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Maternal transfer of nonylphenol drives oxidative, immune, and epigenetic dysregulation in zebrafish offspring.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Maternal transfer of nonylphenol drives oxidative, immune, and epigenetic dysregulation in zebrafish offspring.
Συγγραφείς: Samanta, Anwesha1 (AUTHOR), Maitra, Sudipta1 (AUTHOR) sudipta.maitra@visva-bharati.ac.in
Πηγή: Journal of Environmental Sciences (Elsevier). Oct2026, Vol. 168, p765-780. 16p.
Θεματικοί όροι: Nonylphenol, Epigenetics, Genetic toxicology, Brachydanio, Immunosuppression, Oxidative stress, Chemical transportation, Environmental toxicology
Περίληψη: • Maternal NP exposure increases larval malformations and mortality. • Maternal NP transfer drives oxidative stress, immune suppression, apoptosis. • Direct NP exposure triggers adaptive inflammation without lethality. • Comparative findings highlight maternal NP transfer in ecotoxicological risk. Nonylphenol (NP), a widespread surfactant and endocrine-disrupting pollutant, poses significant ecological and public health risks globally; however, its transgenerational effects remain poorly understood. Using zebrafish (Danio rerio), we compared chronic maternal NP exposure (50 and 100 µg/L, 28 days) with acute embryonic exposure (0.22 µmol/L) during 0–3 days post-fertilization (dpf) to delineate mechanistic differences in toxicity. Maternal NP exposure produced severe developmental defects in offspring, including edema, axial curvature, impaired swim bladder inflation, reduced growth, cardiac dysfunction, and decreased viability. These phenotypes were accompanied by systemic molecular disruptions including oxidative stress, altered estrogen receptor (ER) expression, dysregulated mitogen-activated protein kinase (MAPK) signaling, and suppressed innate immune response characterized by attenuated neutrophil/macrophage density, reduced CD68 and complement protein C3 expression, diminished nitrite load, and downregulation of pro-inflammatory mediators at both transcript and protein levels. Maternal exposure further induced apoptosis and persistent epigenetic reprogramming (alterations in DNA methylation and histone-modifying enzymes), hallmarks of transgenerational toxicity. In contrast, direct embryonic NP exposure elicited morphological abnormalities without significant lethality, accompanied by induction of pro-inflammatory cytokines, nitric oxide (NO) synthesis, and MAPK activation, reflecting an augmented inflammatory response. These mechanistic contrasts reveal that maternal NP exposure is a potent driver of systemic, heritable molecular reprogramming, whereas embryonic exposure triggers acute inflammatory pathways. Together, our findings underscore the global relevance of NP as a transgenerational toxicant, advocating for its urgent inclusion in ecotoxicological risk assessments and regulatory frameworks. [Display omitted] [ABSTRACT FROM AUTHOR]
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Περιγραφή
ISSN:10010742
DOI:10.1016/j.jes.2026.01.084