STUDIES OF CARBONYL SULFIDE TOXICITY - METABOLISM BY CARBONIC-ANHYDRASE
STUDIES OF CARBONYL SULFIDE TOXICITY - METABOLISM BY CARBONIC-ANHYDRASE
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DOI：
10.1016/0041-008x(80)90236-7
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发表时间：
1980-01-01
影响因子：
3.8
通讯作者：
NEAL, RA
中科院分区：
文献类型：
--
作者：
CHENGELIS, CP;NEAL, RA
羰基硫 (COS) [一种工业副产品] 对大鼠有剧毒，腹腔注射 LD50 为 22.5 毫克/千克。 COS 在体内部分代谢为 H2S。用碳酸酐酶抑制剂乙酰唑胺预处理大鼠，降低了血液中 H2S 的水平，同时降低了 COS 的毒性。NaNO2 预处理还可以保护动物免受 COS 毒性。乙酰唑胺本身对 H2S 毒性没有影响。 COS显然被碳酸酐酶代谢为H2S。产生的 H2S 是造成 COS 毒性的原因。
Carbonyl sulfide (COS) [an industrial by-product] is acutely toxic to rats, with an LD50 of 22.5 mg/kg, i.p. COS is partly metabolized in vivo to H2S. Pretreatment of rats with acetazolamide, an inhibitor of carbonic anhydrase, reduced the blood levels of H2S and, concomitantly, decreased the toxicity of COS. NaNO2 pretreatment also protected animals against COS toxicity. Acetazolamide had no effect on H2S toxicity per se. COS is evidently metabolized to H2S by carbonic anhydrase. It is the H2S produced that is responsible for COS toxicity.