In vitro solubility and in vivo toxicity of gallium arsenide.
In vitro solubility and in vivo toxicity of gallium arsenide.
复制标题
砷化镓的体外溶解度和体内毒性。
DOI：
10.1016/0041-008x(84)90032-2
复制
发表时间：
1984
影响因子：
3.8
通讯作者：
Carter,DE
中科院分区：
文献类型：
--
作者：
Webb,DR;Sipes,IG;Carter,DE
砷化镓（GaAs）及其金属氧化物的体外溶解度为：氧化砷>砷化镓>氧化镓。GaAs的溶解也依赖于缓冲阴离子的类型和浓度。不同介质对砷的溶出量为0.2M磷酸盐缓冲液≥ 0.1M磷酸盐缓冲液> Krebs-Hensleit缓冲液>蒸馏水> HCl-KCl缓冲液。GaAs在体内条件下明显可溶。大鼠腹腔内滴注10、30或100 mg/kg GaAs后14天的血砷浓度分别为5.5、14.3和53.6 μg/ml;在任何剂量下均未检测到镓。第14天时肺湿重的增加具有剂量依赖性，这些器官以镓或砷的形式保留了17%至42%的剂量。镓和砷的排泄仅限于粪便。作为毒性指标监测的尿卟啉浓度和体重在14天的研究中发生了显著变化。卟啉分析表明，尿卟啉取代粪卟啉作为主要的尿液代谢产物。大鼠接受10，100，或1000毫克/公斤砷化镓po表现出类似的毒性体征。第14天的血砷浓度分别为3.5、6.8和17.6 μg/ml。在1000 mg/kg GaAs剂量下，卟啉症增加，体重下降。这些值相当于用10至30 mg/kg GaAs的内照射剂量获得的值。我们的研究结果表明，肺和po暴露于砷化镓导致全身砷中毒。尿卟啉浓度大于粪卟啉浓度的发现可以作为GaAs暴露的敏感指标。
The in vitro solubilities of gallium arsenide (GaAs) and its metal oxides were arsenic(III) oxide > GaAs ⪢ gallium(III) oxide. GaAs dissolution was also dependent upon the type and concentration of buffer anion. The amount of arsenic dissolved in 12 hr by various aqueous media was 0.2 m phosphate buffer ≥ 0.1 m phosphate buffer > Krebs-Hensleit buffer > distilled H2O > HClKCl buffer. GaAs was apparently soluble under in vivo conditions. Blood arsenic concentrations in rats 14 days after intratracheal instillation of 10, 30, or 100 mg/kg GaAs were 5.5, 14.3, and 53.6 μg/ml, respectively; gallium was not detected at any doses. An increase in lung wet weight at 14 days was dose dependent with these organs retaining 17 to 42% of the dose as gallium or arsenic. Excretion of gallium and arsenic was limited to the feces. Urinary porphyrin concentrations and body weight, monitored as indices of toxicity, were significantly altered over the 14-day study. The analysis of porphyrins revealed that uroporphyrin replaced coproporphyrin as the primary urinary metabolite. Rats receiving 10, 100, or 1000 mg/kg GaAs po exhibited similar signs of toxicity. Blood arsenic concentrations at 14 days were 3.5, 6.8, and 17.6 μg/ml, respectively. Porphyria was increased, and body weight was decreased at 1000 mg/kg GaAs. These values were equivalent to those obtained with an intratracheal dose of 10 to 30 mg/kg GaAs. Our results showed that pulmonary and po exposure to GaAs resulted in systemic arsenic intoxication. The finding that urinary uroporphyrin concentrations were greater than coproporphyrin concentrations may serve as a sensitive indicator for GaAs exposure.