Effects of vitamin A deficiency on mitochondrial function in rat liver andheart

The aim of this study was to investigate comparative effects of vitamin A d eficiency on respiratory activity and structural integrity in liver and hea rt mitochondria. Male rats were fed a liquid control diet (control rats) or a liquid vitamin A-deficient diet (vitamin A-deficient rats) for 50 days. One group of vitamin-A deficient rats was refed a control diet for 15 days (vitamin A-recovered rats). To assess the respiratory function of mitochond ria the contents of coenzyme Q (ubiquinone, CoQ), cytochrome c and the acti vities of the whole electron transport chain and of each of its respiratory complexes were evaluated. Chronic vitamin A deficiency promoted a signific ant increase in the endogenous coenzyme Q content in liver and heart mitoch ondria when compared with control values. Vitamin A deficiency induced a de crease in the activity of complex I (NADH-CoQ reductase) and complex II (su ccinate-CoQ reductase) and in the levels of complex I and cytochrome c in h eart mitochondria. However, NADH and succinate oxidation rates were maintai ned at the control levels due to an increase in the CoQ content in accordan ce with the kinetic behaviour of CoQ as an homogeneous pool. On the contrar y, the high CoQ content did not affect the electron-transfer rate in liver mitochondria, whose integrity was preserved from the deleterious effects of the vitamin A deficiency. Ultrastructural assessment of liver and heart sh owed that vitamin A deficiency did not induce appreciable alterations in th e morphology of their mitochondria. After refeeding the control diet, serum retinol, liver and heart CoQ content and the activity of complex I and com plex II in heart mitochondria returned to normality. However, the activitie s of both whole electron transfer chain and complex I in liver were increas ed over the control values. The interrelationships between physiological an tioxidants in biological membranes and the beneficial effects of their admi nistration in mitochondrial diseases are discussed.