Impact of oxidative stress induced by heavy metals on ovarian function Original paper

What was studied?

This review examines the detrimental impact of heavy metals, including copper, arsenic, cadmium, mercury, and lead, on ovarian function, particularly through the induction of oxidative stress (OS). These heavy metals are known to generate reactive oxygen species (ROS), leading to cellular damage, apoptosis, and follicular atresia, all of which contribute to premature ovarian insufficiency (POI). The study focuses on the molecular and cellular mechanisms by which these metals affect ovarian health, highlighting their role in disrupting hormone production and accelerating ovarian aging.

Who was studied?

The review incorporates data from both human and animal studies, with a focus on research involving rodents as animal models. These studies explore the physiological effects of heavy metal exposure on ovarian cells, including granulosa cells and oocytes. It also examines the biochemical and physiological consequences of heavy metal toxicity in human populations, particularly those exposed to environmental pollutants, as well as laboratory findings that investigate the molecular mechanisms underlying ovarian damage caused by these metals.

Most important findings

The review underscores the significant role of oxidative stress in mediating the harmful effects of heavy metals on ovarian function. Metals like arsenic, cadmium, and mercury generate excessive ROS, which in turn disrupt mitochondrial function, induce DNA damage, and trigger apoptosis in ovarian cells. These metals also impair the activity of critical antioxidant enzymes, exacerbating oxidative damage. For example, copper exposure leads to follicular disruption and increased cell death, while arsenic accelerates ovarian failure by reducing levels of estrogen and anti-Müllerian hormone (AMH). Overall, the evidence suggests that these metals contribute to a decline in ovarian reserve, leading to early menopause and reduced fertility.

Key implications

The findings highlight the importance of addressing environmental heavy metal exposure as a potential risk factor for POI. The role of oxidative stress in the pathogenesis of ovarian dysfunction suggests that preventive measures, such as reducing exposure to environmental pollutants, could help protect ovarian health. Additionally, antioxidant treatments may offer a promising therapeutic approach to mitigate the damaging effects of oxidative stress caused by heavy metal exposure. Clinicians should consider these environmental factors when diagnosing and treating women with premature ovarian insufficiency.