Tuovinen K, Kaliste-Korhonen E, Raushel F M, Hänninen O
Department of Physiology, University of Kuopio, Finland.
Fundam Appl Toxicol. 1994 Nov;23(4):578-84. doi: 10.1006/faat.1994.1143.
The effect of phosphotriesterase (PTE) on cholinesterase (ChE) activities was studied with exposures to different organophosphates in mice. Paraoxon (PO) (1.0 mg/kg, ip) almost totally inhibited serum ChE activity. This activity, however, recovered to the normal level within 24 hr. The PTE pretreatment (16.8 U/animal, 2.5 micrograms/10 g body wt, iv 10 min before the organophosphate) accelerated this reactivation. The same phenomenon was also seen in vitro. In vitro with human serum, there was only minimal reactivation of the inhibited ChE. PTE, however, reactivated it significantly. The PTE-pretreated mice (168 U/animal, 30 micrograms/10 g body wt, iv) tolerated even 50 mg/kg of PO without showing any remarkable signs of intoxication. In PTE-untreated animals, however, PO doses as low as 1.0 and 1.5 mg/kg caused severe signs of poisoning. PTE (16.8 U/animal, 4 micrograms/10 g body wt, iv) reduced the inhibition of brain and serum ChE activities after PO and diisopropyl fluorophosphate exposure. In sarin and soman intoxications, PTE decreased only slightly the inhibition of ChE activities. The results indicate that PTE pretreatment given iv prevents the inhibition of ChE activities after certain organophosphates and it also hastens the recovery of activities after PO poisoning.
在小鼠中，通过暴露于不同有机磷酸酯来研究磷酸三酯酶（PTE）对胆碱酯酶（ChE）活性的影响。对氧磷（PO）（1.0毫克/千克，腹腔注射）几乎完全抑制血清ChE活性。然而，该活性在24小时内恢复到正常水平。PTE预处理（16.8单位/动物，2.5微克/10克体重，在有机磷酸酯前10分钟静脉注射）加速了这种重新激活。在体外也观察到了相同的现象。在体外用人血清时，被抑制的ChE只有最小程度的重新激活。然而，PTE使其显著重新激活。经PTE预处理的小鼠（168单位/动物，30微克/10克体重，静脉注射）甚至能耐受50毫克/千克的PO，而未表现出任何明显的中毒迹象。然而，在未用PTE处理的动物中，低至1.0和1.5毫克/千克的PO剂量就会引起严重的中毒症状。PTE（16.8单位/动物，4微克/10克体重，静脉注射）降低了在暴露于PO和二异丙基氟磷酸酯后对脑和血清ChE活性的抑制。在沙林和梭曼中毒中，PTE仅略微降低了对ChE活性的抑制。结果表明，静脉注射给予PTE预处理可防止某些有机磷酸酯后对ChE活性的抑制，并且还能加速PO中毒后活性的恢复。
