The effect of the oral iron chelator deferiprone on the liver damage induced by tamoxifen in female rats
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Iron Chelating Agents MeSH
- Deferiprone MeSH
- Enzyme Assays MeSH
- Rats MeSH
- Chemical and Drug Induced Liver Injury drug therapy etiology metabolism MeSH
- Protective Agents MeSH
- Lipid Peroxidation drug effects MeSH
- Rats, Wistar MeSH
- Pyridones pharmacology therapeutic use MeSH
- Tamoxifen adverse effects MeSH
- Treatment Outcome MeSH
- Iron metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Iron Chelating Agents MeSH
- Deferiprone MeSH
- Protective Agents MeSH
- Pyridones MeSH
- Tamoxifen MeSH
- Iron MeSH
Tamoxifen (TAM) is a non-steroidal antiestrogen used in the treatment and prevention of hormone-dependent breast cancer. Tamoxifen therapy may be accompanied with hepatic injury and iron accumulation in this organ. The present study investigates the influence of the effective oral iron chelator, deferiprone (L1), in TAM-induced acute liver injury. Four groups of female Wistar rats were used: I, control; II, TAM; III, TAM+L1; IV, L1. Tamoxifen (75 mg/kg) was administered orally on the first and second day; L1 (50 mg/kg) was administered orally on the first, second and third day of the experiment. On the fourth day, parameters of oxidative state: lipid peroxidation (LP), glutathione (GSH) and catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities were estimated in liver homogenates. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), glutamate dehydrogenase (GLDH) levels and iron hepatic content were also evaluated. The TAM-induced oxidative damage was demonstrated by increased LP (52% above controls) and decreased GPx activity (to 92% of controls). The protective effect of L1 was manifested by attenuation of LP (p <0.05) and preserving of GPx activity. The TAM-induced increase of serum ALT and AST activity remained unchanged by L1 treatment. Significant increase of hepatic iron (Fe) level (41% above controls) was found in TAM-treated rats. Hepatic Fe accumulation was completely prevented by L1 treatment.
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