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Intermittent hypoxia is the most common pattern of hypoxic exposure in humans. The effect of chronic long-term intermittent hypobaric hypoxia (CLTIHH) on bone metabolism is not investigated. We examined the effect of CLTIHH on bone metabolism and the role of nitric oxide (NO) in this process. The rats were divided into three groups in this study. The animals in groups I and II have been exposed to CLTIHH. The animals in group II were also treated with nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester. To obtain CLTIHH, rats were placed in a hypobaric chamber (430 mm Hg; 5 h/day, 5 days/week, 5 weeks). The group III (control) rats breathed room air in the same environment. At the begining of the experiments, bone mineral density (BMD) of the animals were measured, and blood samples were collected from the tail vein. After the 5-week CLTIHH period, the same measurements were repeated. Parathyroid hormone, calcium, phosphate, bone alkaline phosphatase (b-ALP), NO, interleukin 1 beta, interleukin 6, and tumor necrosis factor alpha levels were determined. The cytokines, NO levels, and BMD in CLTIHH-induced rats were higher compared with baseline and control values. The cytokines, b-ALP, and BMD increased while NO levels decreased in the group II compared with baseline values. BMD values of group II were lower than group I but higher than control group. Our results suggested that CLTIHH has positive effects on bone density. Intermittent hypoxia protocols may be developed for treatment and prevention of osteopenia and osteoporosis.

Purpose: Melatonin (N-acetyl-5-methoxy-tryptamine) is synthesized mainly by the pineal gland and its antioxidant properties have been demonstrated both in short and long term studies. Our aim was to clarify the e ects of hyperglycemia and to administer melatonin on lipid peroxidation, protein oxidation and oxidative DNA damage in rat.Methods: Malondialdehyde (MDA), protein carbonyl (PCO) and total thiol (T-SH) levels were determined in plasma and liver tissue, glutathione (GSH) levels in erythrocyte and liver tissue, and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels in plasma and liver.irty-eight male Wistar rats were divided into four groups: 1 -injected with saline (n = 8), 2 -injected with melatonin (n = 10), 3 -injected with STZ (65 mg/kg, i.p.) (diabetic group) (n = 10) and 4 -injected with melatonin (10 mg/kg/day, i.p.) and STZ (65 mg/kg, i.p.) (n = 10) for 8 weeks (diabetic+ melatonin group). Colorimetric methods were used to determine the level of the oxidative stress markers. 8-OhdGwas measured using ELISA.Results: MDA, PCO and 8-OHdG levels in the plasma and the liver homogenates of diabetic rats were higher than controls and were signi cantly reduced a er melatonin treatment. T-SH and GSH levels in samples were markedly reduced in untreated diabetic rats compared with control rats; however, these parameters were increased in diabetic rats following melatonin treatment. Conclusion:Our ndings showed that melatonin administration partially ameliorated oxidative damage in liver injury in STZ-induced diabetic rats. e present study suggests that melatonin functions as a potent antioxidant agent in diabetes. Melatonin, a nutritional supplement, may be a good therapeutic option for diabetic patients.

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In subjects with impaired glucose metabolism, the hyperglycemia is associated with increased IMA, AOPP and PAB concentrations. Increased IMA in subjects with IFG and decreased FRAP concentrations in subjects with IGT after glucose loading suggests that an increase in glucose concentrations can lead to tissue damage by increasing oxidative stress.

Background: Obesity may induce oxidative stress, causing oxidative damage of DNA. We examined associations between decreasing serum and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels and weight loss in morbidly obese patients before and 6 months after laparoscopic adjustable gastric banding (LAGB). Methods:We compared patients who had surgery for morbid obesity with healthy, nonobese controls. Urine and fasting blood samples were collected once from the controls and from the morbidly obese patients before and 6 months after the LAGB. The serum and urinary 8-OHdG levels were evaluated in these groups using an enzyme-linked immunosorbent assay kit. Results:We included 20 patients who had surgery for morbid obesity (8 men, 12 women, mean body mass index [BMI] 46.82 ± 4.47) and 20 healthy, nonobese people (10 men, 10 women, mean BMI 22.52 ± 2.08) in our study. There was no significant difference in serum 8-OHdG levels between the groups, whereas urinary 8-OHdG levels were significantly higher in morbidly obese patients than in controls. Weight, BMI and serum and urinary 8-OHdG levels were significantly decreased in morbidly obese patients 6 months after LAGB. Conclusion:The LAGB provides efficient weight loss in patients with morbid obesity. The systemic oxidative DNA damage was increased by the morbid obesity, but this increase was not related to weight gain, and it was more evident in serum than urine samples. After LAGB for morbid obesity, the oxidative DNA damage declined both in serum and urine.

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