ArticleCellular and molecular life sciences : CMLS2004
Functional and biochemical characteristics of mitochondrial fractions from rat liver in cold-induced oxidative stress.
Article in Cellular and molecular life sciences : CMLS, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 19 citations in OpenAlex.
- Role of ROS and RNS Sources in Physiological and Pathological Conditions.Oxidative medicine and cellular longevity · 2016Review
- The influence of obesity and ambient temperature on physiological and oxidative responses to submaximal exercise.Biology of sport · 2014Article
- Calorie restriction influences key metabolic enzyme activities and markers of oxidative damage in distinct mouse liver mitochondrial sub-populations.Life sciences · 2013Article
- Effect of vitamin E on characteristics of liver mitochondrial fractions from cold-exposed rats.Journal of bioenergetics and biomembranes · 2011Article
- Caloric restriction influences hydrogen peroxide generation in mitochondrial sub-populations from mouse liver.Journal of bioenergetics and biomembranes · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
We determined characteristics of rat liver mitochondrial fractions, resolved at 1000 (M1), 3000 (M3), and 10,000 g (M10) after 2 and 10 days cold exposure. In all groups, the M1 fraction exhibited the highest oxidative capacity, oxidative damage, H2O2 production rate, and susceptibility to stress conditions, and the lowest antioxidant levels. Cold exposure increased cytochrome oxidase activity in all fractions and succinate-supported O2 consumption in the M1 and M10 fractions during state 3 and state 4 respiration, respectively. With succinate, the H2O2 release rate increased in all fractions during state 4 and state 3 respiration, whereas with pyruvate/malate, it increased only during state 4 respiration. Increases in tissue mitochondrial proteins caused a faster H2O2 flow from the mitochondrial to cytosolic compartment, which was limited by the reduction in the M1 fraction. Despite increased liposoluble antioxidant levels, cold also caused enhanced oxidative damage and susceptibility to oxidative challenge and Ca2+-induced swelling in all fractions. These changes leading to elimination of H2O2-overproducing mitochondria avoided excessive tissue damage. We propose that triiodothyronine, whose levels increase in the cold environment, brings about the biochemical changes producing oxidative damage and those limiting its extent.
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