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- W2135127529 abstract "Most biochemistry textbooks still describe mitochondria as the “cellular power plant.” The flurry of experimental interest in mitochondria that began in the 1950s dissipated soon after confirmation and refinement of Mitchell’s chemi-osmotic hypothesis. Scientists knew the mechanism by which ATP production was coupled to electron transport, and that knowledge seemed to make mitochondrial research obsolete. The fact that mitochondria could transport calcium (Ca2+) [ [1] Crompton M. Carafoli E. The measurement of Ca2+ movements in mitochondria. Methods Enzymol. 1979; 56: 338-352 Crossref PubMed Scopus (19) Google Scholar ] and produce reactive oxygen species (ROS) [ [2] Boveris A. Mitochondrial production of superoxide radical and hydrogen peroxide. Adv. Exp. Med. Biol. 1977; 78: 67-82 Crossref PubMed Scopus (344) Google Scholar ] under certain experimental conditions has been known for decades. But even mitochondrial investigators thought that Ca2+ transport occurred only at very late stages of cellular pathology and that ROS production was fixed at low levels by a tightly coupled electron transport chain and the manganese superoxide dismutase." @default.
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- W2135127529 date "2004-11-01" @default.
- W2135127529 modified "2023-09-25" @default.
- W2135127529 title "A ?radical? idea comes of age: mitochondrial oxidant signaling in health and disease" @default.
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- W2135127529 doi "https://doi.org/10.1016/j.yjmcc.2004.10.001" @default.
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