was higher in the nicotine group compared with all other groups. Total and non-enzymatic superoxide scavenger activities and glutathione S-transferase activity were not affected by any of the treatments. Our results suggest that Hippophae rhamnoides extract as well as vitamin E can protect the liver against nicotine-induced oxidative stress.

Vitamin E and Hippophea rhamnoides L. extract reduce nicotine-induced oxidative stress in rat heart.

The effects of vitamin E and Hippophea rhamnoides L. extract (HRe-1) on nicotine-induced oxidative stress in rat heart were investigated. There were eight rats per group and supplementation period was 3 weeks. The groups were: nicotine [0.5 mg kg(-1)day(-1), intraperitoneal (i.p.)]; nicotine plus vitamin E [75 mg kg(-1)day(-1), intragastric (i.g.)]; nicotine plus HRe-1 (250 mg kg(-1)day(-1), i.g.); and the control group (receiving only vehicles). Nicotine increased the malondialdehyde level, which was prevented by both vitamin E and HRe-1. Glutathione peroxidase (GPx) activity in nicotine plus vitamin E supplemented group was higher than the others. Glutathione S-transferase (GST) activity in nicotine plus HRe-1 supplemented group was increased compared with the control group. Catalase activity was higher in nicotine group compared with others. GPx activity in nicotine plus vitamin E supplemented group was elevated compared with the others. Total and non-enzymatic superoxide scavenger activities in nicotine plus vitamin E supplemented group were lower than nicotine plus HRe-1 supplemented group. Superoxide dismutase (SOD) activity was higher in nicotine plus HRe-1 supplemented group compared with others. Glutathione reductase activity and nitric oxide level were not affected. Increased SOD and GST activities might have taken part in the prevention of nicotine-induced oxidative stress in HRe-1 supplemented group in rat heart. Flavonols such as quercetin, and isorahmnetin, tocopherols such as alpha-tocopherol and beta-tocopherol and carotenoids such as alpha-carotene and beta-carotene, reported to be present in H. rhamnoides L. extracts may be responsible for the antioxidant effects of this plant extract.

Hippophae rhamnoides L. and dexpanthenol-bepanthene on blood flow after experimental skin burns in rats using 133Xe clearance technique.

UNLABELLED: The aim of the present experimental study was to determine and compare the effect of Hippophae rhamnoides L. extract (HRe-1) and of dexpanthenol on the blood flow of a wound region, in rats using xenon-133 ((133)Xe) clearance technique. METHODS: Burn wounds were made on both thighs of rats and, HRe-1 and dexpanthenol were applied topically on the wound region only in the right thigh for a period of 8 days. The effect of HRe-1 and of dexpanthenol on blood flow of the wound region was assessed before and after their topical application by using the (133)Xe clearance technique. RESULTS: HRe-1 increased significantly blood flow of the wound region (P<0.05). Dexpanthenol showed a smaller increase in blood flow. In conclusion, our results in rats suggest that HRe-1 increases blood flow of the wound area and can be used for the treatment of skin wound healing, preferably than dexpanthenol.

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.

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.

Effects of sleep deprivation, nicotine, and selenium on wound healing in rats.

Effects of sleep deprivation (SD), nicotine, and selenium (Se) on wound healing were studied in 50 male rats (Sprague-Dawley strain). Full-skin-thickness burns were produced in animals. Then, SD, nicotine, and Se administrations were applied to animals in different groups. Wound healing was assessed by pathological analysis of wound by counting fibroblasts, capillary vessels, polymorphonuclear leucocytes (PNLs), and by measuring radiolabeled immunoglobulin G (IgG) amount in wound area by radio-pharmaceutical and immunoscintigraphic procedures. The number of fibroblasts and capillary vessels were higher in control and Se groups than in sleep deprivation and nicotine groups, and the number of PNLs and the radiolabeled polyvalent IgG levels were higher in SD and nicotine groups than in control and Se groups. The results suggest that SD and nicotine may delay wound healing and that Se supplementation may accelerate wound healing by preventing nicotine-induced oxidative stress and lipid peroxidation.

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.

Right and left visual cortex areas in healthy subjects with right- and left-eye dominance.

The aim of this work was to study the differences between the right- and left-visual cortices in relation to eyedness in healthy subjects. Ocular dominance was determined by means of the near-far alignment test. To assess visual cortical areas, the right and left sagittal scenograms of cranium by magnetic resonance imaging were used. To calculate the visual cortex areas by using scenograms, Cavalieri's method was used. In the subjects with right-eye dominance, the right visual cortex was larger than the left visual cortex, and vice versa in the subjects with left-eye dominance. The right and left cuneal areas were found to be larger in males than in females. In light of these results, it was concluded that the human eyes are predominantly controlled by the ipsilateral visual cortex.