One of the key characteristics of ovarian dysfunction and premature failure, which has been associated with an intense collagen deposition, is polycystic ovarian syndrome [92,93]. Here, the LNI rats had an increase in collagen deposition in their ovaries, demonstrating the improper functioning of ovary physiology, as well as in morphological architecture. Hatzirodos et al. [94] reported high levels of collagen and TNF expression in atretic ovarian follicles of non-pregnant cows. Moreover, TBT is known to have a direct effect on the increase of protein TNF and TNFR1 expression in rat ovarian cells after exposure at 10 mg/kg TBT [95]. Furthermore, OTs led to dysfunction during steroidogenesis and the abnormal ovarian follicular development could be attributable the binding of TNF to TNFR1, activating apoptosis pathways by cleaved caspases [95–98].