Modulation of the PI3K/AKT/mTOR and AMPK/TSC2/mTOR Pathways by N-Acetyl-L-Cysteine as a Protector of Embryonic Bodies from the Toxic Effect of Methylmercury

Methylmercury (MeHg) is a potent environmental contaminant primarily ingested through seafood consumption. Gestational exposure induces profound neurological and developmental deficits in the fetus that often persist throughout childhood. This developmental vulnerability arises from the immature state of the blood–brain barrier and a limited endogenous antioxidant capacity in the developing CNS. Postnatal exposure via breastfeeding further compromises neurodevelopment, specifically impairing visuospatial processing and memory. While fetal and placental mercury accumulation correlates with gestational age, the specific mechanisms of transplacental transport remain poorly defined. Mechanistically, MeHg predominantly accumulates in fetal renal tissue, followed by the brain and liver. This review aims to elucidate MeHg-induced oxidative stress and autophagic collapse mediated by the PI3K/AKT/mTOR and AMPK/TSC2/mTOR pathways. Furthermore, we evaluate neuroprotective candidates, specifically N-acetyl-L-cysteine (NAC) and CCL chemokine modulation, as strategies to mitigate fetal impairment and the associated cellular damage.