Fibre Toxicology Division, Indian Institute of Toxicology Research (CSIR), Lucknow 226 001, UP, India.
Chemosphere. 2011 Apr;83(4):455-60. doi: 10.1016/j.chemosphere.2010.12.074. Epub 2011 Jan 14.
In this in vitro study we investigated the toxic responses in hepatocytes treated with occupational dust to which workers are exposed in bone-based industrial units. The present study investigated the toxicity mechanism of bone-based occupational dust, from a particular industrial unit, on isolated rat hepatocytes. The hepatocytes were isolated by collagenase perfusion method and cell viability was determined by trypan blue exclusion and MTT [3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay treated with occupational dust at 0.1-1.0 mgmL(-1), for 120 min. The cell viability decreased significantly in a concentration-dependent manner. Dust induced significant membrane damage measured by lactate dehydrogenase (LDH) and glutathione (GSH) release in culture media for 30-, 60- and 120 min treatment duration. The toxicity was found to be correlated with the induction of lipid peroxidation (LPO). In addition, nitric oxide (NO), and hydrogen peroxide (H(2)O(2)) generation by occupational dusts were also found to be time- and concentration-dependent. Over all the present study provides initial evidences for the toxic potential of occupational dust generated in bone-based industries and, therefore, the dust exposure to workers in unorganized industrial units should be controlled.
在这项体外研究中,我们研究了暴露于骨基工业单位中工人的职业性粉尘对肝细胞的毒性反应。本研究调查了来自特定工业单位的骨基职业性粉尘对分离的大鼠肝细胞的毒性机制。肝细胞通过胶原酶灌注法分离,用台盼蓝排斥和 MTT[3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴盐]测定细胞活力,用职业性粉尘在 0.1-1.0mgmL(-1)处理 120 分钟。细胞活力呈浓度依赖性显著下降。粉尘诱导的乳酸脱氢酶(LDH)和谷胱甘肽(GSH)释放显著的膜损伤在 30 分钟、60 分钟和 120 分钟处理时间的培养基中。毒性与脂质过氧化(LPO)的诱导有关。此外,职业性粉尘产生的一氧化氮(NO)和过氧化氢(H(2)O(2))的生成也呈时间和浓度依赖性。总之,本研究为骨基工业中产生的职业性粉尘的毒性潜力提供了初步证据,因此,应控制无组织工业单位中工人的粉尘暴露。