ArticleResearch square2026
Prenatal methylmercury exposure disrupts developmental trajectories and induces sex-specific toxicity in pubertal rats.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Prenatal exposure to the environmental toxicant methylmercury (MeHg) remains a significant public health concern, particularly during vulnerable developmental windows when toxicant susceptibility and sex-specific biology may shape long-term health outcomes. This study examined how a maternal diet spiked with environmentally relevant MeHg levels, including low (400 ppb) and high (800 ppb) concentrations reflecting federal and state consumption advisory guidelines for contaminated fish, affects fetal and postnatal growth, developmental maturation, and circulating biomarkers of liver function, inflammation, and oxidative stress in male and female offspring. Methods: Timed-pregnant Sprague-Dawley rats were exposed to diets containing vehicle, 400 ppb MeHg, or 800 ppb MeHg from gestational day (GD) 8 through late gestation (GD20) or parturition (GD22-23). Offspring were evaluated for fetal and placental growth (GD20), postnatal developmental milestones (eye opening and pubertal onset), postnatal growth trajectories, pubertal organ weights, and circulating biomarkers during puberty. Total Hg was quantified using direct thermal decomposition, gold amalgamation, and atomic absorption spectrometry. Plasma liver injury biomarkers and cytokine/chemokine profiles were measured using MILLIPLEZ magnetic bead assays. Circulating oxidized proteins were assessed using an advanced oxidation protein products (AOPP) assay. Results: Gestational MeHg exposure produced dose-dependent Hg accumulation in maternal, placental, fetal, and pubertal offspring tissues, with distinct sex differences in biodistribution. High dose MeHg exposure reduced placental weight but increased placental efficiency and delayed eye opening and male-but not female-pubertal onset. Postnatal growth effects were sex- and dose-dependent, with high dose MeHg-exposed males weighing less and high dose MeHg-exposed females weighing more during late adolescence. Organ weights and circulating biomarkers of liver function (ARG1, SDH, AST, 5'-NT) and inflammatory cytokines (TNF-α, IL-2, IL-1α, IL-17A, IL-6) in pubertal offspring were differentially altered by sex and MeHg dose, indicating persistent metabolic and immune dysregulation. Conclusions: Environmentally relevant prenatal MeHg exposure disrupts developmental trajectories and induces long-lasting, sex-specific alterations in growth, hepatic function, and inflammatory signaling. These findings highlight sex as a critical biological variable in developmental toxicology and underscore the need to consider sex-dependent mechanisms when evaluating early-life environmental exposures and their long-term health consequences.
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