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体外石油烃毒性:正构烷烃、苯和甲苯对肺泡巨噬细胞及肺溶酶体酶的影响

Petroleum hydrocarbon toxicity in vitro: effect of n-alkanes, benzene and toluene on pulmonary alveolar macrophages and lysosomal enzymes of the lung.

作者信息

Suleiman S A

出版信息

Arch Toxicol. 1987 Apr;59(6):402-7. doi: 10.1007/BF00316205.

DOI:10.1007/BF00316205
PMID:3606384
Abstract

The in vitro effects of straight chain alkanes (nC6-nC10), benzene and toluene on pulmonary alveolar macrophages (PAM) of rats and rabbits was studied. The concentrations used ranged from 0.02 to 1.0 mM. All hydrocarbons used in the study were cytotoxic to isolated cultured PAM cells in a dose-dependent manner. The LC50 for these hydrocarbons towards rat PAM cells was estimated to be 1.0 mM for nC8, 2 mM for nC7, 5 mM for nC9 and 10 mM for nC6, nC10, benzene and toluene. Rabbit PAM cells were more sensitive to the hydrocarbons, resulting in and LC50 half that for rat PAM cells. Hydrocarbons also caused extracellular release of the lysosomal enzymes cathepsin D (EC 3.4.23.5) and cathepsin B (EC 3.4.22.1) in a manner corresponding with cell damage. There was more cathepsin D activity released from cells than cathepsin B. In addition, hydrocarbons also caused the release of cathepsin B and D from isolated lysosomes, and there was 10-15% more enzyme activity released in the culture medium of lysosomes exposed to concentrations of 0.5 and 1.0 mM compared to PAM cell cultures of either rats or rabbits. Hydrocarbons also caused loss of cell respiration and stimulated a dose-dependent and a time-dependent increase in lipid peroxidation. The two alkanes nC7 and nC8 caused the greatest increase in lipid peroxidation and the greatest loss of cell respiration. The results indicate that there is a relationship between chain length of alkanes and their cytotoxicity to PAM cells.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了直链烷烃(nC6 - nC10)、苯和甲苯对大鼠和家兔肺泡巨噬细胞(PAM)的体外效应。所用浓度范围为0.02至1.0 mM。研究中使用的所有碳氢化合物对分离培养的PAM细胞均具有剂量依赖性细胞毒性。这些碳氢化合物对大鼠PAM细胞的半数致死浓度(LC50)估计为:nC8为1.0 mM,nC7为2 mM,nC9为5 mM,nC6、nC10、苯和甲苯为10 mM。家兔PAM细胞对碳氢化合物更敏感,其LC50是大鼠PAM细胞的一半。碳氢化合物还导致溶酶体酶组织蛋白酶D(EC 3.4.23.5)和组织蛋白酶B(EC 3.4.22.1)以与细胞损伤相应的方式释放到细胞外。从细胞中释放的组织蛋白酶D活性比组织蛋白酶B更多。此外,碳氢化合物还导致从分离的溶酶体中释放组织蛋白酶B和D,与大鼠或家兔的PAM细胞培养物相比,暴露于0.5和1.0 mM浓度的溶酶体培养基中释放的酶活性多10 - 15%。碳氢化合物还导致细胞呼吸丧失,并刺激脂质过氧化呈剂量依赖性和时间依赖性增加。两种烷烃nC7和nC8导致脂质过氧化增加最多,细胞呼吸丧失最大。结果表明烷烃的链长与其对PAM细胞的细胞毒性之间存在关系。(摘要截断于250字)

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