Abstract:
This study was conducted to investigate the prophylactic effects of lycopene (LC) and ellagic acid (EA) on 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD)-induced testicular and spermatozoal toxicity. These toxicological changes are
associated with the oxidative stress and apoptosis in male rats. Forty-eight male rats were allocated to one of six
groups of 8 rats each: control, LC, EA, TCDD, TCDD+LC, and TCDD+EA. The control group was treated with 0.5 mL/
rat slightly alkaline solution+0.5 mL/rat corn oil every other day. The LC group was treated with 0.5 mL/rat slightly
alkaline solution+0.5 mL/rat corn oil containing 10 mg/kg of LC every other day. The EA group received 0.5 mL/rat
corn oil+0.5 mL/rat slightly alkaline solution containing 2 mg/kg of EA every other day. The TCDD group received
0.5 mL/rat corn oil containing 100 ng/kg/day of TCDD+0.5 mL/rat slightly alkaline solution. The TCDD+LC group was
treated with 0.5 mL/rat TCDD+0.5 mL/rat LC. The TCDD+EA group was treated with 0.5 mL/rat TCDD+0.5 mL/rat EA.
All treatments were made by gavage, and the experimental period was maintained during 8 weeks. Sperm motility,
concentration, and abnormal sperm rate in epididymal tissue, testicular tissue lipid peroxidation (LPO), antioxidant
enzyme activity, histopathological changes, and apoptosis (i.e., Bax and Bcl-2 proteins) were determined. TCDD
exposure resulted in significant decreases in sperm motility, concentration, testicular superoxide dismutase activity,
germinal cell-layer thickness, Johnsen’s testicular score, and significant increases in abnormal sperm rate, testicular
malondialdehyde, glutathione levels, Bax-positive staining, and Bax-positive apoptotic cell score, along with some
testicular histopathological lesions. TCDD treatment did not affect significantly catalase activity. However, combined
treatment with LC or EA, in addition to TCDD, prevented the development of TCDD-induced damages in sperm
quality, testicular histology, and LPO. Improvements in testicular apoptosis after the administration of LC and EA to
TCDD-treated rats were minimal, but not statistically significant. TCDD-induced lipid peroxidation leads to functional
and structural damages, as well as apoptosis, in spermatogenic cells of rats. Both LC and EA protected against the
development of these effects
