ArticleJournal of bioenergetics and biomembranes2011
Effect of vitamin E on characteristics of liver mitochondrial fractions from cold-exposed rats.
Article in Journal of bioenergetics and biomembranes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Mitochondrial Damage and Autophagy Dysregulation in Alzheimer's Disease: Mechanisms and Therapeutic Opportunities.Neurochemical research · 2025Review
- Changes in the Mitochondria in the Aging Process-Can α-Tocopherol Affect Them?International journal of molecular sciences · 2023Review
- Vitamin E Supplementation and Mitochondria in Experimental and Functional Hyperthyroidism: A Mini-Review.Nutrients · 2019Review
- Role of ROS and RNS Sources in Physiological and Pathological Conditions.Oxidative medicine and cellular longevity · 2016Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In cold exposed rats, it is known that vitamin E induces an increase in the respiration of the whole mitochondrial population isolated from liver. To obtain information on the effects of cold exposure and vitamin E treatment on the dynamics of mitochondrial population, we determined characteristics of rat liver mitochondrial fractions, resolved at 1,000 (M(1)), 3,000 (M(3)), and 10,000 g (M(10)). We found that cold exposure increased the liver content of total mitochondrial proteins irrespective of vitamin E treatment. Conversely, protein distribution among the mitochondrial subpopulations was differentially affected by cold and antioxidant integration. In a cold environment, the M(1) fraction, characterized by the highest O(2) consumption and H(2)O(2) production rates, underwent a remarkable protein content reduction, which was attenuated by vitamin E. These changes were dependent on the opposite effects of the two treatments on mitochondrial oxidative damage and susceptibility to swelling. The proteins of the other fractions, in which the above effects were lower, underwent smaller (M(3)) or no change (M(10)) in the treatment groups. The cold also led to an increase in O(2) consumption of the M(1) fraction which was accentuated by vitamin E treatment. This phenomenon and the vitamin-induced recovery of the M(1) proteins supply an explanation of the previously reported increase in the respiration of the whole mitochondrial population induced by vitamin E in the liver from cold exposed rats.
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