Burk R F, Lane J M
Fundam Appl Toxicol. 1983 Jul-Aug;3(4):218-21. doi: 10.1016/s0272-0590(83)80129-8.
Selenium deficiency causes a number of hepatic metabolic alterations in the rat which could lead to changes in chemical toxicity. It causes a decrease in glutathione peroxidase activity, an increase in glutathione S-transferase activity, and an increase in the rate of glutathione synthesis. The hepatotoxicities of three compounds which bind to glutathione S-transferase; iodipamide, acetaminophen, and aflatoxin B1, are decreased by selenium deficiency. The toxicity of redox cycling compounds is generally increased by selenium deficiency and is accompanied by evidence of lipid peroxidation. Thus, nitrofurantoin (100 mg/kg) causes renal tubular necrosis in selenium-deficient rats but not in controls. Selenium-deficient rats are much more sensitive to diquat toxicity than are controls. Lethality of diquat in selenium-deficient rats appears to be causally linked to lipid peroxidation. Lethality of diquat in control rats is not linked to lipid peroxidation. The effect of selenium does not appear to be mediated by glutathione peroxidase, however, indicating that selenium has another oxidant defense function. Another interesting observation made was that increases in inspired O2 tension decreased ethane production (lipid peroxidation) in selenium-deficient and in control rats given diquat. Thus, O2 appears to prevent diquat-induced lipid peroxidation.
硒缺乏会在大鼠体内引发多种肝脏代谢改变，这些改变可能导致化学毒性的变化。它会使谷胱甘肽过氧化物酶活性降低，谷胱甘肽S -转移酶活性增加，以及谷胱甘肽合成速率提高。与谷胱甘肽S -转移酶结合的三种化合物——碘番酸、对乙酰氨基酚和黄曲霉毒素B1的肝毒性，会因硒缺乏而降低。氧化还原循环化合物的毒性通常会因硒缺乏而增加，且伴有脂质过氧化的证据。因此，呋喃妥因（100毫克/千克）会在缺硒大鼠中导致肾小管坏死，但在对照组中不会。缺硒大鼠对百草枯毒性的敏感性远高于对照组。百草枯在缺硒大鼠中的致死性似乎与脂质过氧化有因果关系。百草枯在对照大鼠中的致死性与脂质过氧化无关。然而，硒的作用似乎不是由谷胱甘肽过氧化物酶介导的，这表明硒具有另一种抗氧化防御功能。另一个有趣的观察结果是，提高吸入氧气张力会降低给予百草枯的缺硒大鼠和对照大鼠中的乙烷生成（脂质过氧化）。因此，氧气似乎能预防百草枯诱导的脂质过氧化。
