Abstract
Heavy metals are naturally occurring elements that have numerous applications in industries, agriculture, and other sectors, leading to their widespread distribution in the environment. The constant emission of heavy metals into the environment raises concerns about their impact and harmful effects on living organisms, including human health. Key threats arise from exposure to heavy metals such as lead, cadmium, mercury, and arsenic, all of which are classified as carcinogens. Chronic exposure and bioaccumulation of these metals can result in toxic effects on various body systems, including the female reproductive system. Notably, heavy metals can induce oxidative stress, generate excessive reactive oxygen species, and impair antioxidant defense systems. These metals may also lead to DNA damage, enzyme inactivation, and epigenetic modifications, ultimately disrupting critical cellular processes such as growth, proliferation, differentiation, repair, and apoptosis. Furthermore, some heavy metals can mimic endogenous estrogens, interact with estrogen receptors, and cause hormonal disruptions, a mechanism particularly relevant to the pathogenesis of female-related cancers. Despite significant advances, many gaps remain in our understanding of the molecular mechanisms by which heavy metals contribute to cancer development. Addressing these gaps could facilitate the development of more effective strategies for the prevention and treatment of female cancers. This review highlights the potential effects of heavy metals on molecular pathways in female cancers, suggesting several mechanisms of cancer development.