Respiratory Activities of Hypo- and Hypervitaminotic-A Rat Liver Homogenates

Abstract

Although the role of vitamin A in the visual process is now reasonably well understood, its mechanism of action in intermediary metabolism and particularly in structural integrity of various tissues is not clear. Many investigators have sought to learn more about thle function of vit. A through studies on the metabolic lesions elicited by a deficiency or an excess of the vitamin. Recently DeLuca et aZ( 1) showed an increase in oxygen uptake (measured for 30 min) by liver homogenates of vit. A-deficient rats with a number of Krebs cycle acids. Sampson and co-workers (2) demonstrated that most female rats receiving from 300-525 units of vit. A/g of body weight daily had higher respiratory quotients than litter mate controls. Redfern( 3) recorded an increase in endogenous oxidation by liver homogenates from vit. A-deficient rats. On the other hand, Ray and Sadhu(4) reported that liver slices and homogenates of rats fed excess vit. A, showed a significantly decreased oxidation of succinate. Berdjis(5) reported an increase in number of mast cells in almost all organs of rats given toxic doses of vit. A. They further stated that many pathological conditions and metabolic disturbances are directly related to the variations in mast cell population in tissues. Squibb (6) reported that chickens receiving 100,000 units of vit. A/day for 13 days showed a decrease in liver lipids. Brown et aZ ( 7) suggested that permeability changes associated with hypervitaminosis-A may be due to a change in sulfation of membraneassociated mucopolysaccharides, which appear to be necessary for the integrity of membrane structure.In this paper results are reported which show a marked initial elevation in oxygen uptake by liver homogenates from either hjrpovi tamino tic or hypervi taminotic-A rats. The initial increase in oxygen consumption is fo'llowed by a rapid decline during the follow-ing hour. An effect of tri-o-cresyl phospha.te (TCP) on respiratory control and liver lipids has also been demonstrated. This substance was studied because previous work( 10) had shown it to have a pro-oxidant action in unsaturated lipid systems in vitro, to decrease vit. A, and to produce changes in body fat composition in vivo.Materials and methods. Male weanling ratts of an Osborne-Mendel derived strain (FDA, Division of Nutrition) from dams maintained on a low vit. A stock diet were used in our deficiency studies. The basal diet contained 18% casein (vitamin free), 64% sucrose, 10% lard, 4% salt mixture (Jones-Foster), and 4% vitamin mixture (vit. A and E free). To this was added vit. E as a mixture of dl-alpha tocopherol and dl-alpha tocopherol acetate at 200 mg/kilo. Six weanling rats were used in each of 4 groups: They were fed 1) the basal diet, 2) basal diet supplemented with 5 mg of vit. A acetate per kilo, 3) basal diet with 0.1% TCP, and 4) b a d diet containing both vit. A and TCP. Vit. A deficiency was determined by the onset of loss in body weight, which occurred in 28-40 days. Food and water were available ad libitum. In our excess vit. A expe...

The Roles of Vitamin A in the Regulation of Carbohydrate, Lipid, and Protein Metabolism

“…In the rodent liver, both hypo- and hypervitaminosis A are implicated in the uncoupled oxidative phosphorylation in mitochondria [ 135 , 136 , 137 ]. On the one hand, the dioxygen consumption by liver homogenates of hypo- and hypervitaminotic A rats is significantly increased upon the supply of some TCA intermediates [ 135 , 136 ]. On the other hand, the capacity for oxidative phosphorylation is severely impaired in liver mitochondria of hypo- and hypervitaminotic A rats without affecting ATPase activity [ 137 ].…”

Recherches histochimiques et biochimiques sur des rats en hyper- et hypovitaminose A

“…11 a été observé, avec des m éthodes biochi miques, une activité augm entée de la phosphatase alcaline, lors d'hypervitam ose A, par R a h a lk a r et al [1956] Seward et al [1964] et Seward 11966| ont analysé les enzymes du cycle de Krehs et ils ont pu déterm iner, au moyen de recherches biochimiques sui des hom ogénats de foie de rats en hyper-et hypovitam inose A, une modification avec 2 phases: tout d'abord une augm entation, ensuite une dim inution de l'activité. Le début de l'augm entation a été expliqué par une augm entation de la perm éabilité.…”