Figure 1

A schematic diagram showing the possible mechanism of NLE action at the level of follicle in mammalian ovary. NLE inhibits catalase activity and induces the accumulation of H₂O₂ inside the follicular microenvironment of the ovary. The increased H₂O₂ level induces granulosa cell apoptosis through mitochondria-caspase-mediated pathway. Granulosa cell apoptosis leads to disruption of gap junction, interruption in the transfer of signal molecules from cumulus cells to the oocyte and reduction of estradiol 17-β level further deprive oocyte from nutrients and survival factors. The H₂O₂ also enters directly in the oocyte and trigger oocytes apoptosis. Under this condition, pro-apoptotic factors are upregulated and oocyte becomes susceptible towards apoptosis. NLE induced apoptosis leads to the deterioration in the oocyte quality and limit reproductive outcome in mammals.