scholarly journals The effect of vitamin A deficiency on hepatic, renal and pulmonary glutathione S-transferase activities in the rat

1980 ◽  
Vol 188 (3) ◽  
pp. 889-893 ◽  
Author(s):  
Z H Siddik ◽  
E G Mimnaugh ◽  
M A Trush ◽  
T E Gram
Keyword(s):  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Nutritional State ◽  
Glutathione S Transferase ◽  
Chemical Carcinogens ◽  
Deficient Diet ◽  
Liver Cytosol ◽  
Weanling Rats ◽  
Glutathione S Transferases ◽  
The Relationship

Feeding male weanling rats on a vitamin A-deficient diet for 6 weeks resulted in significant increases (44-57%) in glutathione S-aryl-, S-aralkyl- S-alkyl- and S-epoxidetransferase activities in the liver cytosol. Only the S-aralkyl- (27%) and S-alkyltransferase (14%) activities were significantly increased in the kidney as a result of deficiency. There was no effect on any of the pulmonary glutathione S-transferase activities. The increases in hepatic transferase activities were due primarily to increases (25-96%) in the apparent Vmax. There were no changes in the apparant Km of any of the four drug substrates employed. With 3,4-dichloronitrobenzene as the second substrate, the apparent Km for glutathione was increased by over 2-fold in vitamin A-deficient livers as compared with controls. The relationship between these results and enhanced susceptibility to chemical carcinogens in vitamin A deficiency is briefly discussed, and comparison is made between the effects of this nutritional state and pretreatment with drug inducers on the glutathione S-transferases.

scholarly journals On the relationship between vitamin A and vitamin E in the rat

1968 ◽  
Vol 22 (1) ◽  
pp. 133-143 ◽  
Author(s):  
M. A. Cawthorne ◽  
J. Bunyan ◽  
A. T. Diplock ◽  
Elspeth A. Murrell ◽  
J. Green
Keyword(s):  
Weight Gain ◽  
Vitamin E ◽  
Vitamin A ◽  
Methyl Esters ◽  
Tocopheryl Acetate ◽  
Cod Liver Oil ◽  
Deficient Diet ◽  
Weanling Rats ◽  
The Relationship

1. The effect of vitamin E on the metabolism, utilization and storage of vitamin A has been studied in the rat.2. Male weanling rats were given a vitamin A-deficient, vitamin E-deficient diet until growth had ceased for 3 days, and each rat was then given 50 i.u. vitamin A palmitate. The rats were divided into four groups and given the diet with the addition of 10% methyl oleate or 10% cod-liver oil methyl esters, or either of these diets supplemented with 100 ppm D-α-tocopheryl acetate. There was no increase in maximum weight-gain response in the two groups given vitamin E. There was a significantly lower weight-gain response in the groups given cod-liver oil methyl esters. This effect was not influenced by the presence of vitamin E in the diet.3. Weanling rats of both sexes were made deficient in vitamins A and E and then divided into two groups. One group received, every other day, 1·75 i.u. vitamin A palmitate and 0·6 mg D-α-tocopherol given together; the second group received the two vitamins, in the same amounts, on alternate days. After 28 days there was no difference in the growth of the two groups of rats, irrespective of sex.4. Vitamin A-depleted, vitamin E-deficient rats were given 17·51 μg ‘14C-carbinol’retinyl acetate and then a vitamin A-deficient, vitamin E-deficient diet or that diet supplemented with 100 ppm D-α-tocopheryl acetate. After 6 days, the total remaining ‘14C’retinol and its lipidsoluble metabolites were measured in the carcasses of the rats. Vitamin E administration did not affect the metabolism of the vitamin A dose or its effect on growth.5. Vitamin E-deficient rats were given vitamin A until their liver reserves exceeded 30000 i.u. and were then divided into two groups. One group received a diet deficient in vitamins A and E and the other received, in addition to this diet, a weekly oral supplement of 1 mg D-α-tocopheryl acetate. The vitamin E supplement significantly decreased the rate of vitamin A depletion from the liver during the next 6 weeks. This effect, which was not found to occur when the initial liver reserves were only 3000 i.u., suggests a role for vitamin E in connexion with the capacity of the liver to bind vitamin A.6. The relationship between vitamin A and vitamin E in vivo cannot, in the light of these results, be regarded as that between an antioxidant and a peroxidizable substrate.

Vitamin A Status and Hepatic Drug Metabolism in the Rat

1973 ◽  
Vol 51 (1) ◽  
pp. 6-11 ◽  
Author(s):  
G. C. Becking
Keyword(s):  
Vitamin A ◽  
Drug Metabolism ◽  
Vitamin A Deficiency ◽  
Hepatic Drug Metabolism ◽  
Deficient Diet ◽  
Hepatic Drug ◽  
Vitamin A Status ◽  
Cytochrome P 450 ◽  
Liver Vitamin

The effect of vitamin A status on hepatic drug metabolism was studied in rats. Animals were fed diets with and without vitamin A for 20 and 25 days. Weight gains of control and deficient animals were not significantly different, whereas liver vitamin A levels had decreased to less than 10% of control animals after 20 days and were essentially zero after eating the deficient diet for 25 days. Aniline metabolism in vitro and aminopyrine metabolism in vitro and in vivo were significantly lower in male weanling rats fed a vitamin A deficient diet for 20 days. No alteration in in vitro p-nitrobenzoic acid metabolism was noted after 25 days on the test. Vitamin A deficiency did not alter microsomal protein levels or cytochrome c reductase activity but deficient animals did have a lower microsomal cytochrome P-450 content. Hepatic enzyme activities and cytochrome P-450 levels were restored to values approaching those found in control animals by feeding vitamin A deficient rats the vitamin A containing diet for 21 days. Liver vitamin A levels were markedly increased after re-feeding studies but were still significantly lower than control animals.

scholarly journals Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E−/−Mice and Dietaryβ-Carotene Prevents This Consequence

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Noa Zolberg Relevy ◽  
Dror Harats ◽  
Ayelet Harari ◽  
Ami Ben-Amotz ◽  
Rafael Bitzur ◽  
...  
Keyword(s):  
Vitamin A ◽  
Apolipoprotein E ◽  
Vitamin A Deficiency ◽  
Plasma Cholesterol ◽  
Atherosclerotic Lesion ◽  
Dietary Vitamin ◽  
Control Group ◽  
Chow Diet ◽  
Deficient Diet ◽  
Aortic Sinus

Vitamin A is involved in regulation of glucose concentrations, lipid metabolism, and inflammation, which are major risk factors for atherogenesis. However, the effect of vitamin A deficiency on atherogenesis has not been investigated. Therefore, the objective of the current study was to examine whether vitamin A deficiency accelerates atherogenesis in apolipoprotein E-deficient mice (apoE−/−). ApoE−/−mice were allocated into the following groups: control, fed vitamin A-containing chow diet; BC, fed chow diet fortified withDunaliellapowder containingβc isomers; VAD, fed vitamin A-deficient diet; and VAD-BC group, fed vitamin A-deficient diet fortified with aDunaliellapowder. Following 15 weeks of treatment, liver retinol concentration had decreased significantly in the VAD group to about 30% that of control group. Vitamin A-deficient diet significantly increased both plasma cholesterol concentrations and the atherosclerotic lesion area at the aortic sinus (+61%) compared to the control group. Dietaryβc fortification inhibited the elevation in plasma cholesterol and retarded atherogenesis in mice fed the vitamin A-deficient diet. The results imply that dietary vitamin A deficiency should be examined as a risk factor for atherosclerosis and that dietaryβc, as a sole source of retinoids, can compensate for vitamin A deficiency.

Vitamin A deficiency in Bos indicus heifers fed a wheat straw diet cannot be corrected with algae lick blocks or intramuscular injectable retinyl palmitate treatments

2017 ◽  
Vol 57 (6) ◽  
pp. 1079 ◽  
Author(s):  
A. J. Parker ◽  
J. P. Goopy ◽  
M. J. Callaghan ◽  
J. J. Vermunt ◽  
R. de Nys
Keyword(s):  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Average Daily Gain ◽  
Bos Indicus ◽  
Retinyl Palmitate ◽  
Negative Control ◽  
Deficient Diet ◽  
Treatment Groups ◽  
Protein Deficient Diet ◽  
Β Carotene

Serum and liver retinol concentrations and blood β-carotene concentrations were studied in 30 Bos indicus heifers rendered deficient of vitamin A over 180 days and then given treatments of access to algae-based lick blocks (n = 10), injectable retinyl palmitate and molasses-based lick blocks (n = 10), or a negative control given access to molasses-based lick blocks only (n = 10). All heifers became deficient in blood and liver vitamin A, as well as blood β-carotene by 180 days. There was no treatment effect on bodyweight (P = 0.347). However, a highly significant effect of time (P = 0.001) was detected where all heifers achieved an average daily gain of 0.74 kg/day throughout the depletion phase of the study but lost 0.150 kg/day during the repletion phase. The concentrations of serum and liver retinol and blood β-carotene were not different between treatment groups (P = 0.362, P = 0.535 and P = 0.839) during the depletion or repletion phases of the study. All heifers continued to be rendered deficient in the concentrations of serum and liver retinol and blood β-carotene throughout the experiment demonstrating a highly significant effect of time (P = 0.001). Injectable retinyl palmitate (818 100 IU retinol) or access to algal lick blocks (4180 IU retinol) did not elevate blood or liver retinol concentrations in heifers rendered deficient of vitamin A. It is speculated that the protein-deficient diet fed to the heifers had an adverse effect on the blood retinol transport proteins.

scholarly journals Vitamin E and stress

1967 ◽  
Vol 21 (4) ◽  
pp. 845-864 ◽  
Author(s):  
J. Green ◽  
I. R. Muthy ◽  
A. T. Diplock ◽  
J. Bunyan ◽  
M. A. Cawthorne ◽  
...  
Keyword(s):  
Vitamin E ◽  
Vitamin A ◽  
Dietary Vitamin ◽  
Dietary Pufa ◽  
Weanling Rats ◽  
Depletion Rate ◽  
Gastro Intestinal Tract ◽  
The Relationship ◽  
Liver Vitamin

1. The nature of the relationship between vitamins A and E has been studied in the rat and the chick.2. Stress induced by diets rich in polyunsaturated fatty acids (PUFA) was found to have no effect on the liver vitamin A reserves of vitamin E-deficient rats given dietary vitamin A or repeated small oral doses of vitamin A.3. Dietary PUFA did not affect the liver vitamin A reserves of young rats given necrogenic diets deficient in vitamin E and selenium, nor were these reserves affected by the onset of liver necrosis or its prevention by Se.4. The effect of dietary PUFA on the rate of depletion of liver vitamin A reserves in weanling rats or rats depleted initially of vitamins A and E and then given a single large dose of vitamin A was studied over periods from 2 to 12½ weeks. In three experiments the dietary PUFA did not significantly accelerate vitamin A depletion. In one experiment the depletion rate was increased, but this was not reversed by dietary vitamin E and thus could not be attributed to an enhancement of peroxidation in vivo but rather to a toxic effect. The effect of vitamin E in these experiments was not consistent but, in general, it slightly decreased the rate of depletion.5. Large doses of vitamin A did not affect the metabolism of small amounts of [14C]D-α-tocopherol in the vitamin E-deficient rat or chick, when interaction of the two vitamins in the gastro-intestinal tract was avoided.6. Large doses of vitamin A (40000 i.u. in total) given to vitamin E-deficient chicks receiving a diet containing 1% linoleic acid (as maize oil esters) did not accelerate the onset of encephalomalacia and therefore failed to exert a pro-oxidative effect on tissue tocopherol.7. The conclusion drawn from these experiments was that any relationship that may exist in vivo between vitamins A and E is not concerned with an effect of vitamin E in preventing oxidation of vitamin A. A critical review of the literature on the nature of the relationship in general supports this view.

scholarly journals A study of the structures of the YaYa and YaYc glutathione S-transferases from rat liver cytosol Evidence that the Ya monomer is responsible for lithocholate-binding activity

1981 ◽  
Vol 197 (2) ◽  
pp. 491-502 ◽  
Author(s):  
J D Hayes ◽  
R C Strange ◽  
I W Percy-Robb
Keyword(s):  
Rat Liver ◽  
Lithocholic Acid ◽  
Binding Activity ◽  
Glutathione S Transferase ◽  
Liver Cytosol ◽  
Molecular Weights ◽  
Tryptic Digest ◽  
Glutathione S Transferases ◽  
Limited Digestion ◽  
Rat Liver Cytosol

The two dimeric lithocholic acid-binding proteins previously identified as ligandin (YaYa) and glutathione S-transferase B (YaYc) were isolated from rat liver cytosol. These proteins have molecular weights of 44000 and 47000 respectively. The recovery of these two proteins from liver was not affected by the addition of the proteinase inhibitor Trasylol. No spontaneous interconversion between these two proteins was observed on storage. YaYa and YaYc proteins yielded peptides of identical molecular weight after limited digestion with Staphylococcus aureus V8 proteinase. Analytical and preparative tryptic-digest peptide ‘maps’ showed that all the soluble peptides obtained from YaYa protein were also recovered from YaYc protein. Approximately six extra soluble peptides, which were not recovered from YaYa protein, were obtained from the tryptic digest of YaYc protein. Subdigests of the insoluble tryptic-digest ‘cores’ also resulted in the recovery of identical peptides from both proteins. Evidence is presented that the Ya subunit possessed by both proteins is identical; glutathione S transferase B is a hybrid of ligandin and glutathione S-transferase AA. The Ya monomer is responsible for lithocholate binding.

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