氯丁二烯吸入染毒致大鼠急性肝损害的氧化应激机理

大鼠吸入浓度为6.08 mg·L~(-1)氯丁二烯4 h后。2,12和24 h处死.染毒后2 h时血清SDH即明显升高,继而ALT升高,前者增高的幅度大于后者,肝匀浆GSH明显下降,然后升高,脂质过氧化产物MDA形成增多,肝线粒体膜脂流动性下降,与线粒体膜结合的ANS荧光增强,表明氯丁二烯所致急性肝损害可能与氧化应激机理有关。

Oxidative stress mechanisms in acute liver injury induced by chloroprene in rats

Possible mechanisms in acute liver injury induced by inhalation of chloroprene (2-chloro-l,3-butadiene) in rats were studied. The rats were exposed to concentration of 6.08 mg·L-1 chloroprene for 4 h and killed at 2, 12, 24 h, respectively. Serum sorbital dehydrogenase (SDH) and alanine transaminase (ALT) activities were significantly increased during 2-24 h and 12-24 h, respectively. The glutathione contents showed a ma-rked increase at 12-24 h, after exposure. The significantly increased formation of lipid peroxide malondialdehyde (MDA) in hepatic homogenates was observed 12 and 24 h after exposure. No marked change in serum MDA levels was found during the observation. Fluorescence polarization and microvis-cosity of mitochondrial membranes labeled with l,6-diphenyl-l,3,5-hexatriene (DPH) were increased, denoting the decrease of membrane lipid fluidity. Fluorescence intensity of l-anilino-8-naphthalene sulfonate (ANS) bound to mitochondrial membrane was increased. These findings suggest that the acute liver injury in rat may be associated with reactive intermediates generated by chloroprene in liver and subse-quent oxidative stress mechanisms.