الفهرس 
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Abstract
Aluminum is a silver-white, malleable, and ductile metal and the third most abundant element in the earth’s crust, comprising 8.3 percent of its volume. This study concerns with Al hepatoxicity either in vitro or in vivo and the role of DFO and L1as chelating agents to alleviate this effect. Isolated rat hepatocytes were exposed to different concentrations of AlCl (5, 10, 20 µM) to examine AlCl-induced hepatotoxicity. The isolated hepatocytes at the submaximal dose of ALCl were pre-treated with either DFO or L1 to determine their protective effects. Present results indicated that the viability and enzymatic leakage % of LDH, ALT, and AST were significantly affected by AlCl toxicity. Oxidative stress assessed by GSH & TBA-RS levels was also observed. Addition of DFO & L1 to incubated hepatocytes 60 minutes before AlCl exposure resulted in marked ameliorating effect. In vivo study was performed after oral administration of 100 and 200 mg AlCl /kg for 5 days. DFO and L1 were given 30 min. before AlCl (at the highest dose) administration at a dose of 100 mg/kg. (ip for DFO and orally for L1). Serum LDH, ALT, and AST enzyme activities were significantly increased in the AlCl-treated groups besides oxidative stress induction (decreased glutathione and increased TBA-RS contents of hepatic tissues). The Liver showed several histopathological changes. DFO and L1 treatment improved these adverse effects. from our study we can conclude that AlCl exposure has severe adverse effects on the liver and causes lipid peroxidation which can be alleviated by pre-treatment with DFO or L1 (more effective).