Evidence map›Paper›PMID 42297280›Full record

ArticleEnvironmental research2026

Embryonic lead (Pb) contact impairs lipid, oxidative, and behavioral markers in zebrafish across multiple generations.

Wagner A Tamagno, Hellen Weinschutz Mendes, Sydney C Stradtman, Karthikeyan S N Chelladurai, Christina R Ferreira, Chongli Yuan, Jennifer L Freeman

Abstract read
In one paragraph

Article in Environmental research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Wagner A TamagnoSchool of Health Sciences, Purdue University, West Lafayette, IN, USA.
Hellen Weinschutz MendesSchool of Health Sciences, Purdue University, West Lafayette, IN, USA.
Sydney C StradtmanSchool of Health Sciences, Purdue University, West Lafayette, IN, USA.
Karthikeyan S N ChelladuraiSchool of Health Sciences, Purdue University, West Lafayette, IN, USA.
Christina R FerreiraBindley Bioscience Center, Purdue University, West Lafayette, IN, USA.
Chongli YuanDavidson School of Chemical Engineering, Purdue University, West Lafayette, IN, USA.
Jennifer L FreemanSchool of Health Sciences, Purdue University, West Lafayette, IN, USA. Electronic address: jfreema@purdue.edu.

Funding

Mechanisms of gene-environment interaction in developmental lead exposure leading to Alzheimer's disease phenotypesR01NS130722 · NINDS · PURDUE UNIVERSITY · PI Jennifer L. Freeman, Chongli Yuan · 2022 to 2026
$3.7M
NINDS NIH HHS R01 NS130722
6 · The paper itself

Abstract

The heavy metal lead (Pb) is widely accepted as a toxicant that impairs different physiological functions dependent on dose. The central nervous system (CNS) is highly sensitive to Pb especially when exposure occurs during early developmental periods. Moreover, even low Pb exposures during development can be detrimental and have long-lasting effects on the individual. Pb has also been implicated to exert changes across generations, impairing physiological traits as well as behavioral markers exerting an impairment in the health span. In this study, the developmental effect of environmental-relevant concentrations of Pb (0.01, 0.1, and 1 ppb; μg/L) were assessed in the F1 (multigenerational) and F2 (transgenerational) generations from an F0-exposed zebrafish (Danio rerio). Behavioral, oxidative, and lipid-profiling were assessed for these generations to identify changes inherited from developmental Pb contact. Behavioral assessments revealed an embryonic Pb exposure in the F0 generation led to significant hypolocomotion, anxiolytic- and anxiogenic-like behaviors, impaired social interaction, and reduced decision-making capacity in F1 larvae. On the other hand, minimal effects were observed in the F2 larvae. Lipidomic analysis indicated these behavioral phenotypes were associated with altered levels of sphingomyelins, phosphatidylcholines, and cholesterol esters, suggesting disrupted neuronal signaling and membrane homeostasis. Enzymatic alterations were related to glutathione metabolism and those might be driven by some mechanistic Pb-induced epigenetic modifications. Together, these findings provide evidence that low-level Pb exposure induces multigenerational neurobehavioral toxicity, mediated by lipidomic and redox pathway disruptions, with implications for long-term environmental health risk assessment.

Indexed as

Behavior, AnimalLeadLipid MetabolismOxidative StressWater Pollutants, ChemicalZebrafishAnimalsEmbryo, NonmammalianFemaleLeadWater Pollutants, ChemicalBehaviorMetal toxicityMultigenerationalNeurotoxicityTransgenerational

Identifiers

PMID42297280
PMCPMC13343456

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.