ABSTRACT
Objective:
To investigate the effects of monobromobiphenyl
ether (4-BDE) on the expression of γH2AX in the
rat testis, and the possible mechanism of 4-BDE affecting the reproductive function of the
male rats.
METHODS:
Twenty-four SD
male rats were randomly divided into 4 groups control and low-, medium- and high-
dose 4-BDE, the control
rats treated intragastrically with
olive oil, and the
animals in the latter three groups with 4-BDE at 50, 100 and 200 mg/kg/d, respectively, all for 30 consecutive days. Then all the
rats were killed and the
testis tissues harvested for HE
staining, examination of the
apoptosis of the
cells by
TUNEL and
determination of the expressions of H2AX
mRNA and γH2AX by q-
PCR and
Western blot.
RESULTS:
HE
staining manifested occasional reduction or absence of spermatogonial and
Sertoli cells in the
seminiferous tubules in the medium- and high-
dose 4-BDE groups. Compared with the controls, the
rats exposed to 4-BDE showed a significant
dose-dependent increase in the
apoptosis of the
testis tissue (P < 0.05), even more significant in the medium- and high-
dose 4-BDE groups than in the low-
dose group (P < 0.05). There was a
dose-effect relationship in the
apoptosis index, but with no statistically significant difference between the medium- and high-
dose 4-BDE groups (P > 0.05). The results of q-
PCR exhibited no statistically significant difference in the expression level of H2AX
mRNA either between the control and 4-BDE-exposed
rats (P > 0.05) or among the three 4-BDE groups (P > 0.05). The expression of the γH2AX
protein was remarkably higher in the 4-BDE groups than in the control (P < 0.05), but not significantly different among the 4-BDE groups (P > 0.05).
CONCLUSIONS:
Exposure to 4-BDE at 100 or 200 mg/kg/d damages the structure of
seminiferous tubules, increases the
apoptosis of testicular
cells, significantly up-regulates the expression of the γH2AX
protein, and consequently increases
DNA double-strand breaks (DSB) in the
rat testis. The
apoptosis of testicular
cells may be related to DSB./.