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.

Effect of vitamin E on characteristics of liver mitochondrial fractions from cold-exposed rats

G. Napolitano;
2011-01-01

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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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11367/72442
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