ArticleJournal of bioenergetics and biomembranes2023
Exposure of combination of environmental pollutant, lead (Pb) and β-amyloid peptides causes mitochondrial dysfunction and oxidative stress in human neuronal cells.
Article in Journal of bioenergetics and biomembranes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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.
Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Perinatal lead (Pb) exposure and alterations to amyloid beta and metabolic profiles in the brain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Comparative Efficacy of Coriander Seed Extract-Loaded Selenium Nanoparticles and DMSA in Restoring Antioxidant/Apoptotic Balance of Lead-Induced Hepatotoxicity.Cell biochemistry and biophysics · 2026Article
- Activity-based proteomics analysis revealed that DNJ directly targeted ATP5F1 to alleviate high glucose induced cardiomyocyte injury.Cell communication and signaling : CCS · 2026Article
- Tracing the threads: How toxic metals contribute to neurodegeneration.IBRO neuroscience reports · 2026Review
- Association Between Blood Lead Levels and Diabetic Kidney Disease: A Cross-sectional Analysis of NHANES Data (1999-2018).Current molecular medicine · 2026Article
- Chronic Lead Exposure and Tauopathies: Molecular Mechanisms of Neurotoxicity and Emerging Nanotherapeutic Strategies.Journal of toxicology · 2026Review
- Environmentally relevant lead exposure impacts gene expression in SH-SY5Y cells throughout neuronal differentiation.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Association Between Multiple Plasma Toxic Metal and Metalloid Exposures and Hypertension in Elderly Chinese Adults.Biological trace element research · 2025Article
- Lead Poisoning in the Americas: Sources, Regulations, Health Impacts, and Molecular Mechanisms.Journal of xenobiotics · 2025Review
- Enhanced Neuroprotection by Diosgenin and Pterostilbene Combination Against Neurotoxicity Induced by Amyloid-Β 1-42 in SH-SY5Y Differentiated Cell Models.Annals of neurosciences · 2025Article
- Associations of Environmental Exposure to Arsenic, Manganese, Lead, and Cadmium with Alzheimer's Disease: A Review of Recent Evidence from Mechanistic Studies.Journal of xenobiotics · 2025Review
- Investigation of the relationship between lead exposure in heavy metals mixtures and the prevalence of stroke: a cross-sectional study.BMC public health · 2024Article
- Metal Toxicity and Dementia Including Frontotemporal Dementia: Current State of Knowledge.Antioxidants (Basel, Switzerland) · 2024Review
- Environmental risk factors provoke new thinking for prevention and treatment of dementia with Lewy bodies.Heliyon · 2024Review
- Unveiling Potential Neurotoxic Mechansisms: Pb-Induced Activation of CDK5-p25 Signaling Axis in Alzheimer's Disease Development, Emphasizing CDK5 Inhibition and Formation of Toxic p25 Species.Molecular neurobiology · 2024Article
- Heavy Metal Mediated Progressive Degeneration and Its Noxious Effects on Brain Microenvironment.Biological trace element research · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to the environmental pollutant lead (Pb) has been linked to Alzheimer's disease (AD), in which mitochondrial dysfunction is a pathological consequence of neuronal degeneration. The toxicity of Pb in combination with β-amyloid peptides (1-40) and (25-35) causes selective death in neuronal cells. However, the precise mechanism through which Pb induces Alzheimer's disease, particularly mitochondrial damage, is unknown. Changes in mitochondrial mass, membrane potential, mitochondrial complex activities, mitochondrial DNA and oxidative stress were examined in neuronal cells of human origin exposed to Pb and β-amyloid peptides (1-40) and (25-35) individually and in different combinations. The results showed depolarization of mitochondrial membrane potential, decrease in mitochondrial mass, ATP levels and mtDNA copy number in Pb and β-amyloid peptides (1-40) and (25-35) exposed cells. Also, significant reductions in the expression of mitochondrial electron transport chain (ETC) complex proteins (ATP5A, COXIV, UQCRC2, SDHB, NDUFS3), as well as down regulation of ETC complex gene expressions such as COXIV, ATP5F1 and NDUFS3 and antioxidant gene expressions like MnSOD and Gpx4 were observed in exposed cells. Furthermore, Pb and β-amyloid peptides exposure resulted in elevated mitochondrial malondialdehyde levels and a decrease in mitochondrial GSH levels. Our findings suggest that Pb toxicity could be one of the causative factors for the mitochondrial dysfunction and oxidative stress in Alzheimer's disease progression.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.