Improvement of renal oxidative stress markers after ozone administration in diabetic nephropathy in rats

<p>Abstract</p> <p>Background</p> <p>Several complications of diabetes mellitus (DM) e.g. nephropathy (DN) have been linked to oxidative stress. Ozone, by means of oxidative preconditioning, may exert its protective effects on DN.</p> <p>Aim</p> <p>The aim of the present work is to study the possible role of ozone therapy in ameliorating oxidative stress and inducing renal antioxidant defence in streptozotocin (STZ)-induced diabetic rats.</p> <p>Methods</p> <p>Six groups (n = 10) of male Sprague Dawley rats were used as follows: Group C: Control group. Group O: Ozone group, in which animals received ozone intraperitoneally (i.p.) (1.1 mg/kg). Group D: Diabetic group, in which DM was induced by single i.p. injections of streptozotocin (STZ). Group DI: Similar to group D but animals also received subcutaneous (SC) insulin (0.75 IU/100 gm BW.). Group DO: In which diabetic rats received the same dose of ozone, 48 h after induction of diabetes. Group DIO, in which diabetic rats received the same doses of insulin and ozone, respectively. All animals received daily treatment for six weeks. At the end of the study period (6 weeks), blood pressure, blood glycosylated hemoglobin (HbA_1c), serum creatinine, blood urea nitrogen (BUN), kidney tissue levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxide (GPx), aldose reductase (AR) activities and malondialdehyde (MDA) concentration were measured.</p> <p>Results</p> <p>Induction of DM in rats significantly elevated blood pressure, HbA_1c, BUN, creatinine and renal tissue levels of MDA and AR while significantly reducing SOD, CAT and GPx activities. Either Insulin or ozone therapy significantly reversed the effects of DM on all parameters; in combination (DIO group), they caused significant improvements in all parameters in comparison to each alone.</p> <p>Conclusions</p> <p>Ozone administration in conjunction with insulin in DM rats reduces oxidative stress markers and improves renal antioxidant enzyme activity which highlights its potential uses in the regimen for treatment of diabetic patients.</p

Nitric oxide-mediated regulation of gastric H+, K+-ATPase and alcohol dehydrogenase following ethanol-induced injury in rats

The mucosal protective effect of nitric oxide (NO) was examined by using NG-nitro-L-arginine methyl ester (L-NAME) as nitric oxide synthase (NOS) inhibitor and nitroprusside (NP) as NO donating agent, in ethanol-induced rat gastric lesion model. The results are summarized as follows: (1) As gastric tissue samples were examined by light microscopy, intragastric exposure of ethanol was demonstrated to induce gastric injury; which was more prominent in female rats. The depletion of NO by L-NAME treatment exacerbated the ethanol-induced gastric lesion but NP together with ethanol promoted repair of the mucosal injury, especially in female rats. (2) Gastric H+, K+-ATPase enzyme activity, which was responsible for acid secretion, seemed not to be effected by ethanol treatment. Together with ethanol, L-NAME treatment activated, whereas NP treatment inhibited, the enzyme activity in female rats. (3) Ethanol treatment inhibited gastric alcohol dehydrogenase (ADH) activity, which was responsible for the first-pass metabolism of ethanol. Together with ethanol, L-NAME did not effect the enzyme activity whereas NP treatment disappeared the inhibitory effect of ethanol in both gender. Hydroxyl radical (OH .) scavenger activity was found to increase in ethanol and ethanol + NP groups in both sexes, but superoxide radical (O-2(-.)) scavenger activity did not change. The results indicate that NO may ameliorate the damaging effect of ethanol possibly by regulating acid secretion, ethanol metabolism, and antioxidant content in rat gastric mucosa

The effect of nephropathy on plasma sphingosine 1-phosphate concentrations in patients with type 2 diabetes

Objectives: Sphingosine 1-phosphate (S1P) is carried in plasma by the HDL particles and albumin. It mediates several protective functions of HDL. Because of its barrier-enhancing effect, it has attracted attention in diseases associated with endothelial dysfunction. We examined the impact of circulating levels of S1P in diabetic nephropathy together with apoprotein M, a S1P-binding protein in HDL. Plasma levels of dimethylarginines were evaluated in this context

The evaluation of oxidative stress in patients with chronic renal failure

Background: Free radical-mediated changes are thought to be involved with atherosclerosis in patients with chronic renal failure. Methods: The protein carbonyl and malondialdehyde (MDA) levels in serum as the markers of radical-induced protein and lipid oxidations were measured in chronic renal failure patients. Results: Serum carbonyl and MDA levels in both hemodialysis and peritoneal dialysis patients were not found to be different as compared with healthy subjects. In both patient groups, the approximately twofold increment in total antioxidant activity (ferric reducing/antioxidant power; FRAP) and uric acid values in serum were found. The high uric acid levels in both patient groups might be partly responsible for the increment in FRAP values. In addition, all patients received multivitamin preparations including ascorbate, which was also a major antioxidant in serum. Conclusions: Our data suggest that oxidative stress does not become the major threat for patients with chronic renal failure. The increment in endogenous and exogenous antioxidant capacities in serum might be thought to prevent any possible radical-induced damage in patients with chronic renal failure. In addition, the increased nitric oxide (NO) levels especially in hemodialysis patients might likely favor an antioxidant effect. (C) 2002 Elsevier Science B.V. All rights reserved