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Camandola, S., Aragno, M., Cutrin, J.C., Tamagno, E., Danni, O., Chiarpotto, E., Parola, M., Leonarduzzi, G., Biasi, F. and Poli, G. (1999) Liver AP-1 activation due to carbon tetrachloride is potentiated by 1,2-dibromoethane but is inhibited by alpha-tocopherol or gadolinium chloride. Free Radical Biology and Medicine, 26, 1108-1116. doi:10.1016/S0891-5849(98)00298-6

has been cited by the following article:

• TITLE: Kidney response to L-arginine treatment of carbon tetrachloride-induced hepatic injury in mice

  AUTHORS: Entsar A. Saad

  KEYWORDS: L-arginine; Hepatic Injury; Kidney; Lipid Peroxidation; Antioxidant Enzymes

  JOURNAL NAME: Natural Science, Vol.5 No.1, January 9, 2013

  ABSTRACT: Hepatic injury can be induced by the administration of carbon tetrachloride (CCl4) via the production of free radicals. The present work was initiated to investigate the kidney response to hepatic injury induced by CCl4 and its treatment by L-arginine. Female Swiss albino mice were supplied with L-arginine for 6 days (orally, 200 mg/kg body weight) prior or post to hepatic injury induction through i.p. injection with a single dose of CCl4 (20 mg/kg body weight) for 24 h. After hepatic injury induction, renal MDA content was significantly elevated while renal GSH level and the activities of antioxidant enzymes (GR, GPx, GST, catalase, and SOD) were significantly decreased. These results suggest that CCl4 not only induces hepatic injury but also induces kidney dysfunction side by side. Following the treatment with L-arginine, all levels were almost back to normal. Therefore, Larginine administration is found to be an effective protector of both liver and kidney against CCl4-intoxication.