Background:Triclocarban(3,4,4-trichlorocarbanilide;TCC),an antimicrobial compound largely used in personal and household products, designated as one of the endocrine-disrupting substances(EDS),that adversely affect endocrine function in vitro and in vivo.
Aim:The objective of this study was to investigate whether in maternal exposure to TCC may pose a serious risk to the postnatal development of the ovary.
Materials and Methods:Ten pregnant female rats were equally divided into control dam group and TCC-treated dam group were supplemented with TCC 0.5 mg/L in drinking water from 5th day of gestation till the 14th post natal day(PND14). Then, ten female offspring of the control dams were divided into 2 subgroups (Neonatal and Infantile control offspring). Also, 10 female offspring of TCC-treated dams were divided into (Neonatal and Infantile TCC offspring). At the end of the experimental period, the female offspring were anesthetized and the ovaries were excised and weighed and processed for Hematoxylin and Eosin and immunohistochemical staining of Ki67 and caspse-3.Serumestradiol, progesterone, follicle stimulating hormone(FSH) and luteinizing hormone(LH),c-reactive protein(CRP), malondialdehyde(MDA) and total antioxidant capacity(TAC) were measured.
Results:TCC impaired normal folliculogenesis and impeded the normal primordial transition to other types of more developed follicles.Also,it decreased the mean area% of Ki67 and increase caspase-3 immunoexpression reflecting a decrease of proliferation and a provocation of apoptosis of follicular cells.TCC disturbed the feminine hormonal profile with increasing oxidative stress of the neonatal and infantile offspring.
Conclusion:This work highlighted the deleterious effect of maternal exposure to TCC on the folliculogenesis in the rat ovary offspring that could have implications on fetal outcome.