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目的研究甲基对硫磷对雄性大鼠的睾丸毒性作用,探讨其毒理作用机制。方法选择雄性SD大鼠(220-240g)20只,连续6周灌胃染毒,剂量为1.2,6,30mg/(kg.bw)染毒结束次日处死大鼠。用流式细胞技术分析睾丸细胞周期和细胞凋亡,同时检测睾丸组织超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量。结果1.2,6,30mg/(kg.bw)甲基对硫磷染毒后大鼠精子存活率分别为90.40%,82.99%,73.98%;精子畸形率分别为20.88%,23.91%,29.10%,与对照组相比较差异有统计学意义(P<0.05或(P<0.01)。30mg/kg染毒组的SOD活力185.33U(mg.pro),低于阴性对照组[344.61U/(mg.pro)];MDA含量1.90nmol/(mg.pro)高于其阴性对照组(0.71nmol/mg.pro)(P<0.01)。与对照组比较,中、高剂量染毒组G0/G1期细胞比例(73.43%,75.22%)显著降低,S期细胞(12.10%,9.35%)比例降低;高剂量甲基对硫磷组细胞凋亡率(32.77%)高于对照组(22.17%),差异有统计学意义(P<0.05)。结论甲基对硫磷对大鼠具有明显的生殖毒性,其毒理作用机制可能是氧化应激导致细胞周期的改变和细胞凋亡的增加。
Objective To study the testis toxicity of methyl-parathion on male rats and to explore the toxicological mechanism. Methods Twenty male Sprague-Dawley rats (220-240g) were randomly divided into 6 groups. The rats were killed on the next day after the end of the dose of 1.2, 6 and 30 mg / (kg · bw). Flow cytometry was used to analyze testicular cell cycle and apoptosis, and testicular superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were also detected. Results The sperm survival rates of rats treated with methyl parathion at 1.2, 6 and 30 mg / (kg · bw) were 90.40%, 82.99% and 73.98%, respectively. The sperm deformity rates were 20.88%, 23.91% and 29.10% Compared with the control group, the difference was statistically significant (P <0.05 or (P <0.01) .30 mg / kg SOD activity of 185.33U (mg.pro), lower than the negative control group [344.61U / (mg. (P <0.01). Compared with the control group, the levels of G0 / G1 phase in medium and high dose groups were significantly higher than those in the control group (73.43%, 75.22%) decreased significantly and the proportion of S phase cells (12.10%, 9.35%) decreased. The apoptosis rate of high dose methyl parathion group (32.77%) was higher than that of control group (22.17% (P <0.05) .Conclusion Methyl parathion has obvious reproductive toxicity in rats, its toxicological mechanism may be oxidative stress lead to changes in cell cycle and increase in apoptosis.