Comparative pulmonary toxicity of gallium arsenide, gallium(III) oxide, or arsenic(III) oxide intratracheally instilled into rats.
Comparative pulmonary toxicity of gallium arsenide, gallium(III) oxide, or arsenic(III) oxide intratracheally instilled into rats.
复制标题
气管内滴注砷化镓、氧化镓(III)或氧化砷(III)给大鼠的肺毒性比较。
DOI：
10.1016/0041-008x(86)90276-0
复制
发表时间：
1986
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;Wilson,SE;Carter,DE
通过气管内滴注砷化镓(100 mg/kg)、等摩尔镓As_2O_3(65 mg/kg)或最大耐受量As_2O_3(17 mg/kg)来评价砷化镓及其金属氧化物的相对毒性。给药2周后，每组随机抽取5只大鼠进行肺组织脂质、蛋白质、DNA和胶原(4-羟基脯氨酸；4-HP)含量的生化测定。还测定了镓和/或砷在肺中的滞留以及这些金属在血液中的浓度。对其余3只大鼠的肺进行组织病理学检查。肺暴露于Ga2O_3颗粒物显著(p<；0.05)增加了肺的总脂肪含量，相比于使用赋形剂的对照组动物。这种反应似乎与镓颗粒在肺内的滞留有关(x=镓剂量的36%)。相比之下，As_2O_3颗粒并未滞留在肺中。血砷浓度为36ppm，占总剂量的20%。As_2O_3处理组大鼠肺组织干重、蛋白质、DNA和4-HP含量显著增加。这些数据表明，As_2O_3诱导了急性纤维化反应。气管内滴注砷化镓颗粒产生的效果与单独使用氧化物时的效果相似。肺总脂质、蛋白质和DNA含量显著升高。这些生化改变伴随着肺干重和肺湿重显著增加。在14天的研究结束时，接受砷颗粒的大鼠的肺保留了44%的剂量作为镓，28%的剂量作为砷。血液中的砷浓度为44ppm(砷剂量的7%)，而此时血液中没有检测到镓。气管内注入所有金属微粒14天后，主要的组织病理学观察是炎症反应和肺泡细胞增生。这些病变的生物学严重程度从大到小依次为：As_2O_3、As_2O_3、⪢、Ga_2O_3。然而，必须注意的是，As_2O_3的剂量是0.25摩尔的GaAs。
The relative toxicity of gallium arsenide (GaAs) and its metal oxides was assessed by intratracheally instilling particulate suspensions of GaAs (100 mg/kg), equimolar gallium as Ga2O3(65 mg/kg), or a maximally tolerated nonlethal dose of arsenic as As2O3(17 mg/kg). Two weeks after dosing, five rats from each group were randomly selected for the biochemical determination of lung lipid, protein, DNA, and collagen (4-hydroxyproline; 4-HP) content. The pulmonary retention of gallium and /or arsenic and the concentration of these metals in blood were also determined. Lungs from the remaining rats (n = 3) were examined histopathologically. Pulmonary exposure to Ga2O3particulates significantly (p < 0.05) increased the total lipid content of lungs relative to that observed in the vehicle-treated control animals. This response appeared to be associated with the pulmonary retention of gallium particulates (x = 36% of the gallium dose). In contrast, As2O3particulates were not retained in the lung. Blood arsenic concentrations were 36 ppm which represented 20% of the total arsenic administered. Treatment with As2O3significantly elevated lung dry weight as well as protein, DNA, and 4-HP content. These data suggest that As2O3induced an acute fibrogenic response. The intratracheal instillation of GaAs particulates produced effects similar to those observed with the individual oxides. The total lung content of lipids, protein, and DNA was significantly elevated. These biochemical changes were accompanied by significant increases in lung dry weight and lung wet weight. Lungs from rats receiving GaAs particulates retained 44% of the dose as gallium and 28% of the dose as arsenic at the end of the 14-day study. Blood arsenic concentrations were 44 ppm (7% of the arsenic dose) while gallium was not detected in blood at this time. The primary histopathological observations 14 days after the intratracheal instillation of all metal particulates were an inflammatory response and pneumonocyte hyperplasia. The biological severity of these lesions, in descending order, was GaAs > As2O3⪢ Ga2O3. It must be noted, however, that As2O3was dosed at 0.25 × moles of GaAs.