尖膀胱螺对毒死蜱毒性的生物化学响应

Biochemistry Response of Physa acuta to Chlorpyrifos Toxicity

以尖膀胱螺作为试验动物,研究毒死蜱对尖膀胱螺抗氧化系统、乙酰胆碱酯酶和一氧化氮合酶的影响。通过预试验获得尖膀胱螺72 h LC50为243μg/L,推算的安全浓度为16μg/L,正式试验以16和121.5μg/L浓度组分别暴露尖膀胱螺96 h。在第24、48和96 h分别取材,测定尖膀胱螺体内超氧化物歧化酶(SOD)、乙酰胆碱酯酶(AChE)、一氧化氮合酶(NOS)的活性和丙二醛(MDA)含量变化情况。结果显示,在推算的安全浓度(16μg/L)暴露后,尖膀胱螺体内MDA含量和NOS活性在各时间段变化均不明显,而SOD和AChE活性在96 h被抑制;在高浓度组(121.5μg/L),尖膀胱螺SOD呈现先上升后下降后又有所回升的趋势,MDA水平持续上升,NOS水平被显著性诱导,AChE活性则被显著性抑制,且在48 h时抑制作用最强。试验结果表明毒死蜱对尖膀胱螺抗氧化系统和神经中枢均产生一定的影响,提示尖膀胱螺可作为毒死蜱毒理学试验模型动物,同时MDA和AChE可作为毒死蜱毒性的生物标记物。

The enzymatic activities of SOD, ACHE, and NOS, and MDA contents were determined in visceral mass of the snail Physa acuta after exposure to 16 and 121.5 tLg/L of chlorpyrifos for 96 h. Results showed that no chan- ges in the activities of SOD, ACHE, and NOS, and the MDA content were found in the lower concentration group （ 16 μg/L） during all the periods of exposure, except that the activities of SOD and AChE were inhibited at 96 h of exposure. However, in the higher group （121.5 μg/L）, chlorpyrifos inhibited the activities of SOD and AChE while promoted NOS activity, and induced a sustained increase of MDA content, suggesting that chlorpyrifos may cause lipid peroxidation in the snail and disturb their neural system. The results indicated that chlorpyrifos exposure leaded to lipid perroxidation stress in the nail. The present study revealed that the AChE and MDA could be used as useful biomarker for ditermination of chlorpyrifos.