Maternal exposure to triclosan causes fetal development restriction, deregulation of the oestrous cycle, and alters uterine tissue in rat offspring

Abstract

The aim of the present study was to evaluate the effects of maternal exposure to triclosan (TCS) during pregnancy and lactation on the uterine morphology of rat offspring. For this, 32 Wistar rat dams were distributed into four dose groups (eight mothers per group), and gavage daily, throughout pregnancy and lactation, as follows: Group I–control (GI): corn oil; Group II (GII): TCS diluted in corn oil at a dose of 75 mg/kg/d; Group III (GIII): TCS diluted in corn oil at a dose of 150 mg/kg/d; Group IV (GIV): TCS diluted in corn oil at a dose of 300 mg/kg/d. A female pup of each mother was selected, and at 90 days the pups were euthanized for weighing and collection of the uterus for histomorphometric analysis. The results showed that the mean litter weight was minor in all the groups treated with TCS, when compared with control. The levels thyroid hormones thyroxine (T4) and triiodothyronine (T3) in TCS mother rats were reduced; however the levels of thyroid stimulating hormone (TSH) were increases. The offspring of all groups exposed to TCS presented deregulation of the estrous cycle, compared with control. Analysis of the uterine histological structure demonstrated that all layers of the uterus were affected by the administration of TCS, and the morphometric analysis showed increased uterine layers thickness in the treated groups. We concluded that maternal exposure to TCS during pregnancy and lactation causes intrauterine development restriction, deregulation of the oestrous cycle, and alters uterine tissue in rat offspring.

Advances in understanding the reproductive toxicity of endocrine-disrupting chemicals in women

“…In vitro studies also found that TCS can impair the proliferation, migration, and dedifferentiation of endometrial stromal cells. Stoker et al administered different doses of TCS to rats during early and pre-pregnancy, resulting in a significant advancement of vaginal opening time compared to the control group, indicating TCS’s estrogen-like effects ( Bitencourt et al, 2019 ). When mammals are exposed to low concentrations of TCS, it can be absorbed into placental tissue through the placental channel due to the limited chemical barrier function of the placenta ( Wang et al, 2015 ).…”

Morphofunctional features of the uterus of rodents: morphogenesis, structure, cyclic changes, impact of various negative environmental factors

“…Представляет интерес изучение влияния на репродуктивную систему различных широко используемых в быту бактерицидных веществ. Так, например, было выявлено, что воздействие триклозана (в дозах 75, 150 и 300 мг/кг в сутки) на самок крыс во время беременности и кормления грудью существенным образом нарушается гистофизиология матки потомства [33]. У трехмесячных крыс на фоне снижения массы отмечено нарушение эстрального цикла, во всех оболочках матки наблюдались изменения деструктивного характера в эпителии, соединительной и мышечной тканях, лейкоцитарная инфильтрация.…”

Intrauterine developmental origin, programming mechanism, and prevention strategy of fetal‐originated hypercholesterolemia

“…Offspring with IUGR are more prone to developing cardiometabolic diseases, such as hyperlipidemia, MetS, and coronary atherosclerosis 11–13 . Animal studies have also shown that adverse environmental exposure during pregnancy, such as xenobiotic exposure and food restriction, induces IUGR 14–18 . After birth, offspring with IUGR exhibit increased serum TCH levels and are more susceptible to MetS 19,20 .…”