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Titolo:
Melatonin, mitochondria, and cellular bioenergetics
Autore:
Acuna-Castroviejo, D; Martin, M; Macias, M; Escames, G; Leon, J; Khaldy, H; Reiter, RJ;
Indirizzi:
Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA Univ Texas San Antonio TX USA 78229 truct Biol, San Antonio, TX 78229 USA Univ Granada, Inst Biotechnol, Dept Fisiol, Granada, Spain Univ Granada Granada Spain Inst Biotechnol, Dept Fisiol, Granada, Spain
Titolo Testata:
JOURNAL OF PINEAL RESEARCH
fascicolo: 2, volume: 30, anno: 2001,
pagine: 65 - 74
SICI:
0742-3098(200103)30:2<65:MMACB>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED LIPID-PEROXIDATION; OXIDATIVE STRESS; IN-VITRO; NITRIC-OXIDE; RESPIRATORY-CHAIN; DEFICIENT RATS; FREE-RADICALS; PINEAL-GLAND; COMPLEX-I; DAMAGE;
Keywords:
electron transport chain; free radicals; melatonin; mitochondria; oxidative phosphorylation; oxidative stress;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
71
Recensione:
Indirizzi per estratti:
Indirizzo: Reiter, RJ Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, 7703 Floyd Curl Dr,San Antonio, TX 78229 USA Univ Texas 7703 Floyd Curl Dr San Antonio TX USA 78229 8229 USA
Citazione:
D. Acuna-Castroviejo et al., "Melatonin, mitochondria, and cellular bioenergetics", J PINEAL R, 30(2), 2001, pp. 65-74

Abstract

Aerobic cells use oxygen for the production of 90-95% of the total amount of ATP that they use. This amounts to about 40 kg ATP/day in an adult human. The synthesis of ATP via the mitochondrial respiratory chain is the result of electron transport across the electron transport chain coupled to oxidative phosphorylation. Although ideally all the oxygen should be reduced towater by a four-electron reduction reaction driven by the cytochrome oxidase. under normal conditions a small percentage of oxygen may be reduced by one, two. or three electrons only, yielding superoxide anion, hydrogen peroxide, and the hydroxyl radical, respectively. The main radical produced by mitochondria is superoxide anion and the intramitochondrial antioxidant systems should scavenge this radical to avoid oxidative damage, which leads toimpaired ATP production. During aging and some neurodegenerative diseases,oxidatively damaged mitochondria are unable to maintain the energy demandsof the cell leading to an increased production of free radicals. Both processes, i.e., defective ATP production and increased oxygen radicals, may induce mitochondrial-dependent apoptotic cell death. Melatonin has been reported to exert neuroprotective effects in several experimental and clinical situations involving neurotoxicity and/or excitotoxicity. Additionally, in aseries of pathologies in which high production of free radicals is the primary cause of the disease, melatonin is also protective. A common feature in these diseases is the existence of mitochondrial damage due to oxidative stress. The discoveries of new actions of melatonin in mitochondria supporta novel mechanism, which explains some of the protective effects of the indoleamine on cell survival.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 22:17:35