It is well known that female reproduction ability decreases during the forth decade of life due to age-related changes in oocyte quality and quantity; although the number of women trying to conceive has today increased remarkably between the ages of 36 to 44. The causes of reproductive aging and physiological aspects of this phenomenon are still elusive. With increase in the women's age, during Assisted Reproductive Technologies (ART) we have perceived a significant decline in the number and quality of retrieved oocytes, as well as in ovarian follicle reserves. This is because of increased aneuploidy due to factors such as spindle apparatus disruption; oxidative stress and mitochondrial damage. The aim of this review paper is to study data on the potential role of the aging process impacting oocyte quality and female reproductive ability. We present the current evidence that show the decreased oocyte quality with age, related to reductions in female reproductive outcome. The aging process is complicated and it is caused by many factors that control cellular and organism life span. Although the factors responsible for reduced oocyte quality remain unknown, the present review focuses on the potential role of ovarian follicle environment, oocyte structure and its organelles. To find a way to optimize oocyte quality and ameliorate clinical outcomes for women with aging-related causes of infertility.

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Many recent studies have demonstrated that most nanoparticles (NPs) have an adverse or toxic action on male germ cells. In present study, protective effect of quercetin (Que) on titanium dioxide nanoparticle (NTiO)-induced spermatogenesis defects in mice was investigated. Thirty-two Naval Medical Research Institute (NMRI) mice were randomly divided into four groups. Que group received 75 mg/kg of Que for 42 days. NTiO group received 300 mg/kg NTiO for 35 days. NTiO + Que group initially received 75 mg/kg Que for 7 days and was followed by concomitant administration of 300 mg/kg NTiO for 35 days. Control group received only normal saline for 42 days. Sperm parameters, testosterone concentration, histological criteria, and apoptotic index were assessed. Product of lipid peroxidation (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were also evaluated for oxidative stress in testicular tissue. Administration of NTiO significantly induced histological changes in testicular tissue; increased apoptotic index; and decreased testicular weight, testosterone concentration, and sperm quality (p < 0.01). In the testis, NTiO increased oxidative stress through an increase in lipid peroxidation and a decrease in SOD and CAT activities (p < 0.05). Que pretreatment could significantly attenuate testicular weight; apoptotic index; and histological criteria including vacuolization, detachment, and sloughing of germ cells in seminiferous tubules. Serum and tissue testosterone levels were significantly increased in Que-pretreated mice (p < 0.01). Sperm parameters including sperm number, motility, and percentage of abnormality were also effectively improved by Que pretreatment (p < 0.01). Pretreatment of Que significantly ameliorated oxidative stress and increased the activities of SOD and CAT in testicular tissue. These results indicate that sperm production can be increased by Que pretreatment in NTiO-intoxicated mice. The improved sperm quality and reverse testis histology by Que pretreatment may be a consequence of elevation testosterone concentration, reduction in germ cell apoptosis, and suppression of oxidative stress in testicular tissue.

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