Apoptosis and Ovarian Follicular Atresia in Mammals

The reproductive performance of any mammalian species can be enhanced by enriching nutrition, regulating environmental factors like photoperiod, temperature, humidity etc., through selective breeding, endocrine manipulations and better management practices (Sharma, 2000; Maillet et al., 2002; Bussiere et al., 2002; Iwata et al., 2004, 2005; Rudolf, 2007; Bhardwaj and Sharma, 2011). The endocrine regulation despite being the most complicated is very effective in improving reproductive output of the species. In females, follicular growth and estrous cyclicity are intricately linked (Craig et al., 2007; Sharma and Batra, 2008). Of the thousands of oocytes and primordial follicles present in neonatal ovary only a small fraction i.e. approximately 0.001% are ovulated throughout the active reproductive life span of mammals (Tabarowski et al., 2005; Sharma and Bhardwaj, 2009). Follicular atresia is a wide spread phenomenon that limits the number of ovulations and thus restricting the full reproductive potential of a species. It results in extensive loss of germ cells during development, prenatal, neonatal, prepubertal, pubertal, estrous cycle, pregnancy, lactation and post reproductive life of mammals (Guraya, 1997, 1998; Sharma, 2000; Manabe et al., 2003, 2004; Bhardwaj and Sharma, 2011). Follicular atresia is a natural fertility regulatory mechanism that can best be exploited for increasing or decreasing the fertility of the species by decreasing or increasing the frequency of atresia. It is, therefore a lot of research papers have been published on morphology, histochemistry, biochemistry and endocrinology of follicular atresia (Williams and Smith, 1993; Guraya, 1998, 1999; Monniaux, 2002; Sharma, 2003; Sharma and Batra, 2008; Sharma and Bhardwaj, 2009; Bhardwaj and Sharma, 2011). However, the mechanism of atresia still needs to be further explored and analysed for its effective implementation in fertility regulation programme. The molecular mechanism of atresia can be best explained on the basis of apoptosis (Palumbo and Yeh, 1994; Sharma, 2000; Yu et al., 2004; Sharma and Bhardwaj, 2009). Apoptosis, a type of physiological cell death is the antithesis of mitosis involved in the regulation of tissue homeostasis (Collins and Lopez, 1993; Schwartzman and Cidlowski, 1993). It affects the single scattered cells in the midest of living tissues without eliciting an inflammatory response and is influenced by growth factors and hormones. Many studies on the morphological changes that occur in granulosa cells and theca-interstitial cells of follicles progressing through atresia have documented that apoptosis is, in all likelihood, the primary mechanism by which cell loss is mediated during follicle degeneration (Tsafriri and Braw, 1984; Hirshfield, 1991; Tilly, 1996). The earliest descriptions of apoptosis, the physiological cell death, in the ovary was made in