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目的分析肝脏中甲基转移酶活力与砷代谢产物相关性,探讨不同价态砷体内代谢与其毒性关系。方法雌性Wistar大鼠42只分成7组,对照组,亚砷酸钠高、中、低剂量组;砷酸钠高、中、低剂量组;连续染毒3个月,处死动物,摘取肝脏,于-80℃冷藏保存;采用高效液相色谱-氢化物发生原子荧光光谱法测定并比较不同价态染砷大鼠肝脏中砷形态水平,检测肝脏中甲基转移酶活力,探讨两者相关性。结果亚砷酸钠高、中、低剂量组iAs3+含量分别为(255.9±58.6)、(61.1±10.2)、(62.6±17.3)ng/g,均低于砷酸钠各剂量组(P<0.05);亚砷酸钠高、中、低剂量组二甲砷酸(DMA)含量分别为(2 663.2±203.7)、(118.4±24.2)、(143.5±34.1)ng/g,均低于砷酸钠组(P<0.05);亚砷酸钠高、中、低剂量组甲基转移酶活力分别为(4.81±0.25)、(2.32±0.41)和(1.82±0.25)μg/(s.mg),均低于砷酸钠高、中、低同一剂量组(P<0.05);相关分析显示,肝脏中甲基转移酶活力与DMA和一甲砷酸(MMA)的含量均呈正相关(P<0.01),相关系数分别为0.594和0.497。结论不同价态砷均可通过促进(或抑制)肝脏甲基转移酶活力,诱导肝脏DMA、MMA水平升高(或降低),发挥不同毒性作用。
Objective To analyze the correlation between methyltransferase activity and arsenic metabolites in liver and to explore the relationship between metabolism and toxicity in different valence arsenic. METHODS: Forty-two female Wistar rats were divided into 7 groups: control, sodium arsenite high, medium and low dose groups; sodium arsenate high, medium and low dose groups; continuous exposure for 3 months, animals were killed and livers were harvested , And stored at -80 ℃ for storage. The arsenic speciation of arsenic in different valence arsenic rats was determined by high performance liquid chromatography-hydride generation atomic fluorescence spectrometry, and the activity of methyltransferase in the liver was detected, Sex. Results The concentrations of iAs3 + in high, medium and low doses of sodium arsenite were (255.9 ± 58.6), (61.1 ± 10.2) and (62.6 ± 17.3) ng / g, ). The contents of arsenic trioxide in high, medium and low doses of arsenite were (6623.2 ± 203.7), (118.4 ± 24.2) and (143.5 ± 34.1) ng / g, respectively, (4.81 ± 0.25), (2.32 ± 0.41) and (1.82 ± 0.25) μg / (s.mg) respectively in sodium arsenite group (P <0.05) (P <0.05). The correlation analysis showed that there was a positive correlation between the activity of methyltransferase and the contents of DMA and MMA in the liver (P < 0.01), the correlation coefficients were 0.594 and 0.497 respectively. Conclusion Different valences of arsenic can exert different toxic effects by promoting (or inhibiting) hepatic methyltransferase activity and inducing elevated (or decreased) levels of DMA and MMA in the liver.