Dong H, Buard A, Renier A, Lévy F, Saint-Etienne L, Jaurand M C
Laboratory of Environmental Cellular and Molecular Pathology, Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 139, CHU Henri Mondor, Créteil, France.
Carcinogenesis. 1994 Jun;15(6):1251-5. doi: 10.1093/carcin/15.6.1251.
The role of reactive oxygen metabolites in the toxic effects of asbestos on pleural mesothelial cells is not well defined. We exposed rat pleural mesothelial cells (RPMC) to chrysotile and crocidolite fibers (0-40 micrograms/cm2) in the presence or absence of catalase and superoxide dismutase (SOD). Cell injury was measured using the colorimetric 3-4 (5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and DNA damage was evaluated in terms of unscheduled DNA synthesis (UDS). Catalase (100 U/ml) and SOD (250 U/ml) protected RPMC against asbestos-induced cytotoxicity and DNA damage. However, the inactivated enzymes and bovine serum albumin also showed some protection, suggesting that the effect of antioxidant enzymes may be partly related to their protein nature. These results suggest that oxygen derivatives are partly involved in the toxic effects of asbestos on cultures of RPMC. The presence of extracellular proteins may also decrease asbestos-produced toxicity by reducing the degree of RPMC-fiber interaction.
活性氧代谢产物在石棉对胸膜间皮细胞毒性作用中的角色尚未明确界定。我们将大鼠胸膜间皮细胞(RPMC)暴露于温石棉和青石棉纤维(0 - 40微克/平方厘米)中,同时存在或不存在过氧化氢酶和超氧化物歧化酶(SOD)。使用比色法3 - 4(5 - 二甲基噻唑 - 2 - 基)- 2,5 - 二苯基溴化四氮唑法测定细胞损伤,并根据非程序性DNA合成(UDS)评估DNA损伤。过氧化氢酶(100 U/ml)和SOD(250 U/ml)可保护RPMC免受石棉诱导的细胞毒性和DNA损伤。然而,失活的酶和牛血清白蛋白也显示出一定的保护作用,这表明抗氧化酶的作用可能部分与其蛋白质性质有关。这些结果表明,氧衍生物部分参与了石棉对RPMC培养物的毒性作用。细胞外蛋白质的存在也可能通过降低RPMC与纤维的相互作用程度来降低石棉产生的毒性。