ArticleMedComm2020
Lycopene antagonizes lead toxicity by reducing mitochondrial oxidative damage and mitochondria-mediated apoptosis in cultured hippocampal neurons.
Article in MedComm, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Mitochondrial-targeted actions of lycopene: evidence, mechanisms and future directions.Frontiers in pharmacology · 2026Review
- Chitosan Oligosaccharide-Functionalized Ruthenium-Curcumin Nanodots for Targeted Therapy of Acute Kidney Injury.International journal of nanomedicine · 2026Article
- Lycopene as a Therapeutic Agent against Aflatoxin B1-Related Toxicity: Mechanistic Insights and Future Directions.Antioxidants (Basel, Switzerland) · 2024Review
- Deciphering the role of apoptosis signature on the immune dynamics and therapeutic prognosis in breast cancer: Implication for immunotherapy.Frontiers in genetics · 2024Article
- Exposure of combination of environmental pollutant, lead (Pb) and β-amyloid peptides causes mitochondrial dysfunction and oxidative stress in human neuronal cells.Journal of bioenergetics and biomembranes · 2023Article
- Mitochondrial Modulators: The Defender.Biomolecules · 2023Review
- Mitochondrial impairment and repair in the pathogenesis of systemic lupus erythematosus.Frontiers in immunology · 2022Review
- Sitagliptin Alleviates Radiation-Induced Intestinal Injury by Activating NRF2-Antioxidant Axis, Mitigating NLRP3 Inf--lammasome Activation, and Reversing Gut Microbiota Disorder.Oxidative medicine and cellular longevity · 2022Article
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lead (Pb) exhibits serious adverse effects on the central nervous system, and the major pathogenic mechanism of Pb toxicity is oxidative stress. As one of the carotenoid family members with potent antioxidant properties, lycopene has shown its protections by inhibiting oxidative stress damage in numerous models of neurotoxicity. The current study was designed to explore the possible protective property in primary cultured rat hippocampal neurons challenged with Pb. We observed that 5 μM lycopene pretreatment for 4 h efficiently ameliorated Pb-caused damage in cell viability, accumulation of reactive oxygen species (ROS), and apoptosis in a dose-dependent manner. Moreover, lycopene (5 μM) attenuated the 50 μM Pb-induced mitochondrial ROS production, improved the activities of mitochondrial respiratory chain enzymes and ATP production, and ameliorated the 50 μM Pb-induced depolarization of mitochondrial membrane potential as well as opening of mitochondrial permeability transition pores. In addition, 5 μM lycopene restored the imbalance of Bax/Bcl-2, inhibited translocation of cytochrome c, and reduced caspase-3 activation. Taken together, these findings indicate that lycopene antagonizes against Pb-induced neurotoxicity and the underlying mechanism probably involves reduction of mitochondrial oxidative damage and mitochondria-mediated apoptosis.
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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.