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研究了亚砷酸钠在体内、体外对大鼠肝线粒体丙酮酸脱氢酶（ＰＤＨ）、琥珀酸脱氢酶（ＳＤＨ）和微粒体酶细胞色素Ｐ－４５０、ｂ５、ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶、谷胱甘肽硫转移酶（ＧＳＴ）的影响；并通过观测亚砷酸钠与亚硒酸钠的作用及其对肝谷胱甘肽过氧化物酶、谷胱甘肽含量和线粒体脂质过氧化的影响，探讨亚砷酸钠的作用机理。结果表明：连续７天腹腔注射２０ｍｇ／ｋｇ的亚砷酸钠，线粒体ＰＤＨ、ＳＤＨ被抑制，分别相当于对照组的５１％和５８％。而亚硒酸钠可有效拮抗砷对ＰＤＨ、ＳＤＨ的抑制作用。亚砷酸钠显著降低肝ＧＳＨ的含量，并增强线粒体膜脂质过氧化作用（Ｐ＜０．０５）。在体内试验中，亚砷酸钠对谷胱甘肽过氧化物酶和肝微粒体酶无明显影响。亚砷酸钠在体外实验中，浓度在１０－７～１０－３ｍｏｌ／Ｌ的范围内，抑制ＳＤＨ的活力，提高ＧＳＨ的含量，且呈剂量－效应关系。结果提示，亚砷酸钠对机体的作用与其对ＬＰＯ和体内巯基的影响有关
To study the effects of sodium arsenite on rat liver mitochondrial pyruvate dehydrogenase (PDH), succinate dehydrogenase (SDH) and microsomal enzymes cytochrome P-450, b5, NAD(P)H- Effects of Cytochrome C Reductase and Glutathione Sulfur Transferase (GST); observation of the effects of sodium arsenite and sodium selenite on liver glutathione peroxidase and glutathione The effects of content and mitochondrial lipid peroxidation were investigated to investigate the mechanism of action of sodium arsenite. The results showed that 20 mg/kg sodium arsenite was intraperitoneally injected for 7 consecutive days, and mitochondrial PDH and SDH were inhibited, which was equivalent to 51% and 58% of the control group, respectively. However, sodium selenite can effectively inhibit the inhibitory effect of arsenic on PDH and SDH. The sodium arsenite significantly reduced the content of hepatic GSH and enhanced the mitochondrial lipid peroxidation (P<0.05). In the in vivo test, sodium arsenite had no significant effect on glutathione peroxidase and liver microsomal enzymes. In vitro experiments, the concentration of sodium arsenite in the range of 10-7 ~ 10-3mol / L, inhibition of SDH activity, increased GSH content, and showed a dose-effect relationship. The results suggest that the effect of sodium arsenite on organisms is related to its effect on LPO and sulfhydryl groups in vivo.