Chapter 13 - The Regulation of Cell Energetics and Mitochondrial Signaling by Nitric Oxide
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Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease
2019, Free Radical Biology and MedicineCitation Excerpt :Despite of the overall changes were more markedly in striatum than in frontal cortex, both cerebral areas from rotenone-treated rats for 60 days exhibit a complex I syndrome [5], similar to the one observed in frontal cortex mitochondria from PD patients [54]. Dysfunction of complex I is usually accompanied by changes in mtNOS activity, increases in H2O2 and ONOO− production rates and oxidative and/or nitrosative damage [5,11,12,18–21]. The decline in complex I and in mtNOS activities is consistent with the two enzymes structurally contiguous and functionally associated [10–13].
Diabetes impairs heart mitochondrial function without changes in resting cardiac performance
2016, International Journal of Biochemistry and Cell BiologyMitochondrial nitric oxide production supported by reverse electron transfer
2016, Archives of Biochemistry and BiophysicsHeart mitochondrial nitric oxide synthase. A strategic enzyme in the regulation of cellular bioenergetics
2014, Vitamins and HormonesCitation Excerpt :The mtNOS, same as cytoplasmic NOS isoforms, requires O2, l-arginine, and certain cofactors to produce NO. The apparent O2 KM for heart mtNOS is 36 μM (Alvarez, Valdez, Zaobornyj, & Boveris, 2003), suggesting that under physiological conditions whereby O2 concentration is in the 5–20 μM range (Coburn, Ploegmakers, Gondrie, & Abboud, 1973; Gnaiger, Steinlechner-Maran, Mendez, Eberl, & Margreiter, 1995) the mtNOS activity is O2-limited. To note, the reported KM values for mtNOS indicate a quite low affinity of mtNOS for O2, as compared with other NOS (KM values of eNOS, nNOS, and iNOS are in the range 12–20 μM O2), certainly a point that deserves further research (Boveris, Carreras, & Poderoso, 2009). In this way, the in vivo enzymatic activity of heart mtNOS might be 6–25% of its maximal activity (Boveris & Boveris, 2007).
Metabolic acidosis corrected by including antioxidants in diets of fattening lambs
2013, Small Ruminant ResearchComplex i syndrome in myocardial stunning and the effect of adenosine
2011, Free Radical Biology and MedicineCitation Excerpt :It has been reported by others [38], and also shown in this work, that in myocardial stunning the infarct area is not significant (Fig. 2) and the functional injury is completely reversible (Fig. 1). The mitochondrial dysfunction is properly described as “complex I syndrome” with decreased tissue O2 uptake, decreased malate–glutamate-supported mitochondrial respiration, reduced complex I (NADH-dehydrogenase) activity, increased phospholipid and protein oxidation and protein nitration products, and increased O2•− and H2O2 production rates [39]. Interestingly, high doses of vitamin E were able to restore to normal the age-dependent complex I syndrome in hippocampus and brain cortex [40].