دانلود مقاله ISI انگلیسی شماره 126249
ترجمه فارسی عنوان مقاله

حفاظت از سمیت تولید مثل در مردان در موش صحرایی در معرض دیان بیوتی فتالات در طول رشد جنین بوسیله تستوسترون

عنوان انگلیسی
Protection of male reproductive toxicity in rats exposed to di-n-butyl phthalate during embryonic development by testosterone
کد مقاله سال انتشار تعداد صفحات مقاله انگلیسی
126249 2017 11 صفحه PDF
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Biomedicine & Pharmacotherapy, Volume 87, March 2017, Pages 355-365

پیش نمایش مقاله
پیش نمایش مقاله  حفاظت از سمیت تولید مثل در مردان در موش صحرایی در معرض دیان بیوتی فتالات در طول رشد جنین بوسیله تستوسترون

چکیده انگلیسی

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.