Ameliorative Effects of Sodium Hydrogen Sulphide in The Renal Tissues of Diabetic Rats Orally Exposed to Monosodium Glutamate

Diabetic mellitus is an autoimmune disease afflicting millions of population around the world. The concern is the increasing rate of the disease in spite of the advancement in medical education. Of the factors that predispose to the disease is the life style such as diet. Monosodium glutamate is a flavour enhancer widely believed to predispose to diabetes mellitus that is probably related to its obesogenic potential. However MSG direct involvement in the aetiology of diabetes mellitus remains controversial. The controversy is hinged on the finding that the portal blood levels of glutamate is lowly increased even after chronic ingestion since it is readily metabolized. This project therefore aimed to investigate the contribution of MSG to diabetes and possible amelioration by a sulphur compound specifically NaHS through attenuation of oxidative stress. Male Sprague Dawley rats were made diabetic by subcutaneous administration of alloxan and were fed MSG and or NaHS at 2 g/kg/day and 2.8 mg/kg/day respectively for 14 days. Non-diabetic rats were similarly treated or not treated. Rats renal post mitochondrial supernatants were analyzed for the specific activities of superoxide dismutase (SOD) and xanthine oxidase (XO) as well as reduced glutathione (GSH) concentration. N acetyl-?-D-glucosaminidase (NAG) specific activity and creatinine concentration in the urine and cystatin C (CysC) and urea in the serum were investigated. Histologic studies were carried out on the kidney tissues. Altered biochemical indices including induction of oxidative stress and pathological changes in cellular architecture were recorded among the diabetics, diabetics fed MSG as well as the non-diabetics fed MSG. Administration of NaHS to the rats attenuated the oxidative stress and ameliorated the pathological changes in the tissues. This work supports the theory that MSG induces renal dysfunction which is mediated by oxidative stress.