Oxidative stress, apoptosis and cellular proliferation in uterus exposed to endocrine-active compounds - an ex vivo study on sow-fed and formula-fed piglets - research data

Our study investigates whether neonatal exposure to endocrine-active compounds that modulate androgen and estrogen signaling induces oxidative stress and disrupts cellular proliferation and apoptosis in the developing porcine uterus. Furthermore, we hypothesize that these effects differ between piglets fed maternal milk and those receiving a milk replacer. To test this, we employed an ex vivo model to assess the solely effects of the antiandrogen 2-hydroxyflutamide, the environmental estrogen 4-tert-octylphenol, and the organochlorine insecticide methoxychlor metabolite 2,2-bis-(p-hydroxyphenyl)-1,1,1-trichloroethane (HPTE), which exhibits mixed steroidal properties (estrogenic, antiestrogenic and/or antiandrogenic), on oxidative stress, apoptosis, and cellular proliferation in uterine explants from 10-day-old sow-fed or formula-fed piglets. The dataset includes results from the quantification of reactive oxygen and nitrogen species levels and antioxidant enzyme activities, identification and measurement of proliferating and apoptotic cells via immunohistochemistry and TUNEL assays, and semi-quantitative analysis of apoptosis- and proliferation-associated protein abundance using Western blotting.