Journal
FREE RADICAL RESEARCH
Volume 45, Issue 1, Pages 37-52Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/10715762.2010.516254
Keywords
Mitochondria; free radicals; peroxynitrite; 3-nitrotyrosine
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Funding
- Howard Hughes Medical Institute (HHMI)
- International Centre of Genetic Engineering and Biotechnology (ICGEB)
- Agencia Nacional de Investigacion e Innovacion - Fondo Clemente Estable [398]
- Agencia Nacional de Investigacion e Innovacion (ANII), Uruguay
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Mitochondria are primary loci for the intracellular formation and reactions of reactive oxygen and nitrogen species including superoxide (O-2(radical anion)), hydrogen peroxide (H2O2) and peroxynitrite (ONOOradical anion). Depending on formation rates and steady-state levels, the mitochondrial-derived short-lived reactive species contribute to signalling events and/or mitochondrial dysfunction through oxidation reactions. Among relevant oxidative modifications in mitochondria, the nitration of the amino acid tyrosine to 3-nitrotyrosine has been recognized in vitro and in vivo. This post-translational modification in mitochondria is promoted by peroxynitrite and other nitrating species and can disturb organelle homeostasis. This study assesses the biochemical mechanisms of protein tyrosine nitration within mitochondria, the main nitration protein targets and the impact of 3-nitrotyrosine formation in the structure, function and fate of modified mitochondrial proteins. Finally, the inhibition of mitochondrial protein tyrosine nitration by endogenous and mitochondrial-targeted antioxidants and their physiological or pharmacological relevance to preserve mitochondrial functions is analysed.
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