Open AccessCyclosporine A-induced nitration of tyrosine 34 MnSOD in endothelial cells: role of mitochondrial superoxide
Author(s) -
Mariano RedondoHorcajo,
Natália Romero,
Pablo Martínez-Acedo,
Antonio MartínezRuiz,
Celia Quijano,
Cátia F. Lourenço,
Nieves Movilla,
José Antonio Enrı́quez,
Fernando Rodrı́guez-Pascual,
Eduardo Rial,
Rafael Radí,
Jesús Vázquez,
Santiago Lamas
Publication year - 2010
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvq028
Subject(s) - peroxynitrite , superoxide , mitochondrion , peroxynitrous acid , chemistry , biochemistry , nitric oxide , endothelial stem cell , endothelium , nitrotyrosine , superoxide dismutase , reactive oxygen species , nitric oxide synthase , microbiology and biotechnology , biology , oxidative stress , enzyme , endocrinology , in vitro , organic chemistry
Cyclosporine A (CsA) has represented a fundamental therapeutic weapon in immunosuppression for the past three decades. However, its clinical use is not devoid of side effects, among which hypertension and vascular injury represent a major drawback. Endothelial cells are able to generate reactive oxygen and nitrogen species upon exposure to CsA, including formation of peroxynitrite. This may result in endothelial cell toxicity and increased tyrosine nitration. We have now studied the subcellular origin of superoxide formation in endothelial cells treated with CsA and the biochemical consequences for the function of mitochondrial enzymes.
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