H. Iguchi et al., LIPID-PEROXIDATION AND DISINTEGRATION OF THE CELL-MEMBRANE STRUCTURE IN CULTURES OF RAT LUNG FIBROBLASTS TREATED WITH ASBESTOS, Journal of applied toxicology, 13(4), 1993, pp. 269-275
Rat lung fibroblasts were cultured for 24 and 48 h with UICC standard
reference asbestos samples of amosite, crocidolite or Canadian chrysot
ile at various concentrations, and thiobarbituric acid-reactive substa
nces (TBARS) in the media and the cells were measured. Tests by the tr
ypan blue dye-exclusion method showed that cell viability was 80 +/- 5
% (mean +/- SD) and 71 +/- 6% when cultured for 48 h in the presence o
f 500 mug ml-1 of amosite and crocidolite, respectively, but was not a
ffected by chrysotile. In cultures for 24 and 48 h, both chrysotile an
d crocidolite at > 250 mug ml-1 significantly increased TBARS in the m
edium, whereas amosite did so at > 500 mug ml-1. TBARS in the cells wa
s not increased significantly by chrysotile at any concentration in th
e cultures for 24 and 48 h, but crocidolite at > 250 mug ml-1 signific
antly increased TBARS in the cells when cultured for 24 or 48 h. Altho
ugh amosite at all concentrations tested did not increase significantl
y TBARS in the cells of the 24-h culture, it did increase TBARS signif
icantly in the cells when cultured for 48 h at a concentration of 500
mug ml-1 amosite. The increases of TBARS in media of the cultures with
asbestos were accompanied by increases of lactate dehydrogenase (LDH)
activity in the media, indicating the leakage of the enzyme from the
cell into the media. The activity of LDH and the amount of TBARS showe
d a good correlation with each other, with a significant correlation c
oefficient value of 0.655. Thus, the amount of TBARS produced during t
he culture seemed to change, depending on both the asbestos concentrat
ion and the inherent properties. The findings suggest that when certai
n types of asbestos are cultured with rat lung fibroblasts the cell me
mbranes are peroxidized to cause disintegration of the membrane struct
ure, followed by leakage of cellular LDH into the medium.