Protective effects of vitamin U on kidney tissue in hepatotoxicity caused by galactosamine

Galactosamine (GalN) is used for the construction of hepatic disease models like viral hepatitis. This active ingredient forms hepatic injury via generating free radicals and oxidative molecules. The kidney is one of the most affected organs due to GalN exposure. Vitamin U (Vit. U) is a well-proven antioxidant molecule and scavenges free radicals and many toxic molecules. In this study, we intended to investigate the protection by Vit. U on GalN induced kidney injury. The Sprague-Dawley rats were randomly split into four groups. Control group (given physiological saline, for 3 days), Vit. U group (given 50 mg/kg, orally, 3 days), GalN group (injected 500 mg/kg, a single dose, intraperitoneally), GalN+Vit. U group (given the substances at the same dose and time). Vit. U was given to rats one hour before GalN administration. After 6 hours of GalN injection, all rats were sacrificed by anesthesia. The kidney samples were taken and homogenized in cold physiological saline. The homogenates were centrifuged. The supernatants were collected and biochemical experiments were performed. The kidney reduced glutathione levels, carbonic anhydrase, paraoxonase and sodium potassium ATPase activities were decreased while serum urea, uric acid and creatinine levels, kidney lipid peroxidation and advanced oxidized protein products levels, antioxidant enzyme, myeloperoxidase, xanthine oxidase, adenosine deaminase, lactate dehydrogenase activities were increased in GalN group as compared to control group. Administration of Vit. U to GalN group reversed these parameters. According to these results, we can conclude that Vit. U protected kidney tissue against GalN induced toxicity.