Impactos da exposição prolongada a uma mistura ambientalmente relevante de desreguladores endócrinos no testículo de ratos

Abstract

Endocrine disruptors (EDs) are environmental contaminants commonly found in personal care products, food preservatives, domestic and agricultural pesticides, construction materials, plastics, and cleaning products. These compounds interfere with hormone dependent organs such as the testes, negatively affecting male fertility. This study aimed to evaluate testicular histoarchitecture in rats chronically exposed to an environmentally relevant mixture of EDs from gestation through adulthood. Pregnant Sprague Dawley rats were randomly assigned to two groups: Control (corn oil, 2 mL/kg) and ED Mix (32.11 mg/kg/day of a mixture of 12 compounds, including phthalates, pesticides, UV filters, bisphenol A, and butylparaben, in corn oil, 2 mL/kg). Dosing by oral gavage occurred from gestational day 7 (GD7) to postnatal day 21 (PND21). After weaning (PND22), male offspring (F1 generation) continued to receive the ED mixture until PND220. Testes were collected, fixed in Metacarn, and processed for histological analysis. Sections were stained with hematoxylin eosin and picrosirius red for morphometric assessment and collagen quantification. Chronic exposure to the ED mixture significantly reduced seminiferous tubule diameter and germinal epithelium height, and decreased the number of Sertoli and Leydig cells compared to control animals. Notably, the proportion of seminiferous tubules in early spermatogenic stages (I–VI) increased from 53.17 ± 1.98 in controls to 61.00 ± 0.87 in the exposed group (p = 0.002), while stages VII–VIII decreased from 46.5 [38.25–48.0] to 37.0 [33.0–39.0] (p = 0.017), indicating delayed spermatogenic progression. The incidence of abnormal tubules also increased significantly (from 0 [0–1] to 2 [1–3], p = 0.002), characterized primarily by vacuolization and the presence of immature germ cells. In contrast, no significant difference was observed in relative interstitial collagen volume between groups (p = 0.0603). These findings demonstrate that chronic ED exposure from prenatal life through adulthood induces substantial structural and functional alterations in the testis, consistent with evidence showing that endocrine active compounds disrupt steroidogenesis and spermatogenesis in male reproductive systems.