出生前氯氰菊酯与甲基对硫磷暴露对大鼠脑细胞DNA损伤的探讨

目的探讨大鼠出生前暴露于农药氯氰菊酯和甲基对硫磷混配对胎鼠和子鼠脑细胞DNA的毒性效应。方法48只Wistar大鼠在怀孕第1~15天每日一次采用甲基对硫磷、氯氰菊酯混配农药灌胃,1个对照组和3个暴露组,剂量分别为0、(0.0230+0.8000)、(0.0725+2.5265)和(0.2300+8.0000)mg/kgbw,相当于(0、1/300、1/95和1/30)LD50。分别取24只孕16天胎鼠大脑和24只出生后30天龄子鼠大脑,采用单细胞凝胶电泳技术分析脑细胞DNA的损伤。结果甲基对硫磷和氯氰菊酯混配在中、高剂量水平可明显引起妊娠16天胎鼠脑细胞DNA的断裂(P<0.05),并存在明显的剂量-反应关系(r=0.836,P=0.000)。在高剂量水平可引起出生后30天子鼠脑细胞DNA损伤的断裂(P<0.05);子鼠脑细胞DNA损伤程度比胎鼠减轻(F=15.81,P<0.05)。结论大鼠出生前暴露于甲基对硫磷和氯氰菊酯混配可引起神经细胞DNA链断裂损伤,呈现剂量-反应关系,在较低剂量水平DNA损伤能够被修复,而在较高剂量水平DNA损伤不能够被修复。

Studies on DNA damage of the neuron cell in rat offspring induced by cypermerthrin and methylparathrion during embryo exposure

Objective To explore DNA damage of rat's brain prenatal exposure to mixed pesticides of cypermerthrin and methylparathrion. Methods 48 pregnant Wistar rats were divided into 4 groups. During the 1st to 15th day of gestation, all rats were force fed with mixed pesticides of cypermerthrin plug methylparathrion. The dosage of the two pesticides were (0, 1/300, 1/95 and 1/30)LD_ 50 , respectively. The brains of 24 embryos at the gestation day 16th (6 each group) and 24 rat offspring (6 each group) at the 30-day-old after birth were taken out respectively, and the single cell gel electrophoresis (SCGE or comet assay) was utilized to access DNA damage. Results At the exposure does of 1/95LD_ 50 and 1/30LD_ 50 , the mixed pesticides could induce the neuron cell DNA strain rupture of the neuron cell of embryos remarkably (P<0.05), while the high dose could induce the DNA damage in brain of 30-day-old rats (P<0.05).The DNA damage in brain neurons of rat offspring was more severe with increased doses of mixed pesticides (correlation analysis: DNA damage at embryos, r=0.836,P=0.000). Especially at dose of 1/95 LD_ 50 , 1/30 LD_ 50 , the DNA damage in brain of the 30-day-old rats was more severe than the embryo rats(F=15.81, P<0.0001). Conclusion Prenatally exposed to mixed pesticides of cypermerthrin plus methyl parathion could cause neuron cell DNA damage. At the lower level, DNA damage of the neuron of rat offspring could be repaired, but the repair was difficult at the higher level.