Propofol attenuates toxic oxidative stress by CCl4 in liver mitochondria and blood in rat

ABSTRACT

Anti-oxidant effects of propofol [2, 6-diisopropylphenol] were evaluated agains carbon tetrachloridet CCl[4] -induced oxidative stress in rat liver. 30 male rats were equally divided in to 6 groups [5 rats each]. Group I [control], while Group II was given CCl[4] [3 mL /Kg/day, IP]. Animals of Groups III received only propofol [10 mg/Kg/day, IP]. Group IV was given propofol+ CCl[4]. Group V was administered vitamin E [alpha-tocopherol acetate 15 mg/Kg/day, SC] .Animals of Group VII received alpha-tocopherol acetate + CCl[4] once daily for two weeks. After treatment, blood and liver mitochondria were isolated. Anti-oxidant enzymes activity such as glutathione peroxidase [GPx], superoxide dismutase [SOD] and oxidative stress marker such as reduced glutathione [GSH] and lipid peroxidation [LPO] concentration were measured. Oxidative stress induced with CCl[4] in liver mitochondria was evident by a significant increase in enzymatic activities of GPx, SOD, and LPO and decreased of GSH and vailability of mitochondria. Propofol and vitamin E restored CCl[4]-induced changes in GSH, GPx, SOD and LPO in blood and liver mitochondria. CCl[4] decreased viability of mitochondria that was recovered by propofol and vitamin E. It is concluded that oxidative damage is the mechanism of toxicity of CCl[4] in the mitochondria that can be recovered by propofol comparable to vitamin E