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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #107260
Title: COPPER DEFICIENCY DOES NOT INCREASE HEPATIC MITOCHONDRIAL HYDROGEN PEROXIDE PRODUCTION

Author
item Johnson, William

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/10/1999
Publication Date: 3/15/2000
Citation: Johnson, W.T. 2000. Copper deficiency does not increase hepatic mitochondrial hydrogen peroxide production [abstract]. The Federation of American Societies for Experimental Biology Journal. 14:A773.

Interpretive Summary:

Technical Abstract: Mitochondrial electron transport consumes about 85-90% of the oxygen utilized by the cell. However, not all of the oxygen consumed is converted to water, about 1-2% is converted to superoxide. The generation of reactive oxygen species (ROS) is largely determined by the redox state of the respiratory complexes and is highest when electron flow is blocked near the end of the electron transport chain (ETC). By inhibiting cytochrome c oxidase, which catalyzes the terminal reaction of the ETC, copper (Cu) deficiency should increase mitochondrial ROS production. Because much of the superoxide formed in mitochondria is converted into hydrogen peroxide (H2O2) by manganese-superoxide dismutase (MnSOD), increased ROS production during Cu deficiency could lead to increased release of hydrogen peroxide from mitochondria. In the present study, four groups of male, weanling rats were fed diets containing 0.3 ppm Cu (CuD), 1 ppm Cu (Cu1), 2 ppm Cu (Cu2), and 6 ppm Cu (Cu6) for five weeks. CCO activities in liver mitochondria isolated from rats fed Cu1 and CuD were 50% and 89% lower, respectively, than CCO activity in rats fed Cu6 (p<0.05). Respiratory complex I activities, assayed as NADH-cytochrome c reductase, also were 30% and 64% lower in mitochondria from rats fed Cu1 and CuD, respectively, compared to rats fed Cu6. Both activities were unchanged in rats fed Cu2. However, mitochondrial H2O2 production in the presence of 7mM succinate was 53% lower in rats fed CuD than in those fed Cu6 (p<0.05), but was unaffected in rats fed Cu1 and Cu2. Furthermore, H2O2 production was directly correlated (r=0.77, p<0.01) to CCO activity in mitochondria from rats fed CuD. These findings indicate that mitochondria are not a major source of H2O2 during Cu deficiency.