Effects Of TCA On Metabolism Of Oxygen-Derived Free Radicals In Mice

Taurocholic acid (TCA) is one of effective component which exists in cattle, goat bile andso on, and it to bring into full play pharmacological action. It is the first time that the effects of TCA on Oxygen derived free radicals were investigated in mice in this paper. The xanthine oxidase method, DTNB method, ultraviolet spectrotometry, barbital acid method and ELISA method were used to determine the activities of total super-superoxide dismutase (T-SOD), glutathioneperoxidase (GSH-Px), catalase (CAT), NOS,and the content of maleicdialdehyde (MDA) in healthy mice, And the xanthine oxidase method and ELISA method were used to determine the activities of total super-superoxide dismutase (T-SOD) ,NOS of plasma and hepatic tissue with acute damage caused by carbon tetracholoride in mice.The results show that TCA can increase the activity of GSH-PX remarkably in plasma, liver and brain at low dose and the activity of CAT in liver and brain, but decrease the activity of GSH-PX in plasma and brain. TCA can increase the activity of T-SOD remarkably in plasma and liver, and degrade the activity of NOS in plasma in acute liver damaged mice by carbon tetracholoride poisonig. The high dose of TCA can increase the activity of GSH-PX in plasma, T-SOD and GSH-PX in liver and brain and CAT in liver remarkably, increase the activity of T-SOD remarkably in plasma in acute liver damaged mice by carbon tetracholoride poisonig. At both low and high dose, TCA can decrease the content of MDA significantly in plasma, liver and brain, but increase the activity of NOS in healthy mice. The results demonstrated that TCA has the noticeable antioxidation, its antioxidation can be due to the increase of activity of T-SOD, GSH-PX, CAT, NOS and decrease of MDA. And TCA can protect mice from acute liver damaged by carbon tetracholoride poisoning, which can be due to the increase of activity of T-SOD in plasma and liver, and the decrease of activity of NOS in plasma.