Effect of the organophosphorus compounds leptophos and TOCP on creatine kinase activity in hens.

Abstract

The time trend of plasma Creatine Kinase (CK) activity in hens after a single intravenous injection (iv) of orgaonphosphorus compounds (OPs), such as leptophos, TOCP (tri-ortho-cresyl phosphate) or parathion were measured. CK activities in muscles and nervous tissues of hens on day 21 after iv injection of OPs were also measured.In all hens injected with 30mg/kg body weight of leptophos or 40mg/kg body weight of TOCP, the onset of neurotoxic signs was delayed 8 to 10 days after each treatment, while hens injected with 15mg/ kg body weight of leptophos showed no neurotoxic signs. Hens which were injected intravenously with sublethal doses (2mg/kg body weight) or lethal doses (3mg/kg body weight, saved by atropine) of parathion did not show any abnormalities after recovering from acute toxicity.Plasma CK activity in all hens except hens injected with 2mg/kg body weight of parathion rose significantly on the 1st day after OPs injection. A few days later, plasma CK activity recovered to normal levels in hens injected with 15mg/kg body weight of leptophos or 3mg/kg body weight of parathion. However, the high activity levels were prolonged until the 9th to 11th day in hens injected with 30mg/ kg body weight of leptophos or 40mg/kg body weight of TOCP. After developing delayed neurotoxic signs, plasma CK activities rose again in paralitic hens, though ataxic hens maintamed a normal CK level.On the 21st day after OPs injection, CK activities in some parts of the leg muscles and nervous tissues of hens were relatively higher than those of control hens. It is assumed that there was some correlation between the changes of CK activity in muscles and the severity of delayed neurotoxicity in those hens.It is suggested that plasma CK activity is useful for evaluating the severity of delayed neurotoxic damage, and that there are associations between the prolonging of high plasma CK activity in the several days after OPs exposure and the development of delayed neurotoxic symptoms.