The effects on oxidative DNA damage of laparoscopic gastric band applications in morbidly obese patients.

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.

CONTEXTE: L'obésité peut provoquer stress oxydatif qui endommage l'ADN. Nous avons analysé les liens entre une baisse des taux de 8-OHdG (8-hydroxy-2'-désoxyguanosine) sériques et urinaires et la perte de poids chez des patients atteints d'obésité morbide avant, puis 6 mois après la pose d'un anneau gastrique ajustable par laparoscopie (AGAL). MÉTHODES: Nous avons comparé des patients qui ont subi cette chirurgie pour un problème d'obésité morbide à des témoins non obèses en bonne santé. Nous avons prélevé des échantillons d'urine et de sang à jeun chez les témoins 1 fois et chez les patients atteints d'obésité morbide, avant, puis 6 mois après l'intervention pour AGAL. Les taux de 8-OHdG sériques et urinaires ont été mesurés dans les 2 groupes à l'aide d'une trousse de test ELISA (enzyme-linked immunosorbent assay). RÉSULTATS: Notre étude a inclus 20 patients soumis à la chirurgie pour obésité morbide (8 hommes, 12 femmes; indice de masse corporelle [IMC] moyen 46,82 ± 4,47) et 20 témoins non obèses en bonne santé (10 hommes, 10 femmes; IMC moyen 22,52 ± 2,08). Nous n'avons noté aucune différence significative des taux de 8-OHdG sériques entre les 2 groupes, mais les taux de 8-OHdG urinaires étaient significativement plus élevés chez les patients souffrant d'obésité morbide que chez les témoins. Le poids, l'IMC et les taux de 8-OHdG sériques et urinaires avaient significativement diminué chez les patients atteints d'obésité morbide 6 mois après l'intervention pour AGAL. CONCLUSION: L'AGAL est une technique efficace de perte de poids chez les patients souffrant d'obésité morbide. L'atteinte oxydative systémique de l'ADN était exacerbée par l'obésité morbide, mais cette hausse n'était pas reliée au gain pondéral, et elle était plus évidente dans les échantillons sériques que dans les échantillons urinaires. Après la pose d'un AGAL pour obésité morbide, l'atteinte oxydative de l'ADN a diminué dans le sérum et dans l'urine.

The effect of chronic long-term intermittent hypobaric hypoxia on bone mineral density in rats: role of nitric oxide.

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.

The association of oxidative stress markers with conventional risk factors in the metabolic syndrome.

BACKGROUND AND AIMS: The metabolic syndrome (MetS) is a common and complex disorder that consists of various abnormalities, including dyslipidemia, obesity, hypertension and hyperglycemia. We investigated the relationships between the levels of advanced protein oxidation products (AOPPs), the total antioxidant capacity (TAC) and the pro-oxidant-antioxidant balance (PAB) in MetS patients. METHODS: A total of 55 patients (37 women, 18 men) with MetS and 20 healthy controls (14 women, 6 men) with a body mass index (BMI) less than 25 kg/m(2) were enrolled in the study. Colorimetric methods were used to determine the levels of AOPPs, the TAC, and the PAB. RESULTS: AOPP, TAC, and PAB values were significantly higher in patients with MetS than in control subjects (p<0.001, p=0.050, and p<0.001, respectively). A positive correlation was observed between the AOPP levels and the glucose, triglyceride, insulin and HOMA-IR levels. PAB values also exhibited significant positive correlations with diastolic blood pressure and fibrinogen levels. Logistic regression analysis revealed that higher serum PAB values were positively and independently associated with the MetS (odds ratio: 1.110; 95% confidence interval: 1.006-1.224; P<0.37). CONCLUSIONS: Increased AOPP levels and higher PAB values are likely to be a result of oxidative stress, a condition in which an imbalance occurs between the production and inactivation of reactive oxygen species. In addition, it appears that serum PAB values may accurately reflect the levels of oxidative stress in MetS patients.

Melatonin ameliorates oxidative damage in hyperglycemia-induced liver injury.

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 effects 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. Thirty-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 significantly reduced after 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 findings showed that melatonin administration partially ameliorated oxidative damage in liver injury in STZ-induced diabetic rats. The 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.