Turrens, J. F. & Boveris, A. Generation of superoxide anion by the NADH dehydrogenase of bovine heart mitochondria. Biochem. J. 191, 421-427

Biochemical Journal (Impact Factor: 4.4). 12/1980; 191(2):421-7. DOI: 10.1042/bj1910421
Source: PubMed


Submitochondrial particles from bovine heart in which NADH dehydrogenase is reduced by either addition of NADH and rotenone or by reversed electron transfer generate 0.9 +/- 0.1 nmol of O2-/min per mg of protein at pH 7.4 and at 30 degrees C. When NADH is used as substrate, rotenone, antimycin and cyanide increase O2- production. In NADH- and antimycin-supplemented submitochondrial particles, rotenone has a biphasic effect: it increases O2- production at the NADH dehydrogenase and it inhibits O2- production at the ubiquinone-cytochrome b site. The generation of O2- by the rotenone, the uncoupler carbonyl cyanide rho-trifluoromethoxyphenylhydrazone and oligomycin at concentrations similar to those required to inhibit energy-dependent succinate-NAD reductase. Cyanide did not affect O2- generation at the NADH dehydrogenase, but inhibited O2- production at the ubiquinone-cytochrome b site. Production of O2- at the NADH dehydrogenase is about 50% of the O2- generation but the ubiquinone-cytochrome b area at pH 7.4. Additivity of the two mitochondrial sites of O2- generation was observed over the pH range from 7.0 to 8.8. AN O2- -dependent autocatalytic process that requires NADH, submitochondrial particles and adrenaline is described.

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Available from: Julio Francisco Turrens, Oct 08, 2015
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    • "When the ROS productions are not scavenged sufficiently by antioxidant system, it causes oxidative stress and shows harmful effect. These dangerous reactive species are formed by (1) enzymes such as nicotinamide adenine dinucleotide phosphate (NADPH) [9] or nitric oxide synthase [10], (2) non-enzymatic reactions through the mitochondrial electron transport chain [11], or (3) reduced transition metals [12]. ROS can also interact with nitric oxide (NO), whose expression is usually accompanied by inflammatory lesions. "
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    • "In addition, the respiratory chain complex 1 inhibitor rotenone increased mitochondrial ROS production as previously reported [20, 77]. The ROS increasing effect of NO was abolished by rotenone indicating that the regulation of ROS formation by Cx43 could be through interaction with complex 1. Modulation of complex 1, rather than other complexes, by Cx43 has been previously reported for oxygen consumption as well [2]. "
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    • "The mitochondrion has been widely considered as the major site for production of endogenous ROS. Incomplete metabolism of approximately 1–3% of consumed oxygen leads to production of superoxide, hydrogen peroxide, and hydroxyl radical. Damage to complex I and III, which have been reported as important sites of electron leakage, may lead to the increased production of ROS [12] [13] [14] [15]. Mitochondrial ROS has been repeatedly described to induce the opening of mitochondrial permeability transition pore (mPTP), accompanied with collapse of mitochondrial membrane potential, mitochondrial swelling, and release of cytochrome c [16] [17] [18] [19]. "
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