ArticleJournal of clinical biochemistry and nutrition2008
Flow cytometric analysis of ca-induced membrane permeability transition of isolated rat liver mitochondria.
Article in Journal of clinical biochemistry and nutrition, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 7 citations in OpenAlex.
- Fishing for contaminants: identification of three mechanism specific transcriptome signatures using Danio rerio embryos.Environmental science and pollution research international · 2018Article
- Induction of mitochondrial dysfunction by poly(ADP-ribose) polymer: implication for neuronal cell death.Molecules and cells · 2013Article
- Characterization of functionally distinct mitochondrial subpopulations.Journal of bioenergetics and biomembranes · 2013Article
- Effect of trifluoperazine on toxicity, HIF-1α induction and hepatocyte regeneration in acetaminophen toxicity in mice.Toxicology and applied pharmacology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The membrane permeability transition (MPT) of mitochondria plays an important role in the mechanism of apoptotic cell death in various cells. Classic type MPT is induced by Ca(2+) in the presence of inorganic phosphate and respiratory substrate, and is characterized by various events including generation of reactive oxygen species (ROS), membrane depolarization, swelling, release of Ca(2+) and high sensitivity to cyclosporine A. However, the sequence of these events and the effect of antioxidants on their events remain obscure. Flow cytometry is a convenient method to investigate the order of events among various functions occurring in MPT using a limited amount of mitochondria (200 microl of 0.02 mg protein/ml) without contamination by other organelles. Flow cytometric analysis revealed that Ca(2+) sequentially induced ROS generation, depolarization, swelling and Ca(2+) release in mitochondria by a cyclosporine A-inhibitable mechanism. These results were supported by the finding that Ca(2+)-induced MPT was inhibited by antioxidants, such as glutathione and N-acetylcysteine. It was also revealed that various inhibitors of Ca(2+)-induced phospholipase A(2) suppressed all of the events associated with Ca(2+)-induced MPT. These results suggested that ROS generation and phospholipase A(2) activation by Ca(2+) underlie the mechanism of the initiation of MPT.
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Registered trials
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