암탉에서 지발성 신경 독작용에 의한 혈장 및 뇌 효소 활성치의 경시별 변동에 관한 연구

A study on the time related alteration of the plasma and brain enzyme activity by organohosphorus-induced delayed neurotoxicity (OPIDN)in adult hen

Organophosphorus insecticides are direct or indirect inhibitors of esterases and have been known to induce an organophosphorus-induced delayed neurotoxicity(OPIDN), which is characterized by a delayed onset of prolonged locomotor ataxia resulting from a single or repeated exposure to some organophophorus compounds by affecting central and peripheral nervous systems. Their effects are known to be species specific and old animal is more sensitive to this effect. The effects of EPN, a well known potent OPIDN-producing inseciticide and parathion, non-OPIDN-producing insecticide were investigated on some enzyme activities in laying hens which are known as the most sensitive species to OPIDN. The puropse of this work was to find out the biochemical marker enzyme of OPIDN and elucidate the role of some plasma or brain enzymes in the etiology of OPIDN. Additionally, the possibility of brain cell mitochondria as a target site of OPIDN was evaluated by observing the time course alteration of mitochondria succinate dehydrogenase activity. EPN(50mg/kg) or parathion(3mg/kg) were administered subcutaneously in a single dose in hens pretreated with atropine sulfate(10mg/kg). The enzyme activities were measured on the day 1, 2, 3, 4, 8 and 28 after treatment of insecticides. In conclusion, plasma BuChE and brain AChE are thought to play a role on the development of OPIDN and brain CNPase can be considered as a biochemical marker enzyme of OPIDN. However, brain cell mitochondria may not be the target site of OPIDN.