Respiratory chain dysfunction

It is clear that no single biochemical event is responsible 

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Thorniley, M.S., Lane, N.J., Manek, S. and Green, C.J. (1994). Non-invasive measurement of respiratory chain dysfunction following hypothermic renal storage and transplantation. Kidney Int. 45, 1489-1496. 

Brivet FG, Nion I, Megarbane B, Slama A, Brivet M, Rustin P, Munnich A. Fatal lactic acidosis and liver steatosis associated with didanosine and stavudine treatment a respiratory chain dysfunction J Hepatol 2000 32(2) 364-5. 

Moran, M., D. Moreno-Lastres, L. Marin-Buera et al. Mitochondrial respiratory chain dysfunction Implications in neurodegeneration. 53(3), 2012 595-609. 

LHON is caused by a mutation in the mitochondrial DNA encoding one of the complex I subunits. It appears that the optic nerve is especially vulnerable to this respiratory chain dysfunction. This condition occurs in adults and results in loss of vision. 

The condition known as fatal infantile mitochondrial myopathy and renal dysfunction involves severe diminution or absence of most oxidoreductases of the respiratory chain. MELAS (mitochondrial encephalopathy, lactic acidosis, and stroke) is an inherited condition due to NADHiubiquinone oxidoreductase (complex I) or cytochrome oxidase deficiency. It is caused by a muta-... 

Nitrite is also an important source of nitric oxide, molecule that could rapidly react with superoxide to form peroxynitrite (ONOO ), a potent cytokine which is very reactive (Kohn et al., 2002). Reactive species of oxygen and nitrogen could initiate a toxic oxidative chain, including lipid peroxidation, protein oxidation, directly inhibiting some enzymes from the mitochondrial respiratory chain, and causing dysfunctions of the antioxidant defense systems. 

Kruidering M, Van de Water b, de Fleer E, Mulder GJ, Nagelkerke JF. Cisplatin-induced nephrotoxicity in porcine proximal tubular cells Mitochondrial dysfunction by inhibition of complexes I to IV of the respiratory chain. J Pharmacol Exp 1997 280 638-649. Gunter T, Pfeiffer D. Mechanisms by which mitochondria transport calcium. Am J. Physiol 1990 258 C755-C786 (Abstract). LemastersJJ, Nieminen AE,QianT,Trost EC, Elerman B.The mitochondrial permeability transition in toxic, hypoxic and reperfusion injury. Mol Cell Biochem 1997 174 159-165. 

Mitochondrial dysfunction has long been considered to play a central role in the development of cell injury during ischemia-reperfusion and hypoxia-reoxygenation [19]. Besides the inhibition of fatty acid oxidation, mitochondrial energy generation is diminished because of defects in respiratory chain function. Inhi-hition of the FO-Fl-ATPase leading to impaired function of respiratory complex I has been observed in I/R injury. Similar to ischemia, dsplatin has been shown to affed mitochondrial respiratory complexes and func-... 

Kmidering M, Van de Water B, de Heer E, Mulder GJ, Nagelkerke JR Cisplatin-induced nephrotoxicity in porcine proximal tubular cells Mitochondrial dysfunction by inhibition of complexes I to IV of the respiratory chain. J Pharmacol Exp 1997 280 638-649. 

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