Catecholamine and acetylcholine levels of the kidney in weanling rats fed a choline-deficient diet

1980 ◽  
Vol 47 (1) ◽  
pp. 79-87 ◽  
Author(s):  
M. A. Rossi ◽  
R. S. Costa
Keyword(s):  
1980 ◽  
Vol 188 (3) ◽  
pp. 889-893 ◽  
Author(s):  
Z H Siddik ◽  
E G Mimnaugh ◽  
M A Trush ◽  
T E Gram

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.


1980 ◽  
Vol 43 (2) ◽  
pp. 367-373 ◽  
Author(s):  
W. M. Tsagn ◽  
J. Belin ◽  
A. D. Smith

1. When weanling rats were fed on a diet containing 0.1 g/kg of the diet as polyunsaturated fatty acid, it was found that after 2 weeks the level of linoleate in the lymphocyte total lipids was 56 mg/ g total fatty acids, as compared with a level of 138 mg/ g in rats on a normal diet (P < 0.005). Similar levels were obtained from rats which had been fed for up to 16 weeks on the deficient diet, but in a group killed after 28 weeks on the diet the level was found to be only 20 mg/ g total fatty acids. The arachidonate level was found to be approximately 220 mg/ g total fatty acids, regardless of whether the rats were fed on a diet deficient in linoleate for up to 16 weeks or on a normal diet. In the group of rats killed after 28 weeks on the linoleate deficient diet, however, the arachidonate level was only 60 mg/ g total fatty acids.2. Percentage values for total fatty acids are given for plasma, adipose tissue, and lymphocytes for rats on normal and experimental diets.3. Scatter diagrams of the levels of linoleate v. arachidonate in the lymphocyte total fatty acids showed no correlation between the levels of the two acids (r 0.05), but similar plots of linoleate and oleate levels showed an inverse correlation (r – 0.68).


1988 ◽  
Vol 60 (1) ◽  
pp. 57-68 ◽  
Author(s):  
Ingo H. Waschulewski ◽  
Roger A. Sunde

1. The effect of dietary methionine on the utilization of selenium from dietary selenomethionine ([Se]Met) for tissue Se deposition and for glutathione peroxidase (EC 1.11.1.9; GSH-Px) synthesis was studied in male weanling rats.2. When rats were given 0.5 mg Se as [Se]Met/kg diet supplemented with 0, 4 or 9 g methionine/kg, Se in plasma, erythrocytes, liver and muscle increased significantly over the 20 d period for all methionine-treatment groups. The increases in erythrocyte and muscle Se, however, were significantly higher in rats fed on the methionine-deficient diet compared with the methionine-supplemented diets.3. In contrast to the increases in tissue Se, GSH-Px activity in liver, plasma and muscle decreased in methionine-deficient rats given 0.5 mg Se as [Se]Met/kg whereas GSH-Px activity was maintained or increased in rats supplemented with methionine.4. The percentage of tissue Se associated with GSH-Px was calculated from the measured Se concentration and GSH-Px activity. A significantly lower percentage of Se was associated with GSH-Px in methionine-deficient rats compared with methionine-supplemented rats.5. These results show that Se from dietary [Se]Met is preferentially incorporated into body proteins rather than used for GSH-Px synthesis when methionine is limiting in the diet.6. These results further suggest that [Se]Met might not be the optimum Se compound to use for Se supplementation because metabolism of dietary [Se]Met to a biochemically active form, such as GSH-Px, was impaired when [Se]Met was provided in diets low in methionine.


1987 ◽  
Vol 242 (2) ◽  
pp. 383-386 ◽  
Author(s):  
C G Fraga ◽  
R F Arias ◽  
S F Llesuy ◽  
O R Koch ◽  
A Boveris

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.


1989 ◽  
Vol 23 (4) ◽  
pp. 328-332 ◽  
Author(s):  
H. Van Herck ◽  
J. P. Van Wouwe ◽  
M. Veldhuizen ◽  
V. Baumans ◽  
F. R. Stafleu ◽  
...  

In order to gain experience about the detection of adverse effects during a scientific procedure, we carried out a clinical examination of rats with zinc deficiency. In weanling rats fed a zinc-deficient diet (30 μmol zinc/kg) for 10 days, the mean tibial concentration of zinc was reduced by 53% and body weight gain by 73070 when compared with rats fed a diet containing an adequate amount of zinc (150 μmol zinc/kg). In a small open field on day 9 of the experiment, the deficient rats more frequently displayed the posture standing upright with elevated heels. On day 10 of the experiment a clinical examination was carried out at random and 'blind' by three independent assessors. Out of 20 variables scored quantitatively on each individual animal, only body size differed between normal and deficient rats. Other classical signs of zinc deficiency, such as alopecia, dermatitis and diarrhoea, were not detected. It is concluded that in this rat model of zinc deficiency, no evidence for extreme discomfort can be demonstrated.


1968 ◽  
Vol 22 (1) ◽  
pp. 133-143 ◽  
Author(s):  
M. A. Cawthorne ◽  
J. Bunyan ◽  
A. T. Diplock ◽  
Elspeth A. Murrell ◽  
J. Green

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.


2008 ◽  
Vol 101 (4) ◽  
pp. 492-498 ◽  
Author(s):  
Motoyuki Nakao ◽  
Shoko Hironaka ◽  
Naoki Harada ◽  
Tetsuya Adachi ◽  
Tomohiro Bito ◽  
...  

The aim of the present study was to examine the effects of cobalamin (Cbl) on the activity and expression ofl-methylmalonyl-CoA mutase (MCM) in rat liver and cultured COS-7 cells. The MCM holoenzyme activity was less than 5 % of the total (holoenzyme+apoenzyme) activity in the liver although rats were fed a diet containing sufficient Cbl. When weanling rats were maintained on a Cbl-deficient diet, the holo-MCM activity became almost undetectable at the age of 10 weeks. In contrast, a marked increase in the total-MCM activity occurred under the Cbl-deficient conditions, and at the age of 20 weeks it was about 3-fold higher in the deficient rats than in the controls (108 (sd14·5)v.35 (sd8·5) nmol/mg protein per min (n5);P < 0·05). Western blot analysis confirmed that the MCM protein level increased significantly in the Cbl-deficient rats. However, the MCM mRNA level, determined by real-time PCR, was rather decreased. When COS-7 cells were cultured in a medium in which 10 % fetal bovine serum was the sole source of Cbl, holo-MCM activity was barely detected. The supplementation of Cbl resulted in a large increase in the holo-MCM activity in the cells, but the activity did not exceed 30 % of the total-MCM activity even in the presence of Cbl at 10 μmol/l. In contrast, the total-MCM activity was significantly decreased by the Cbl supplementation, indicating that Cbl deficiency results in an increase in the MCM protein level in COS-7 cells as well as in rat liver.


1975 ◽  
Vol 33 (1) ◽  
pp. 73-85 ◽  
Author(s):  
R. F. Krause ◽  
K. C. Beamer ◽  
A. M. Mccormick ◽  
R. J. Canterbury ◽  
G. P. Tryfiates

1. The effects of retinol and retinoic acid supplementation of retinol-deficient rats were studied for a variety of metabolic processes shown to be affected by retinol deficiency.2. Retinol-deficient rats were found to have decreased body-weight, liver and testes weights, a degeneration of testicular germinal cells, an increased incorporation of labelled choline into liver and testes phospholipids, an increased protein synthetic activity (in vitro) of liver ribosomes, an increased transfer-RNA methyltransferase activity in liver and a decreased activity in testes, an increased DNA content of testicular nuclei, and a decreased uptake of [3H]thymidine by testicular nuclear DNA.3. In retinol-deficient rats supplemented for 8 weeks with retinol these changes were reversed, measurements returning to control levels.4. In retinol-deficient rats supplemented for 8 weeks with retinoic acid all changes were reversed except those in the testes.5. Testicular signs of retinol deficiency appeared to be delayed when retinoic acid was added to the retinol-deficient diet of weanling rats. This suggests a sparing action of retinoic acid on the rat's utilization of retinol.6. Suggestions are offered as to why retinoic acid will support growth and development but not spermatogenesis in the rat.


1965 ◽  
Vol 85 (4) ◽  
pp. 362-366 ◽  
Author(s):  
Linda Morris ◽  
Dorothy Arata ◽  
Dena C. Cederquist

1974 ◽  
Vol 104 (11) ◽  
pp. 1496-1502 ◽  
Author(s):  
Alberto J. Monserrat ◽  
Eduardo A. Porta ◽  
Amiya K. Ghoshal ◽  
S. B. Hartman
Keyword(s):  

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