Green tea ameliorates renal oxidative damage induced by gentamicin in rats

Recent studies indicate that free radicals are important mediators of renal damage induced by gentamicin [GM], an aminoglycoside antibiotic widely used in treating severe gram-negative infections. Green tea extract [GTE] was reported to have antioxidant and free radical scavenging activities. Therefore, the aim of this work was to investigate the possible protective effect of GTE against gentamicin-induced nephrotoxicity. For this purpose, rats were divided into four groups. Group-1 [control] received normal saline. Group-2 received GTE [300 mg/kg/d, orally]. Group-3 received gentamicin [80 mg/kg/d, intraperitoneally]. Group-4 was injected with GTE plus gentamicin simultaneously. Daily urinary total protein levels were estimated to assess kidney dysfunction. The rats were sacrificed on the seventh day and kidneys were collected for histopathological studies. Blood urea nitrogen [BUN] and creatinine levels were measured in the blood. Moreover, glutathione [GSH], lipid peroxide expressed as thiobarbituric acid reactive substance [TBARS] levels, superoxide dismutase [SOD] and catalase [CAT] activities were determined in renal tissues. GM produced elevation in urinary total protein, BUN, serum creatinine and TBARS levels. On the other hand, GM reduced the GSH level and SOD, CAT activities. The simultaneous administration of GTE plus gentamicin protected kidney tissues against nephrotoxic effect of gentamicin as evidenced from amelioration of histopathological alterations and normalization of kidney biochemical parameters

Role of NADPH oxidase in the endothelial dysfunction and oxidative stress in aorta of aged spontaneous hypertensive rats

Increased reactive oxygen species [ROS] production is implicated in the pathogenesis of arterial hypertension and the development of endothelial dysfunction. NADPH oxidase type enzyme family has been suggested to form ROS and to interfere with endotheli urn-dependent relaxation. However, the specific isoform of NADPH oxidases that may predominantly contribute to these events remains to be clarified. Here we investigated the expressional regulation of NADPH oxidase isoforms [NOX[1], NOX[2] and NOX[4]] in aorta of aged spontaneously hypertensive rats [SHR] in comparison to age matched Wistar Kyoto rats [WKY]. Moreover, we examined the effect of in vitro inhibition of NADPH oxidase by apocynin or the novel NADPH oxidase inhibitor, VAS2870 on the vascular reactivity and ROS production. Our results showed that ROS formation was largely increased in aorta of SHR as measured by dihydroethidine [DHE] fluorescence and inhibited by apocynin or VAS2870. NADPH oxidase activity, measured by lucigenin-enhanced chemiluminescence and of NOX[1] and NOX[2] protein levels were increased in aortic homogenates from SHR compared to WKY. However, NOX[4] protein expression was not significantly changed. Furthermore, the impaired acetylcholine-induced relaxation of SHR aorta was significantly improved in the presence of either apocynin or VAS2870. Collectively, our data suggest that NADPH oxidases, particularly NOX[1] and NOX[2] are relevant sources of ROS in the aorta of aged SHR thereby cause endothelial dysfunction, and VAS2870 is effective as apocynin in reversing these consequences