Microcystins and Reproductive Dysfunction: Mechanisms and Consequences

Accelerating eutrophication of aquatic ecosystems worldwide has increased concern regarding cyanotoxin exposure as an emerging environmental and public health issue, with Microcystin-LR (MC-LR) among the most extensively studied congeners due to its widespread occurrence and high toxicity. Evidence from experimental animal and cellular studies indicates that MC-LR elicits pronounced toxic impacts on both the male and female reproductive systems. In males, MC-LR induces overt testicular injury, compromises the structural and functional integrity of the blood–testis barrier, and triggers severe disorders in reproductive hormone synthesis and secretion. In females, it precipitates ovarian dysfunction, impedes normal follicular maturation and development, and induces distinct embryotoxic effects. The underlying pathogenic mechanisms involve the synergistic interplay of multiple signaling pathways, primarily including oxidative stress induction, aberrant apoptosis activation, endocrine disruption, and epigenetic modifications. Of particular significance, emerging evidence suggests that parental exposure to MC-LR may induce intergenerational or potentially transgenerational reproductive effects through epigenetic modifications in germ cells, impairing fertility and developmental outcomes in subsequent offspring and thus posing a sustained, long-term threat to population-level health. This review systematically delineates the reproductive toxicity profiles and underlying molecular mechanisms of MC-LR, evaluates its transgenerational health hazards, and aims to furnish robust scientific evidence for the formulation of targeted environmental health policies and risk management strategies.