Article citationsMore>>
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:
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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.
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