Study on the body effects of arsenic, indium and antimony as the semiconductive materials

InAs在体内部分解离形成无机砷和铟。砷在仓鼠尿中的主要代谢产物为DMA。铟被证明是专门积累在肾脏和肝脏。但砷的浓度较低。这些结果表明，代谢和毒性的InAs之间的可能关系。砷化铟是一种低毒的砷化合物，小鼠皮下LD_<50>（32.5）g/kg。然而，铟在肝脏中的积累会产生慢性毒性作用。血浆生化显示与铟沉积相关的GOT、GPT、γ-GTP、LDH和LDH活性显著、一致和统计学显著增加。血ALAD活性被砷或砷抑制。结果表明，血红素途径中的酶可能具有作为这些药剂的暴露/毒性的标记物的效用。尿中无机砷、DMA和发中无机砷浓度均大于铟浓度，可作为砷化铟暴露的敏感生物学指标。

InAs is partially dissociated in vivo to form inorganic arsenic and indium. The principal metabolite of arsenic in the urine of hamsters was DMA. Indium was shown to specifically accumulate in the kidney and liver. but the concentration of arsenic was low. These results suggested a possible relationship between the metabolism and toxicity of InAs. InAs proved to be an arsenic compound of low toxicity, with an sc LD_<50> of 32.5 g/kg in mice. Indium accumulation in the liver, however, produced chronic toxic effects. Plasma biochemistries showed marked, consistent and statistically significant increases in the activities of GOT, GPT, gamma-GTP, LAP and LDH associated with indium deposition. Blood ALAD activity was inhibited by InAs or arsenic exposure. The results suggest that the enzymes in the heme pathway may have utility as markers of exposure/toxicity for these agents. The finding that urinary inorganic arsenic, DMA and inorganic arsenic in hair are greater than indium concentrations way serve as a sensitive biological indicator for InAs exposure.