Follicle atresia

Homeostasis of tissues Hematopoietic system (M9) Ovarian follicle atresia (Kl) Remodeling of endometrium during menstruation (Tl)... 

Hsueh, A.J.W., H. Billig and A. Tsafriri. Ovarian follicle atresia a hormonally controlled apoptotic process. 

Intermediate-duration studies with treated females show that exposure to chlordecone may result in persistent vaginal estrus, decreased ovulation, and reproductive failure. Persistent vaginal estrus was observed in female mice at doses as low as 2 mg/kg/day for 3-6 weeks (Huber 1965 Swartz and Mall 1989 Swartz et al. 1988). Increased atresia of follicles (Swartz and Mall 1989), decreased ovulation (Swartz et al. 1988), and small and medium-sized follicles (Swartz and Mall 1989) have been observed after 4 weeks of exposure to 8 mg/kg/day of chlordecone. Similarly, decreased corpora lutea have been observed following administration of 3.9 mg/kg/day for 130 days (Huber 1965). Decreased numbers of litters or complete reproductive failure have been observed after exposure of female rats to 1.62-1.71 mg/kg/day for 4.5 months or female mice to 5.2 mg/kg/day for 160 days (Huber 1965). 

Delayed follicular atresia If follicular development occurs, atresia of the follicle is sometimes delayed and the follicle may continue to grow beyond the size it would attain in a normal cycle. 

The corpus luteum arises from the ruptured follicle and secretes progesterone, which has an important role in the estrous or menstrual cycle. Luteal progesterone is also required to maintain early pregnancy in most mammalian species, including humans (Csapo Pulkkinen, 1978). Therefore, establishment and maintenance of normal corpora luteaare essential for normal reproductive function. However, with the exception of evaluations to establish their presence or absence, these structures are not evaluated in routine testing. Increased rates of follicular atresia and oocyte toxicity may lead to premature menopause in humans. Altered follicular development, failure to ovulate or altered corpus luteum formation and function can disrupt cyclicity, reduce fertility and interfere with normal sexual behaviour. Therefore, significant increases in the rate of follicular atresia, evidence of oocyte toxicity, interference with ovulation or altered corpus luteum formation or function should be considered adverse effects. 

All primary oocytes are already present about a week before birth. Many of these remain in an arrested diplotene stage of meiosis for many months before ovulation or loss by atresia. Stages of primary oocyte development are defined by the cytologic appearance of the oocyte and its follicle. 

Q1 The primordial follicles in which ova develop, form in the embryo and the maximal number 1-2 million, is present at birth. Follicles are located in the cortex of the ovary and each contains a primary oocyte. Following sexual maturation at puberty about 200 000 follicles remain, some of these will develop into primary follicles. During reproductive life a number of the primary follicles develop further, leading to ovulation, the remainder decline (a process known as atresia). 

Characteristics of the human menstrual cycle throughout reproductive life have been well described. A woman is born with approximately two million primordial follicles in her ovaries. During a normal reproductive life span, she ovulates less than 500 times. The vast majority of follicles undergo atresia. 

The morphologic hallmark is mild enlargement of both ovaries, which contain multiple small cysts surrounding the increased central ovarian stroma. The follicles may concurrently exist in different stages of growth, maturation, or atresia. 

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