Table III.

Effect of stress on ovary.

Cell type	Type of stress	Test subject	Mediators	Impact	(Refs.)
Oocyte	CUS	Mice	HPA axis	Increased follicle atresia with suppressed GDF9 expression	(84)
	CRS	Mice	HPA axis	Increased abnormal bipolar spindle rates; reduced the expression of CCNB1; increased meiotic arrest failure of oocytes by inhibition of the cAMP pathway; overactivation of primordial follicles due to activation of the PI3K/AKT pathway	(20,21,93)
	N/A	Rats	NE	Decreased ovarian sympathetic activity decreases KISS1 levels and increases FSHR expression and follicle growth	(177)
	Injection of cortisol	Mice	Cortisol	Impaired oocyte development and mitochondrial membrane potential	(128,161)
Granulosa	CUS	Mice	HPA axis	Increased apoptosis due to the ROS accumulation and MAPK pathway activation	(85)
	CRS	Mice	HPA axis	Increased apoptosis via activating the Fas/FasL and TNFα system	(97,103))
	N/A	Humans	NE	Induced generation of ROS in granulosa cells	(178)
	Injection of cortisol	Mice	Cortisol	Decreased expression of IGF1 and BDNFl increased apoptosis	(128,161)
	N/A	Rats	NE	Activation of TGFβ-SMAD7 pathway and apoptosis	(179)

CUS, chronic unpredictable stress; HPA, hypothalamic-pituitary-adrenal; GDF9, growth differentiation factor 9; CRS, chronic restraint stress; CCNB1, cyclin B1; cAMP, cyclic AMP; KISS, kisspeptin; FSHR, follicle-stimulating hormone receptor; ROS, reactive oxygen species; NE, norepinephrine; IGF1, insulin-like growth factor 1; BDNF, brain-derived neurotrophic factor; TGFβ, transforming growth factor β; ET-AR, endothelin-receptor type A.