Abstract
► Al-intoxication caused severe liver damage biochemically and histopathologically. ► Taurine administration alleviated Al-induced oxidative damaging effects. ► Taurine elevated the antioxidant milieu of the cells. ► The rate of recovery was better when taurine was administered prior to Al. ► Taurine had anaphylactic and therapeutic activity against Al-induced hepatotoxicity.
Aluminum is a well known neurotoxin and a possible candidate of hepatotoxins to humans. Using natural antioxidants against metal-induced hepatotoxicity is a modern approach. In the present study, Aluminum (AlCl
3) intoxication (a single injection of 25
mg Al
3+/kg, i.p.) for 24
h in mice resulted in elevations in serum alanine aminotransferase activity and serum tumor necrosis factor and hepatic malondialdehyde levels. Aluminum reduced the activities of glutathione peroxidase, glutathione S-transferase, quinone oxidoreductase, and catalase in liver. In addition, Al caused hepatic hemorrhage, cellular degeneration as well as necrosis of hepatocytes. Ultrastructure examination showed swelling of mitochondria, derangement of rough endoplasmic reticulum cisternae and pleomorphic nuclei with abnormal chromatin distribution. Taurine, a sulfur-containing amino acid was administered to mice daily for 5
days before (at 100
mg/kg, i.p.) or 2
h after (a single dose of 1
g/kg, i.p.) aluminum administration. Treating mice with taurine at either dosing regimens, pre- or post-aluminum administration alleviated aluminum oxidative damaging effects. The rate of recovery was better when taurine was administered prior to Al. Taurine had anaphylactic and therapeutic activity against hepatotoxicity induced by aluminum in mice.