HEAVY METAL TRANSFER FROM MOTHER TO FETUS DURING PREGNANCY: MOLECULAR MECHANISMS AND CLINICAL OUTCOMES (REVIEW)

Abstract

Environmental contamination with heavy metals poses a serious global health threat, with pregnant women being particularly vulnerable due to physiological changes that enhance metal absorption and distribution. This review synthesizes current knowledge on heavy metal intake pathways, molecular mechanisms of transplacental transfer, and subsequent fetal damage. Metals enter the maternal body through alimentary, inhalation, and endogenous routes, with lead mobilization from bone depots during the third trimester being especially dangerous. The placental barrier is not impermeable; metals exploit "ionic mimicry" to utilize transport systems for essential nutrients: lead uses calcium channels, cadmium employs DMT1 and ZIP transporters, methylmercury utilizes the L-amino acid system, and arsenic uses aquaporins. The transplacental transfer index is highest for methylmercury (0.9-1.2) and lead (0.7-0.9). Once in fetal circulation, metals trigger oxidative stress, driving mitochondrial dysfunction, inflammation via proinflammatory cytokines and NLRP3 inflammasome activation, steroidogenesis disruption through StAR and CYP11 suppression, and competitive displacement of essential micronutrients. Clinically, these disturbances increase risks of preterm birth (OR = 1.4 for lead), low birth weight (OR = 1.10 for cadmium), and long-term neurodevelopmental impairments, with no safe exposure threshold. The review addresses heavy metal contamination in several Russian regions, including Siberia and the Urals. Prevention requires multi-tiered strategies: exposure reduction, nutritional correction with calcium, iron, zinc, and selenium, and early detection through screening. Understanding these molecular mechanisms provides a foundation for effective preventive measures against anthropogenic environmental contamination.