OBJECTIVETo study the effects of chrysotile on the activities of some enzymes for xenobiotics metabolism.

METHODSUICC chrysotile (UC) and China Mangya chrysotile (MC) asbestos fibers were used at different doses (0, 25, 50, 100, 200 mg/L) to study its effects on the activities of cytochrome P4501A1 and glutathione S-transferase (GST) in A549 cell line. Also, the effects of chrysotile on the activities of CYP1A1 and GST induced by benzo(a)pyrene were studied.

RESULTSThe activity of EROD increased slowly with the increasing dose of UC, as A549 cells were incubated with UC for 24 h, and EROD activity increased by 40% at a dose of 200 mg/L UC. However, activity of EROD decreased by 32% with 48 h incubation at the same dose, indicating that lower dose of UC and short time could induce the activity of EROD in A549 cells, whereas higher doses and long time could inhibit its activity. MC exhibited a multiphasic effects on the activity of EROD, whether at a dose of 25 mg/L for 24 h or 48 h all gave the strongest induction, 1.86 times or 1.28 times as controls, respectively. However, EROD activity decreased with the increases in MC doses and incubation time, with the lowest as 35% of the controls. The effect of UC on GST activity was not so obvious, with the highest as the increase in its activity by 20%. The highest induction of MC to GST activity was at a dose of 25 mg/L, 2, 5 times as that in controls. With the increases in its doses, effects of MC on GTS activity became inhibition from induction, like that on EROD activity. MC at a dose of 200 mg/L could lower the activity of GST by 18.7%. A549 cells were incubated with chrysotile fiber for 24 h firstly, and then incubated with benzo(a)pyrene to induce the activities of EROD and GST. The results showed that neither UC nor MC could affect the activity of EROD induced by benzo(a)pyrene. However, UC at a dose of 200 mg/L and MC at 100 mg/L could increase the activity of GST induced by benzo(a)pyrene.

CONCLUSIONChrysotile at different doses or its different types showed varied effects on the activities of EROD and GST in A549 cell lines, probably because of different physicochemical characteristics and surface activity of two kinds of asbestos.

Asbestos, Serpentine ; toxicity ; Cytochrome P-450 CYP1A1 ; metabolism ; Dose-Response Relationship, Drug ; Enzyme Induction ; Glutathione Transferase ; metabolism ; Humans ; Lung Neoplasms ; enzymology ; Tumor Cells, Cultured

OBJECTIVETo understand the effects of exposure to asbestos and GSTM1 genotypes on plasma activity of glutathione S-transferases (GSTs).

METHODSNinety-four workers exposed to asbestos and 51 controls were selected, and their general information, occupational history and personal behavior were collected by questionnaire. Venous blood specimen was collected from each of them and plasma was separated for detection of GSTs activity and lymphocytes for DNA extraction and GSTM1 genotyping.

RESULTSPlasma activity of GSTs in the asbestos-exposed workers (23.0 +/- 6.9) U/L was significantly lower than that in the controls (32.6 +/- 11.8) U/L, which declined with the length of employment in asbestos industry and the increase of cumulated dose of asbestos. Stratification of workers by GSTM1 genotypes showed that plasma activity of GSTs in asbestos-exposed workers with GSTM1+/+ or GSTM1-/- were (24.0 +/- 6.1) and (22.5 +/- 7.3) U/L, respectively, lower than those in the controls with the same genotypes (38.1 +/- 13.2) and (26.8 +/- 6.6) U/L. Plasma activity of GSTs in the control workers with GSTM-/- was significantly lower than in those with GSTM+/+, and, so did in asbestos-exposed workers, but without statistically significant difference.

CONCLUSIONExposure to asbestos could significantly decrease plasma activity of GSTs, and GSTM1 genotypes could affect on the activity of GSTs in the control workers, which was not so obvious in asbestos-exposed workers.

Adult ; Asbestos ; adverse effects ; Gene Frequency ; Genotype ; Glutathione Transferase ; blood ; drug effects ; genetics ; Humans ; Middle Aged ; Occupational Exposure ; adverse effects ; Time Factors