Evidence map›Paper›PMID 40465124›Full record

ReviewEnvironmental science and pollution research international2025

Metal mechanisms of mitochondrial toxicity: recent review of arsenic, cadmium, and lead-induced nephrotoxicity.

Rachel E Turkington, Neil A Hukriede, Jacqueline Ho, Nishad Jayasundara, Alison P Sanders

Abstract readReview
In one paragraph

Review in Environmental science and pollution research international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

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  12. Chronic exposure to low levels of glyphosate and metals induces kidney dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2026
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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

5 authors.

Rachel E TurkingtonDepartment of Environmental and Occupational Health, School of Public Health, University of Pittsburgh, 130 De Soto St, Pittsburgh, PA, 15261, USA.
Neil A HukriedeCenter for Integrative Organ Systems, Department of Cell Biology, Biological Sciences Tower 3, University of Pittsburgh, 5065, 3501 Fifth Avenue, Pittsburgh, PA, 15213, USA.
Jacqueline HoDepartment of Pediatrics, School of Medicine, University of Pittsburgh, UPMC Children's Hospital of Pittsburgh, 4401 Penn Ave, Pittsburgh, PA, 15224, USA.
Nishad JayasundaraNicholas School of the Environment, Duke University, 9 Circuit Dr, Durham, NC, 27710, USA.
Alison P SandersDepartment of Environmental and Occupational Health, School of Public Health, University of Pittsburgh, 130 De Soto St, Pittsburgh, PA, 15261, USA. APS109@pitt.edu.ORCID http://orcid.org/0000-0001-8252-4016

Funding

Resource Development CoreU54DK137329 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Gerard L Apodaca · 2023 to 2026
$4.8M
Metal mixture effects on mitochondrial dysfunction in kidney development and maturation: Towards a whole mixture risk assessmentR01ES033466 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SANDERS, ALISON P · 2023 to 2025
$2.2M
NIDDK NIH HHS U54 DK137329NIEHS NIH HHS R01 ES033466NIEHS NIH HHS R01ES033466
6 · The paper itself

Abstract

The kidney is rich in mitochondria that are vulnerable to toxic metal injury during the filtration, secretion, and reabsorption processes required for the excretion of wastes, solutes, and xenobiotics. Understanding the mechanisms of mitochondrial toxicity of metals can provide critical insights into the mitochondrial etiology of kidney damage and the susceptible nephron segments. Recent research has revealed potential new mechanisms of mitochondrial toxicity and related adverse bioenergetic effects due to metal and metalloid exposure. Here we reviewed 20 studies on the mitotoxic effects from exposure to arsenic (n = 6), cadmium (n = 10), and lead (n = 3) as individual toxicants and as mixtures (n = 1) to gain insights into mitochondrial mechanisms of nephrotoxicity and to identify current research gaps. Studies have shown that exposure to toxic metals is associated with adverse kidney health and function with underlying changes in gene expression and enzymatic activity, loss of mitochondrial membrane potential, cellular oxidative imbalance, and inhibited electron transport. The mechanisms of damage and the severity of injury were metal and dose dependent. The proximal tubule was the most prevalent target segment of the nephron for metal-induced mitochondrial toxicity, specifically to cadmium exposure as an individual toxicant and as part of a mixture. There is a clear need to understand metal-induced mitochondrial nephrotoxicity and key research gaps that need to be filled, including the need for sex-specific and time-series studies.

Indexed as

ArsenicCadmiumKidneyLeadMitochondriaAnimalsHumansArsenicCadmiumLeadArsenicCadmiumKidney diseaseLeadMechanismsMitochondrial toxicityNephrotoxicity

Identifiers

PMID40465124
PMCPMC12202593

What OpenQuestion holds

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Registered trials

None linked

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 OpenQuestion graph.