Am. Avunduk et al., DETERMINATIONS OF SOME TRACE AND HEAVY-METALS IN RAT LENSES AFTER TOBACCO-SMOKE EXPOSURE AND THEIR RELATIONSHIPS TO LENS INJURY, Experimental Eye Research, 65(3), 1997, pp. 417-423
Cigarette smoking has been implicated in the pathogenesis of cataract,
but the pathogenic mechanism by which cigarette smoke causes cataract
is yet to be completely understood. There has been suggestion that ox
idative damage caused by accumulation of Fenton reagents (iron and cop
per) in the lens can cause lens damage and possibly cataract. To inves
tigate the accuracy of this theory the study was planned. A number of
twenty-four male Wistar rats were divided randomly into experimental a
nd control groups. The experimental group of rats were exposed to ciga
rette smoke for two hours in each day over sixty consecutive days and
the controls were treated in identical fashion but only exposed to roo
m air. At the end of the study period, both eyes of all the animals we
re enucleated and one eye prepared for histopathological examination a
nd the other used for the measurement of metal levels. The lenses of e
xperimental animals showed significantly decreased zinc and increased
iron, and calcium concentration relative to those of sham exposed cont
rols. However, no significant difference was found in the copper conte
nts of the lenses of both groups. Distinct histopathological changes s
uch as hyperplasia, hypertrophia, and multilayering of epithelial cell
s and elevations of calcium concentration detected in the lenses of ex
perimental group animals suggested that the lens damage was a result o
f in-vivo exposure to tobacco smoke. We propose that increased metal c
ontents in the lens can cause lens damage by the mechanism of oxidativ
e stress through formation of oxygen radicals via metal catalysed Fent
on reaction. (C) 1997 Academic Press Limited.