Protection of male reproductive toxicity in rats exposed to di-n-butyl phthalate during embryonic development by testosterone

- In-utero exposure of DBP causes fertility alteration by increased pre and post-implantation losses.
- In-utero exposure of DBP effects on testes and seminal vesicle weight with decreased sperm count, motility, viability and HOS tail coiled sperm.
- In-utero exposure of DBP effects on testicular 3β, 17βHSD enzymes and serum testosterone, FSH and LH levels.
- In-utero exposure of DBP increases testicular oxidative stress with decreased antioxidant enzymes such as SOD, CAT and GPx.
- Testosterone supplement to in-utero DBP exposed rats, deteriorates DBP induced reproductive toxicity.

Di-n-butyl phthalate (DBP) widely spread industrial chemical that made drastic alteration in male reproductive system. The present study elucidates the protective role of testosterone on reproductive toxicity in prenatal DBP exposed adult male rats. Pregnant rats were injected with corn oil or 100 and 500 mg/kg body weight of DBP on gestation day (GD) 1, 7 and 14. F1 male rats were weaned, injected with either testosterone or vehicle. On postnatal day (PND) 100 F1 adult male rats were cohabited with untreated female rats. Then rats were sacrificed and analyzed for other reproductive end points. Prenatal DBP exposed male rat testes, seminal vesicle weight, sperm count, motility, viability and HOS tail coiled sperm were significantly decreased with increased sperm morphological abnormalities. The levels of testicular 3β, 17βHSD, serum testosterone were significantly decreased with increased FSH, LH levels in experimental rats. The fertility studies revealed that increased pre, post-implantation losses and resorptions in normal females cohabited with experimental rats. Higher testicular LPO with lower SOD, CAT and GPx activity levels in experimental rats. Administration of testosterone to prenatal DBP treated male rats showed significant protection in above all parameters. In conclusions, testosterone deteriorates prenatal DBP induced reproductive and fertility toxicity by decreased oxidative stress and increased testicular antioxidant enzymes.