Kidney and liver functions and stress oxidative markers of monosodium glutamate-induced obese rats.

Abstract

The purpose of the present study was to determine the function and oxidative status in kidney and liver using a model of obesity induced by neonatal treatment of rats with monosodium glutamate, and to investigate the association of these metabolic changes with antioxidant enzymes, oxidative stress and NO generation. Methods: neonate male Wistar rats were subcutaneously injected, with monosodium L-glutamate (MSG), at a dose of 4 g/kg body weight at days 2, 4, 6, 8 and 10 of life. We evaluated: anthropometrical parameters and obesity markers, intravenous glucose and insulin tolerance tests, liver function, bile flow and pharmacokinetic parameters, biochemical and histological studies in renal and hepatic tissues, measurement of oxidative stress markers and histopathological examination. Results: glutathione decreased in kidney; glutathione peroxidase (GPx), glutathione reductase and superoxide dismutase (SOD) increased activities. These suggest that the oxidative defences of kidney reacts positively giving to such tissue more resistance against to the oxidative stress. There may be a ROS mediate inactivation of NO and as a result reduced renal plasma flow and glomerular filtration rate. In liver redox status induces decrease in SOD and increase in GPx activity. Changes in redox status would be responsible of the functional and histological alterations observed both in kidney and liver.