Table 1.

Related OS factors leading to ovarian aging

Influence Factors	Injury Effects Summary
Aging	• Decreased pregnancy and live birth rates • Increased ROS production, decreased antioxidant system defense • Frequent DSBs, inefficient DDR repair, accumulation of DNA damage • Mitochondrial dysfunction • Accumulation of biomacromolecules damage
Cigarette smoking	• Extension of conception time, reduction of fertility incidence, extension of IVF-ET treatment cycles • Increased ROS formation, depletion of protective antioxidants • Impairment of ovarian function in female offspring
High-sugar diet	• Increasing levels of ROS through AGEs production • Dysregulation of insulin signaling pathway • Hyperplasia of extracellular matrix • Impairment of blood vessel • Induction of inflammation and hypoxia
Pressure	• Reduced pregnancy rate • Direct negative effects on HPO and HPA axes • Decrease of antioxidant expression • Accelerated cellular autophagy, apoptosis and paraptosis • Disorder of endocrine hormone
Superovulation	• Increased ROS levels and inflammatory response • Reduced primordial follicles • Increased risk of osteoporosis and cardiovascular disease in the long term
Chemotherapy	• Depletion of antioxidant enzymes • Mitochondrial dysfunction, lipid peroxidation • Exacerbated cell apoptosis • Atresia of growing follicles, overactivation of primordial follicular
Industrial Pollution	• Reduction of mitochondrial membrane potential • Exacerbated DNA damage • Spindle assembly destruction • Increased cell apoptosis and autophagy • Inhibition of steroid synthesis

ROS Reactive oxygen species, DSBs DNA double-strand breaks, DDR DNA damage response, IVF-ET In vitro fertilization-embryo transfer, AREs Antioxidant response elements, HPO Hypothalamic-pituitary-ovarian, HPA hypothalamus–pituitary–adrenal