Irisin as an emerging target in the regulation of reproductive functions in health and disease.

Germ cells are highly conserved in the gonads, nurtured to either develop into a gamete or self-renew into a stem cell reserve. Preserving the germ cell pool and protecting the reproductive organs is essential for maintaining an individual's fertility. Several factors, including a sedentary lifestyle, pollutants, hormonal disruption, drugs, and a disease condition, have been shown to impair normal reproductive function. Irisin has recently been identified as an adipomyokine involved in modulating physiological functions based on the body's metabolic status. It is being studied for its role in various functions, including fertility. Findings show the localization of irisin in various parts of the reproductive axis, with the highest levels observed during puberty and pregnancy. This raises questions about its role and function in reproduction. Studies support irisin's role in protecting against disease-induced reproductive abnormalities and infertility. Therefore, the current review focuses on how irisin influences spermatogenesis and ovarian follicular development and plays a significant role in indirectly preserving the germ cell pool by protecting the gonads against oxidative stress and inflammation.

Arsenic-Induced Thyroid Hormonal Alterations and Their Putative Influence on Ovarian Follicles in Balb/c Mice.

Thyroid issues are common among women in their reproductive years, and women with thyroid dysfunction often encounter challenges with fertility. Arsenic is known for its toxic effects on the thyroid and ovaries, investigated independently. However, there is no known study directly or indirectly addressing the association between arsenic, thyroid function, and ovarian reserve. This study aims to investigate the effect of arsenic on thyroid function and its possible implications on ovarian follicular reserve. Female Balb/c mice were given sodium arsenite (0.2 ppm, 2 ppm, and 20 ppm) via drinking water for 30 days. Findings showed that arsenic decreased thyroid hormone levels (fT3 and fT4) while increasing TSH levels, which might have led to elevated levels of FSH and LH. Furthermore, arsenic treatment not only decreased thyroid follicle sizes but also altered the ovarian follicular count. The finding demonstrates that arsenic significantly reduced the expression of LAMP1, a lysosomal marker protein. This reduction leads to increased lysosomal permeability in the thyroid, resulting in a significant release of cathepsin B. These changes led to hypothyroidism, which might indirectly affect the ovaries. Also, the elevated levels of growth differentiation factor-8 in arsenic-treated ovaries indicate impaired folliculogenesis and ovulation. Furthermore, arsenic significantly increased the expressions of pAkt and pFoxo3a, implying that arsenic accelerated the activation of the primordial follicular pools. In conclusion, arsenic disrupts lysosomal stabilization, potentially leading to a decline in circulating fT3 and fT4 levels. This disturbance could, in turn, affect the estrous cycle and may alter the pattern of follicular development.

Developmental and reproductive toxic effects of exposure to microplastics: A review of associated signaling pathways.

Microplastics (MPs), small pieces of plastic (∼5 mm), are released into the environment not only as a result of the decomposition of large-sized plastics but also from day-to-day use of plastic products. Chronic exposure to MPs has been attributed to harmful effects on aquatic organisms and rodents. Effects include gastrointestinal toxicity, hepatotoxicity, neurotoxicity, and reproductive and developmental toxicities. Exposure to MPs may also potentially affect human health. Herein, we reviewed the impact of MPs on male and female reproductive systems and the associated mechanisms involved in the reproductive and developmental toxicities of MPs. We performed a literature search in Google Scholar and PubMed using the following keywords: MPs and reproductive toxicity; MPs and developmental studies; MPs and infertility; MPs and aquatics; and MPs and rodents. Evidence of MPs accumulation has been reported in many organs of humans and experimental models. The harmful effects of MPs have been manifested in male and female reproductive systems of mammalian and aquatic animals, including developmental effects on gametes, embryos, and their offspring. This review describes various signaling pathways involved in MPs-associated male and female reproductive and developmental toxicities.