Evidence map›Paper›PMID 22094459›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2012

Subchronic polychlorinated biphenyl (Aroclor 1254) exposure produces oxidative damage and neuronal death of ventral midbrain dopaminergic systems.

Donna W Lee, Sarah A Notter, Mona Thiruchelvam, Daniel P Dever, Richard Fitzpatrick, Paul J Kostyniak, Deborah A Cory-Slechta, Lisa A Opanashuk

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.5field-weighted citation impact, top 20% of its field
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

33 citing papers in PubMed, 57 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Donna W LeeDepartment of Environmental Medicine, School of Medicine and Dentistry, University of Rochester, Rochester, New York 14642, USA.
Sarah A Notter
Mona Thiruchelvam
Daniel P Dever
Richard Fitzpatrick
Paul J Kostyniak
Deborah A Cory-Slechta
Lisa A Opanashuk
University of Rochester · USUniversity at Buffalo, State University of New York · USEnvironmental and Occupational Health Sciences Institute · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Katrina S Korfmacher · 1985 to 2026
$42.8M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
PCB Neurotoxicity: Effects on Cerebellar DevelopmentK22ES000375 · NIEHS · UNIVERSITY OF ROCHESTER · PI OPANASHUK, LISA A · 2002 to 2004
$324k
NIEHS NIH HHS K22 ES00375NIEHS NIH HHS P30 ES01247NIEHS NIH HHS T32 ES07026
6 · The paper itself

Abstract

Recent epidemiologic studies have demonstrated a link between organochlorine and pesticide exposure to an enhanced risk for neurodegenerative disorders such as Parkinson's disease (PD). A common biological phenomenon underlying cell injury associated with both polychlorinated biphenyl (PCB) exposure and dopaminergic neurodegeneration during aging is oxidative stress (OS). In this study, we tested the hypothesis that oral PCB exposure, via food ingestion, impairs dopamine systems in the adult murine brain. We determined whether PCB exposure was associated with OS in dopaminergic neurons, a population of cells that selectively degenerate in PD. After 4 weeks of oral exposure to the PCB mixture Aroclor 1254, several congeners, mostly ortho substituted, accumulated throughout the brain. Significant increases in locomotor activity were observed within 2 weeks, which persisted after cessation of PCB exposure. Stereologic analyses revealed a significant loss of dopaminergic neurons within the substantia nigra and ventral tegmental area. However, striatal dopamine levels were elevated, suggesting that compensatory mechanisms exist to maintain dopamine homeostasis, which could contribute to the observed increases in locomotor activity following PCB exposure. Biochemical experiments revealed alterations in OS markers, including increases in SOD and HO-1 levels and the presence of oxidatively modified lipids and proteins. These findings were accompanied by elevated iron levels within the striatal and midbrain regions, perhaps due to the observed dysregulation of transferrin receptors and ferritin levels following PCB exposure. In this study, we suggest that both OS and the uncoupling of iron regulation contribute to dopamine neuron degeneration and hyperactivity following PCB exposure.

Indexed as

Administration, OralAnimalsCell DeathChlorodiphenyl (54% Chlorine)DopamineDopamine Plasma Membrane Transport ProteinsDopaminergic NeuronsDose-Response Relationship, DrugEnvironmental PollutantsHeme Oxygenase-1HyperkinesisIronLipid PeroxidationMaleMembrane ProteinsMesencephalonChlorodiphenyl (54% Chlorine)DopamineDopamine Plasma Membrane Transport ProteinsEnvironmental PollutantsHeme Oxygenase-1Hmox1 protein, mouseIronMembrane ProteinsSuperoxide DismutaseTyrosine 3-Monooxygenase

Identifiers

PMID22094459
PMCPMC3262858
OpenAlexW2146008657

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.