甲氨基阿维菌素胁迫下福寿螺肝脏抗氧化酶活性及显微结构的变化

Changes in antioxidant enzyme activities and microstructure of liver of Pomacea canaliculata exposed to methylamino abamectin

为明确甲氨基阿维菌素对福寿螺肝脏的损伤机制,测定了不同浓度甲氨基阿维菌素对福寿螺肝脏抗氧化酶活性的影响,并比较了正常福寿螺和用药福寿螺肝脏的组织结构。甲氨基阿维菌素胁迫下,福寿螺肝脏超氧化物歧化酶(SOD)、酚氧化酶(PO)、过氧化氢酶(CAT)活性均出现了波动,呈先升高后降低的趋势,暴露48 h时,除低浓度组福寿螺肝脏SOD活性与对照组无显著差异外,各浓度组福寿螺肝脏SOD、CAT、PO酶活性均显著低于空白对照组,说明短时间甲氨基阿维菌素胁迫作用下,福寿螺体内抗氧化酶的保护作用被激活,但随着胁迫时间延长,抗氧化酶活性下降。甲氨基阿维菌素作用后,福寿螺肝脏结缔组织血管中出现少量淤血,随着暴露时间延长和浓度增加,结缔组织内出现弥漫性淤血甚至坏死现象,细胞变性、畸形、坏死甚至溶解。推测甲氨基阿维菌素通过破坏福寿螺肝脏抗氧化酶功能产生氧化损伤,发挥毒性作用,从而损害其结构和功能。

To explain the injury mechanism of methylamino abamectin exposure to the liver of Pomacea canaliculata, the acute toxicities of different concentrations of methylamino abamectin for P. canaliculata were measured, the changes of antioxidant enzyme activities were detected, and the microstructures of liver of treated and untreated P. canaliculata were compared. The treated P. canaliculata went up first in the activities of SOD, CAT, and PO in liver and then down, indica-ting that enzyme activities were induced by methylamino abamectin initially and were inhibited over time. A small amount of blood stasis was observed in the liver tissue of P. canaliculata in a short period of exposure time. However, high-concentra-tion and long-time stress of methylamino abamectin induced diffuse coagulation even acute necrosis of liver connective tissue, and cell degeneration, malformation, necrosis and cytolysis. The results suggested that oxidative damage might be a causal factor for methylamino abamec-tin toxicity to P. canaliculata.