Nakashima H
Department of Preventive Medicine and Public Health, School of Medicine, Keio University, Tokyo, Japan.
Arch Toxicol. 1994;69(1):59-64. doi: 10.1007/s002040050138.
To clarify the time course of toxicological effects of tetraethoxysaline [Si(OC2H5)4, TEOS] on the kidney and the relationship between blood silicon levels (Si-B) and the effects, 250 mg/kg or 500 mg/kg TEOS was intraperitoneally administered to ten 5-week-old male ICR mice (SPF grade) in each group, and morphological and functional changes of the kidney were assessed at 12 h, 24 h, 3 days and 2 weeks after administration of TEOS. Injury to tubular epithelial cells was observed in mice killed 12 and 24 h after administration, and its severity increased with increasing dosage. The mean values of blood urea nitrogen exhibited dose-related increase in mice sacrificed 24 h after the administration. The concentrations of Si-B increased in order of the administered doses of TEOS, and then decreased steadily. The results of Si-B were consistent with the concept that renal toxicity of TEOS is mediated by siliceous compounds. The kidney was recovering from injury 3 days after administration, and had developed tubulointerstitial nephritis, which could be regarded as repaired lesion of acute injury, by 2 weeks after administration.
为阐明四乙氧基硅烷[Si(OC2H5)4, TEOS]对肾脏毒理学效应的时间进程以及血硅水平(Si-B)与这些效应之间的关系,每组10只5周龄雄性ICR小鼠(SPF级)腹腔注射250 mg/kg或500 mg/kg TEOS,在注射TEOS后的12小时、24小时、3天和2周评估肾脏的形态和功能变化。给药后12小时和24小时处死的小鼠中观察到肾小管上皮细胞损伤,且损伤严重程度随剂量增加而加重。给药后24小时处死的小鼠中,血尿素氮平均值呈剂量相关增加。Si-B浓度随TEOS给药剂量增加而升高,然后稳定下降。Si-B结果与TEOS肾毒性由硅质化合物介导的概念一致。给药后3天肾脏损伤开始恢复,给药后2周发展为肾小管间质性肾炎,可视为急性损伤的修复性病变。