ArticleMolecular and cellular biochemistry2010
Cytochrome c redox state influences the binding and release of cytochrome c in model membranes and in brain mitochondria.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- NMR Reveals the Conformational Changes of Cytochrome C upon Interaction with Cardiolipin.Life (Basel, Switzerland) · 2021Article
- Article
- Specific methionine oxidation of cytochrome c in complexes with zwitterionic lipids by hydrogen peroxide: potential implications for apoptosis.Chemical science · 2015Article
- Low levels of IgM antibodies to oxidized cardiolipin increase and high levels decrease risk of cardiovascular disease among 60-year olds: a prospective study.BMC cardiovascular disorders · 2013Article
- RNA oxidation catalyzed by cytochrome c leads to its depurination and cross-linking, which may facilitate cytochrome c release from mitochondria.Free radical biology & medicine · 2012Article
- Bromopyruvate mediates autophagy and cardiolipin degradation to monolyso-cardiolipin in GL15 glioblastoma cells.Journal of bioenergetics and biomembranes · 2012Article
- Ribose 5-phosphate glycation reduces cytochrome c respiratory activity and membrane affinity.Biochemistry · 2011Article
- Tyrosine phosphorylation turns alkaline transition into a biologically relevant process and makes human cytochrome c behave as an anti-apoptotic switch.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytochrome c (cyt c), a component of the respiratory chain, promotes apoptosis when released into the cytosol. Cyt c anchorage within mitochondria depends on cardiolipin (CL). Detachment and release have been related to CL loss and peroxidation. We report that NaN(3)-dependent complex IV inhibition, accompanied by impairment of respiration, resulted in cyt c release. Contrarily, inhibition of respiration upstream cyt c with complex I and III inhibitors was not accompanied by the release of the protein, despite CL decrease and monolyso-CL increase. No CL changes and H(2)O(2) formation were observed by inhibiting complex IV. In cyt c-CL liposomes, breaching cyt c-CL hydrophilic interactions produced a higher release of the reduced, compared to the oxidized form, suggesting that the hydrophobic component of cyt c-CL binding is prevalent in the oxidized form. Free or liposome-reconstituted cyt c was able to form fatty acid-protein complexes (palmitate < linoleate < oleate) only in its reduced form. We hypothesize that reduced cyt c-fatty acid binding favors the dislocation of the protein from anchoring CL. A mechanism for cyt c release independent of CL peroxidation by H(2)O(2) is feasible. It could weaken the hydrophobic component of cyt c-CL interactions and might function following complex IV inhibition or in oxygen lack, both conditions producing accumulation of reduced cyt c and free fatty acids.
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