ArticleOxidative medicine and cellular longevity2019
Chronic Lead Exposure Results in Auditory Deficits and Disruption of Hair Cells in Postweaning Rats.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Subtype-Specific Vulnerability of Spiral Ganglion Neurons in Sensorineural Hearing Loss Across the Lifespan.Brain sciences · 2026Review
- Bisphenol A induces ototoxic injury by ferroptosis pathway: integrated analysis of network toxicology, RNA-sequencing and experimental validation.Frontiers in molecular neuroscience · 2026Article
- Lead exposure and physical frailty in patients with type 2 diabetes mellitus: cross-sectional results from the METAL study.Endocrine · 2025Article
- Baicalein ameliorates DSS-induced ulcerative colitis in mice by inhibiting ferroptosis and regulating gut microbiota.Frontiers in pharmacology · 2025Article
- Unraveling the molecular landscape of lead-induced cochlear synaptopathy: a quantitative proteomics analysis.Frontiers in cellular neuroscience · 2024Article
- Lutein-Rich Beverage Alleviates Visual Fatigue in the Hyperglycemia Model of Sprague-Dawley Rats.Metabolites · 2023Article
- Neurotoxicity and Outcomes from Developmental Lead Exposure: Persistent or Permanent?Environmental health perspectives · 2023Article
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Authors and funding
3 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
objectiveThe effects of lead exposure on cognitive function have been studied intensively over the past decade, but less attention has focused on its impact on auditory function. This study is aimed at investigating the effect of lead on the cochlea and the molecular mechanisms responsible for its actions.
methods0.2% lead acetate was administered to rats in drinking water for 30, 60, and 90 days. Brainstem auditory evoked responses (ABR) were recorded, and morphological changes in the hair cells were observed. We also measured glutathione (GSH) and malondialdehyde (MDA) concentrations and antioxidant enzyme activities such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) activities in the cochlea.
resultsLead exposure increased the ABR threshold and slightly prolonged the latencies of wave II and wave IV in rats. Abnormally shaped hair cells and loss of hair cells were found in the cochlea basilar membrane, together with degenerative changes in spiral ganglion neurons following lead exposure. The activities of some antioxidant enzymes were also reduced in association with upregulation of MDA expression. These effects may be caused by impaired catalytic function of the enzymes as a result of lead interaction.
conclusionThe antioxidant system of the cochlea in the immature rat brain is highly vulnerable to developmental lead exposure. Oxidative stress may therefore represent a possible mechanism for lead-induced auditory deficits.
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