In vivo protection by protein A of hepatic microsomal mixed function oxidase system of CCl 4-administered rats

Abstract

The in vivo protection by protein A of hepatic mixed function oxidase system of carbon tetrachloride (CCl 4) administered rats, has been investigated in the present communication. Aryl hydrocarbon hydroxylase activity was decreased by 63% in CCl 4 administered rats while in protein A + CCl 4 administered rats the decrease was in the range of 22–25% (group IV–V). The aryl hydrocarbon hydroxylase activity in protein A + CCl 4 administered rats showed significant increase in group IV (P < 0.005) and group V (P < 0.001) in comparison to CCl 4 alone (group II). Similarly, aniline hydroxylase and aminopyrene N-demethylase were decreased, by 75 and 84% respectively in CCl 4 administered rats and 31% and 54–64%, respectively in protein A + CCl 4 administered rats (groups IV and V). The aniline hydroxylase activity was also found enhanced in protein A + CCl 4 administered group IV and V (P < 0.001). In addition the aminopyrene N-demethylase also showed significant increase in its activity in group IV (P < 0.001) and group V (P < 0.001) in comparison to CCl 4 alone. In accordance with these data, serum glutamic oxaloacetic transaminase and glutamic pyruvic transaminase exhibited significantly less increase in their activity in animals receiving protein A and CCl 4 than those treated with CCl 4 alone. Protein A alone was found to have no effect on any of these enzymes. Our results indicate that protein A protects CCl 4 induced injury as judged by the biochemical alterations and suggests that it may be useful in providing an excellent system for the investigation on the regeneration of the hepatic enzyme activity following toxic insult of CCl 4.