ArticleCell calcium2009
A comparison of Zn2+- and Ca2+-triggered depolarization of liver mitochondria reveals no evidence of Zn2+-induced permeability transition.
Article in Cell calcium, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Metabolic cell death in cancer: ferroptosis, cuproptosis, disulfidptosis, and beyond.Protein & cell · 2024Review
- The zinc transporter ZIP7 (Slc39a7) controls myocardial reperfusion injury by regulating mitophagy.Basic research in cardiology · 2021Article
- The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction.Biomedicines · 2021Review
- The role of labile ZnMolecular and cellular biochemistry · 2021Review
- ZnExperimental neurology · 2020Article
- Mitochondrial ZnThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019Article
- ZnExperimental neurology · 2018Article
- Labile Low-Molecular-Mass Metal Complexes in Mitochondria: Trials and Tribulations of a Burgeoning Field.Biochemistry · 2016Review
- Zinc Modulates Nanosilver-Induced Toxicity in Primary Neuronal Cultures.Neurotoxicity research · 2016Article
- The Critical Roles of Zinc: Beyond Impact on Myocardial Signaling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015Review
- The interactive roles of zinc and calcium in mitochondrial dysfunction and neurodegeneration.Journal of neurochemistry · 2014Article
- Mitochondrial permeability transition induced by different concentrations of zinc.The Journal of membrane biology · 2011Article
- Zinc: new clues to diverse roles in brain ischemia.Trends in pharmacological sciences · 2011Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Intracellular Zn(2+) toxicity is associated with mitochondrial dysfunction. Zn(2+) depolarizes mitochondria in assays using isolated organelles as well as cultured cells. Some reports suggest that Zn(2+)-induced depolarization results from the opening of the mitochondrial permeability transition pore (mPTP). For a more detailed analysis of this relationship, we compared Zn(2+)-induced depolarization with the effects of Ca(2+) in single isolated rat liver mitochondria monitored with the potentiometric probe rhodamine 123. Consistent with previous work, we found that relatively low levels of Ca(2+) caused rapid, complete and irreversible loss of mitochondrial membrane potential, an effect that was diminished by classic inhibitors of mPT, including high Mg(2+), ADP and cyclosporine A. Zn(2+) also depolarized mitochondria, but only at relatively high concentrations. Furthermore Zn(2+)-induced depolarization was slower, partial and sometimes reversible, and was not affected by inhibitors of mPT. We also compared the effects of Ca(2+) and Zn(2+) in a calcein-retention assay. Consistent with the well-documented ability of Ca(2+) to induce mPT, we found that it caused rapid and substantial loss of matrix calcein. In contrast, calcein remained in Zn(2+)-treated mitochondria. Considered together, our results suggest that Ca(2+) and Zn(2+) depolarize mitochondria by considerably different mechanisms, that opening of the mPTP is not a direct consequence of Zn(2+)-induced depolarization, and that Zn(2+) is not a particularly potent mitochondrial inhibitor.
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Registered trials
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