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Abstract
The objective of the present study was to characterize
and investigate potential mechanisms for the male
reproductive toxicity of trichloroethylene (TCE). Male
rats exposed to TCE in drinking water exhibited a dose-
dependent decrease in the ability to fertilize oocytes
from untreated females. This reduction in fertilizing
ability occurred in the absence of treatment related
changes in combined testes/epididymides weight, sperm
concentration, or sperm motility. In addition, flow
cytometric analysis showed that there were no treatment-
related differences in sperm mitochondrial membrane
potential or acrosomal stability. TCE caused slight
histological changes in efferent ductule epithelium,
coinciding with the previously reported ductule
localization of cytochrome P450 2E1. However, no
alterations were noted in the testis or in any segment of
the epididymis. Because there were no treatment-related
changes to sperm indices and no clear pathological lesion
to explain the reduced fertilization, the present study
investigated TCE-mediated sperm oxidative damage.
Oxidized proteins were detected by immunochemical
techniques following the derivatization of sperm protein
carbonyls with dinitrophenyl hydrazine. Immunochemical
staining of whole intact sperm showed the presence of
halos of oxidized proteins around the head and midpiece
of sperm from TCE-treated animals. The presence of
oxidized sperm proteins was confirmed by Western blotting
using in vitro oxidized sperm as a positive control.
TBARS analyses showed a dose-dependent increase in the
level of lipid peroxidation in sperm from treated
animals, as well. Oxidative damage to sperm may explain
the diminished fertilizing capacity of exposed animals
and provide another mechanism by which TCE can adversely
affect reproductive capabilities in the male.
Key words:
Male Reproductive Tract
Toxicology
Epididymis
In vitro fertilization
Sperm
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