ArticleOxidative medicine and cellular longevity2016
Zinc Chelation Mediates the Lysosomal Disruption without Intracellular ROS Generation.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Induced Zinc Loss Produces Heterogenous Biological Responses in Melanoma Cells.International journal of molecular sciences · 2022Article
- Does roundup affect zinc functions in a bivalve mollusk in ex vivo exposure?Ecotoxicology (London, England) · 2022Article
- Zinc Modulates Several Transcription-Factor Regulated Pathways in Mouse Skeletal Muscle Cells.Molecules (Basel, Switzerland) · 2020Article
- Islet protection and amelioration of type 2 diabetes mellitus by treatment with quercetin from the flowers ofDrug design, development and therapy · 2018Article
- Natural and redesigned wasp venom peptides with selective antitumoral activity.Beilstein journal of organic chemistry · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
We report the molecular mechanism for zinc depletion caused by TPEN (N,N,N',N'-Tetrakis(2-pyridylmethyl)ethylenediamine) in neuroblastoma cells. The activation of p38 MAP kinase and subsequently caspase 3 is not due to or followed by redox imbalance or ROS generation, though these are commonly observed in literature. We found that TPEN is not responsible for ROS generation and the mechanism involves essentially lysosomal disruption caused by intracellular zinc depletion. We also observed a modest activation of Bax and no changes in the Bcl-2 proteins. As a result, we suggest that TPEN causes intracellular zinc depletion which can influence the breakdown of lysosomes and cell death without ROS generation.
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