THE CAUSE OF THE DISAPPEARANCE OF ARGININE FROM THE BLOOD OF RATS WITH ACUTE HEPATIC NECROSIS INDUCED BY DIETARY MEANS

1961 ◽  
Vol 39 (6) ◽  
pp. 977-980 ◽  
Author(s):  
Guy N. Emery ◽  
J. M. R. Beveridge
Keyword(s):  
Vitamin E ◽  
Amino Acid ◽  
Liver Damage ◽  
Hepatic Necrosis ◽  
Liver Necrosis ◽  
Sprague Dawley ◽  
Acute Liver Damage ◽  
Blood Samples ◽  
Weanling Rats ◽  
Basal Ration

One hundred and fifteen male weanling rats of the Sprague–Dawley strain were placed on a basal ration designed to deplete their tissue reserves of vitamin E and selenium. They were then placed on a diet capable of precipitating acute hepatic necrosis within a few days. At 0, 12, 24, 36, 48, 60, 72, 78, 84, 90, 96, 114, 120, 132, 144, and 160 hours, groups of rats, including any which showed obvious signs of liver damage, were anesthetized with pentobarbital and blood samples were taken from the aorta via a syringe. Determinations of arginase activity of the plasma showed that greatly elevated values occurred only at the time of development of the acute liver damage. It is concluded that the disappearance of arginine from the blood of rats in which acute liver necrosis has developed is due to the liberation of arginase from the dead and dying liver cells thus destroying the amino acid.

Nutritional Hepatic Necrosis in Beef Cattle “Sawdust Liver”

1966 ◽  
Vol 3 (4) ◽  
pp. 379-400 ◽  
Author(s):  
Glen C. Todd ◽  
Lennart Krook
Keyword(s):  
Fatty Acids ◽  
Vitamin E ◽  
Selenium Deficiency ◽  
Diagnostic Value ◽  
Hepatic Necrosis ◽  
Common Denominator ◽  
Liver Necrosis ◽  
Liver And Kidney ◽  
Tissue Changes ◽  
The Common

A histologic examination of spontaneous cases of sawdust livers in cattle indicated that the focal liver necrosis was an expression of vitamin E-selenium deficiency. The condition was reproduced in Hereford steers by feeding a diet rich in polyunsaturated fatty acids and poor in protein, vitamin E. and selenium. Lesions also occurred in the kidney, heart, skeletal muscled and pylorus. Addition of dictary protein or injection of selenium partially prevented the condition. Cellular anoxia with formation of hyalinc bodies in the liver and kidney was considered to be the common denominator of the degenerative changes. Due to the relatively mild tissue changes, plasma GOT and OCT determinations were found to be of no diagnostic value.

scholarly journals Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence

1987 ◽  
Vol 242 (2) ◽  
pp. 383-386 ◽  
Author(s):  
C G Fraga ◽  
R F Arias ◽  
S F Llesuy ◽  
O R Koch ◽  
A Boveris
Keyword(s):  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Selenium Deficiency ◽  
Serum Levels ◽  
Hepatic Necrosis ◽  
Deficient Diet ◽  
Control Value ◽  
Weanling Rats

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.

AMINO ACID PATTERN IN THE BLOOD OF RATS WITH DIETARY HEPATIC NECROSIS

1960 ◽  
Vol 38 (1) ◽  
pp. 365-373
Author(s):  
L. S. Valberg ◽  
J. M. R. Beveridge
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Glutamic Acid ◽  
Reduced Glutathione ◽  
Liver Lesion ◽  
Hepatic Necrosis ◽  
Chromatographic Study ◽  
Oxidized Glutathione ◽  
Liver Necrosis ◽  
Beta Alanine

A paper chromatographic study of the amino acids and peptides in the blood of rats with dietary liver necrosis has been made.The relative levels of alanine, methionine, tyrosine, glutamic acid, threonine, citrulline, glutamine, oxidized glutathione, and gamma aminoisobutyric acid were increased. The level of reduced glutathione was slightly reduced and levels of valine, taurine, and proline remained unchanged. Beta-alanine, which could not be detected in the blood of normal rats, was found in the case of those with acute liver damage.Although arginine was present in the blood of normal animals and in those on a necrogenic diet prior to the development of the liver lesion, it was not detectable in those animals with acute hepatic necrosis. The possible implications of this finding have been discussed.

Effect of Policosanol on Carbon Tetrachloride-Induced Acute Liver Damage in Sprague-Dawley Rats

Drugs in R&D ◽  
2003 ◽  
Vol 4 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Miriam Noa ◽  
Sarah?? Mendoza ◽  
Rosa M??s ◽  
Nilda Mendoza
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Damage ◽  
Sprague Dawley ◽  
Acute Liver Damage ◽  
Sprague Dawley Rats

THE PREVENTION OF LIVER NECROSIS BY ALPHA-TOCOPHEROL, METHIONINE, AND CYSTEINE BY ORAL AND PARENTERAL ROUTES

1953 ◽  
Vol 31 (5) ◽  
pp. 417-420
Author(s):  
J. R. McLean ◽  
J. M. R. Beveridge
Keyword(s):  
Alpha Tocopherol ◽  
Daily Ration ◽  
Liver Necrosis ◽  
Sprague Dawley ◽  
Weanling Rats ◽  
Site Of Action

Groups of 10 male weanling rats of the Sprague-Dawley strain were fed a basal necrogenic diet supplemented with alpha-tocopherol, DL-methionine, and L-cysteine. The amount of supplement contained in the daily ration was administered parenterally to similar groups of rats. All three antinecrogenic agents employed exerted some action when given either in the diet or by injection. Alpha-tocopherol completely prevented the development of liver necrosis by both routes. On an equisulphur basis, methionine was obviously more effective than cysteine by either method of administration. The experiment threw no light on the question of the site of action of these compounds. The low antinecrogenic potency of cysteine compared to methionine or to cystine has posed a problem yet to be explained.

THE EFFECT OF UNSATURATION OF DIETARY FAT AND OF ANTIOXIDANTS ON THE DEVELOPMENT OF LIVER DAMAGE

1959 ◽  
Vol 37 (1) ◽  
pp. 493-499 ◽  
Author(s):  
L. S. Valberg ◽  
Rose A. Young ◽  
J. M. R. Beveridge
Keyword(s):  
Amino Acids ◽  
Fatty Acids ◽  
Antioxidant Activity ◽  
Vitamin E ◽  
Liver Damage ◽  
Dietary Fat ◽  
Unsaturated Fatty Acids ◽  
Alpha Tocopherol ◽  
Liver Necrosis ◽  
Gamma Tocopherol

The addition of unsaturated fatty acids, even in small amounts, to diets low in vitamin E, selenium, and the sulphur-containing amino acids greatly accelerated the development of acute liver necrosis in rats. The production of this lesion was shown also to be affected in a similar manner by the nature of the dietary fat in the ration consumed immediately prior to the removal of protective substances such as the sulphur-containing amino acids; unsaturated fatty acids or lipid again acted as predisposing factors.Gamma-tocopherol incorporated in the diet at a level of 0.02% and injected at a level of 1.5 mg/rat/day was equally as effective as alpha-tocopherol in preventing liver necrosis. The protective effect of gamma-tocopherol against the development of liver necrosis lends support to the thesis that alpha-tocopherol protects against liver damage by virtue of its antioxidant activity.

THE EFFECT OF UNSATURATION OF DIETARY FAT AND OF ANTIOXIDANTS ON THE DEVELOPMENT OF LIVER DAMAGE

1959 ◽  
Vol 37 (3) ◽  
pp. 493-499 ◽  
Author(s):  
L. S. Valberg ◽  
Rose A. Young ◽  
J. M. R. Beveridge
Keyword(s):  
Amino Acids ◽  
Fatty Acids ◽  
Antioxidant Activity ◽  
Vitamin E ◽  
Liver Damage ◽  
Dietary Fat ◽  
Unsaturated Fatty Acids ◽  
Alpha Tocopherol ◽  
Liver Necrosis ◽  
Gamma Tocopherol

The addition of unsaturated fatty acids, even in small amounts, to diets low in vitamin E, selenium, and the sulphur-containing amino acids greatly accelerated the development of acute liver necrosis in rats. The production of this lesion was shown also to be affected in a similar manner by the nature of the dietary fat in the ration consumed immediately prior to the removal of protective substances such as the sulphur-containing amino acids; unsaturated fatty acids or lipid again acted as predisposing factors.Gamma-tocopherol incorporated in the diet at a level of 0.02% and injected at a level of 1.5 mg/rat/day was equally as effective as alpha-tocopherol in preventing liver necrosis. The protective effect of gamma-tocopherol against the development of liver necrosis lends support to the thesis that alpha-tocopherol protects against liver damage by virtue of its antioxidant activity.

Preventative Effect of Vitamin E on Mast Cells in Carbon Tetrachlorideinduced Acute Liver Damage

2017 ◽  
Vol 16 (3) ◽  
pp. 205-212 ◽  
Author(s):  
Ayhan Eralp ◽  
Nur Menguc ◽  
Elif Polat ◽  
Mehmet Yuncu ◽  
Mehmet Koruk ◽  
...  
Keyword(s):  
Vitamin E ◽  
Mast Cells ◽  
Liver Damage ◽  
Acute Liver Damage

scholarly journals Vitamin E and stress

1967 ◽  
Vol 21 (1) ◽  
pp. 115-125 ◽  
Author(s):  
A. T. Diplock ◽  
J. Green ◽  
J. Bunyan ◽  
D. Mchale ◽  
I. R. Muthy
Keyword(s):  
Vitamin E ◽  
Terminal Illness ◽  
Methyl Esters ◽  
Tocopheryl Acetate ◽  
Liver Necrosis ◽  
Deficient Diet ◽  
Weanling Rats ◽  
High Incidence ◽  
Gastro Intestinal Tract ◽  
Oxidant Effect

1. When weanling rats were given a vitamin E-deficient diet and 0.15% (w/v) silver acetate in their drinking water, there was a high incidence of liver necrosis and death after 2–4 weeks. This was prevented by 120 ppm D-α-tocopheryl acetate in the diet, was partially prevented by selenium at 1 ppm but not at 0.05 ppm and was only marginally prevented by 0.15% DL-methionhe.2. All these effects were observed when the diet was free of fat and when it contained either methyl oleate or polyunsaturated methyl esters. The polyunsaturated lipid slightly increased the velocity of the terminal illness.3. In spite of the ‘anti-vitamin E’ effect of Ag and the clear demonstration that α-tocopherol played a major part in preventing toxicity, experiments with tracer amounts of [5-Me-14C]-D-α-tocopherol showed that rather than there being any destruction of tocopherol in the critical period preceding the onset of disease, there was an increase in tocopherol in the liver due to Ag administation. The metabolism of tocopherol in the remainder of the animal was unaffected during the pre-necrotic phase.4. The results are inconsistent with the view that the stress induced by Ag is caused by a pro-oxidant effect, either in the gastro-intestinal tract or in the tissues of the rat. They show that lipid peroxidation is not a causal factor in the aetiology of Ag-induced liver necrosis and suggest that stress in the vitamin E-deficient animal probably raises the requirement for tocopherol.

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