Arecoline tumorigenicity in swiss strain mice on normal and vitamin B deficient diet

1984 ◽  
Vol 107 (3) ◽  
pp. 169-171 ◽  
Author(s):  
S. V. Bhide ◽  
S. V. Gothoskar ◽  
N. M. Shivapurkar
Keyword(s):  
Vitamin B ◽  
Deficient Diet ◽  
Swiss Strain

Effects of cobalt deficiency in the pregnant ewe on neonatal lamb survival

1992 ◽  
Vol 15 ◽  
pp. 169-171 ◽  
Author(s):  
G. E. J. Fisher ◽  
A. MacPherson
Keyword(s):  
Reproductive Performance ◽  
Dry Matter ◽  
Methylmalonic Acid ◽  
Milk Powder ◽  
Vitamin B ◽  
Deficient Diet ◽  
Cobalt Deficiency ◽  
Acid Status ◽  
Pregnant Ewe ◽  
Skimmed Milk Powder

It has been suggested (Mills, 1981) that there was a lack of research on the effects of cobalt (Co) deficiency on the reproductive performance of sheep. Duncan, Morrison and Garton (1981) reported that clinically Co-deficient ewes produced fewer lambs with a higher incidence of stillbirths and neonatal mortalities than Co-sufficient animals. Garton, Duncan and Fell (1981) related these findings to the vitamin B12 and methylmalonic acid status of dams. However, their investigations used few animals and were therefore inconclusive. The objectives of this work were to investigate the effects of subclinical Co deficiency in pregnant hill sheep on reproductive performance and neonatal lamb viability.Experiment 1 (1985/86) comprised 60 Scottish Blackface × Swaledale ewes, while experiment 2 (1986/87) included 30 of these animals plus 30 pure Scottish Blackface sheep. In both experiments the ewes were housed and bedded on sawdust and a Co-deficient diet of timothy hay, micronized maize, maize gluten, dibasic calcium phosphate and sodium chloride was offered. Skimmed milk powder was introduced to the diet during lactation. The Co content of the diet was 0.06 mg Co per kg dry matter.

Thiamine (Vitamin B1)

2011 ◽  
Vol 16 (1) ◽  
pp. 12-20 ◽  
Author(s):  
Aviva Fattal-Valevski
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Metabolism ◽  
Oxidant Stress ◽  
Vitamin B1 ◽  
Vitamin B ◽  
Deficient Diet ◽  
Common Cause ◽  
Korsakoff Syndrome ◽  
Reducing Substances ◽  
B Vitamin

Thiamine (vitamin B1) was the first B vitamin to have been identified. It serves as a cofactor for several enzymes involved in energy metabolism. The thiamine-dependent enzymes are important for the biosynthesis of neurotransmitters and for the production of reducing substances used in oxidant stress defenses, as well as for the synthesis of pentoses used as nucleic acid precursors. Thiamine plays a central role in cerebral metabolism. Its deficiency results in dry beriberi, a peripheral neuropathy, wet beriberi, a cardiomyopathy with edema and lactic acidosis, and Wernicke—Korsakoff syndrome, whose manifestations consist of nystagmus, ophthalmoplegia, and ataxia evolving into confusion, retrograde amnesia, cognitive impairment, and confabulation. Patients on a strict thiamine-deficient diet display a state of severe depletion within 18 days. The most common cause of thiamine deficiency in affluent countries is either alcoholism or malnutrition in nonalcoholic patients. Treatment by thiamine supplementation is beneficial for diagnostic and therapeutic purposes.

EXCRETION OF 4(5)-AMINO-5(4)-IMIDAZOLECARBOXAMIDE AND FORMIMINO-L-GLUTAMIC ACID IN FOLIC ACID AND VITAMIN B12 DEFICIENT RATS

1965 ◽  
Vol 43 (8) ◽  
pp. 1367-1374 ◽  
Author(s):  
P. L. McGeer ◽  
N. P. Sen ◽  
D. A. Grant
Keyword(s):  
Folic Acid ◽  
Glutamic Acid ◽  
Fold Increase ◽  
Urocanic Acid ◽  
Vitamin B ◽  
Deficient Diet ◽  
Intraperitoneal Dose ◽  
Group A ◽  
Acid Load ◽  
Deficient Group

The excretion of 4(5)-amino-5(4)-imidazolecarboxamide (AIC) in the urines of normal rats, rats raised on a folic acid deficient diet, and rats raised on a vitamin B12 deficient diet was measured. The AIC excretion was elevated 3-fold above normal in the B12 deficient group and 1.5-fold above normal in the folic acid deficient group.No evidence could be found that the raised AIC excretion was associated with a block in the conversion of AIC to purines. The recovery of radioactive AIC in the urine after an intraperitoneal dose of 2 μmoles AIC per kg was not increased over normal in any of the deficient groups, and was significantly less than normal in the B12-deficient group. Most of the urinary radioactivity in all groups was in allantoin, uric acid, and purines.When a load of 220 μmoles of AIC per kg was administered there was no difference between the vitamin B12 deficient and the normal groups in AIC recovery in the urine. When a load of 220 μmoles of urocanic acid per kg was administered, however, the B12-deficient group had an 18-fold increase over normal in Figlu excretion, and the folic acid deficient group a 17-fold increase. Thus, a substantial block in formimino-L-glutamic acid (Figlu) metabolism, but not in AIC metabolism, existed in the vitamin-deficient groups.Feeding a B12-deficient group a 2% methionine supplement reduced the Figlu excretion after a urocanic acid load to less than half that observed in B12-deficient groups without methionine supplementation, but had no influence on the AIC excretion.

scholarly journals Role of pyridoxal phosphate in mammalian polyamine biosynthesis. Lack of requirement for mammalian S-adenosylmethionine decarboxylase activity

1977 ◽  
Vol 166 (1) ◽  
pp. 81-88 ◽  
Author(s):  
A E Pegg
Keyword(s):  
Ornithine Decarboxylase ◽  
Pyridoxal Phosphate ◽  
Vitamin B ◽  
Decarboxylase Activity ◽  
Deficient Diet ◽  
Polyamine Biosynthesis ◽  
Adenosylmethionine Decarboxylase ◽  
Ornithine Decarboxylase Activity

1. Polyamine concentrations were decreased in rats fed on a diet deficient in vitamin B-6. 2. Ornithine decarboxylase activity was decreased by vitamin B-6 deficiency when assayed in tissue extracts without addition of pyridoxal phosphate, but was greater than in control extracts when pyridoxal phosphate was present in saturating amounts. 3. In contrast, the activity of S-adenosylmethionine decarboxylase was not enhanced by pyridoxal phosphate addition even when dialysed extracts were prepared from tissues of young rats suckled by mothers fed on the vitamin B-6-deficient diet. 4. S-Adenosylmethionine decarboxylase activities were increased by administration of methylglyoxal bis(guanylhydrazone) (1,1′-[(methylethanediylidine)dinitrilo]diguanidine) to similar extents in both control and vitamin B-6-deficient animals. 5. The spectrum of highly purified liver S-adenosylmethionine decarboxylase did not indicate the presence of pyridoxal phosphate. After inactivation of the enzyme by reaction with NaB3H4, radioactivity was incorporated into the enzyme, but was not present as a reduced derivative of pyridoxal phosphate. 6. It is concluded that the decreased concentrations of polyamines in rats fed on a diet containing vitamin B-6 may be due to decreased activity or ornithine decarboxylase or may be caused by an unknown mechanism responding to growth retardation produced by the vitamin deficiency. In either case, measurements of S-adenosylmethionine decarboxylase and ornithine decarboxylase activity under optimum conditions in vitro do not correlate with the polyamine concentrations in vivo.

Effects of vitamin B12 deficiency on lipid metabolism of the rat liver and nervous system

1978 ◽  
Vol 39 (3) ◽  
pp. 501-513 ◽  
Author(s):  
C. Fehling ◽  
Margaretha JÄgerstad ◽  
B. Åkesson ◽  
J. Axelsson ◽  
A. Brun
Keyword(s):  
Fatty Acids ◽  
Nervous System ◽  
Fatty Acid ◽  
Motor Nerve ◽  
Vitamin B12 Deficiency ◽  
Neurological Dysfunction ◽  
Vitamin B ◽  
Deficient Diet ◽  
Neurological Signs ◽  
The Central Nervous System

1. Rats bred from vitamin B12-depleted dams were fed on a vitamin B12-deficient diet for 12–15 months and developed a severe vitamin B12 deficiency, as judged from methylmalonic acid excretion and tissue vitamin B12 levels at slaughter. Control rats were supplemented with vitamin B12 in the drinking-water.2. Neurological signs were recorded after 7 months but the motor nerve conduction velocities remained normal. Neuropathological examination revealed mild changes in the peripheral nerves but no changes in the central nervous system.3. The amounts of total lipids and phospholipids were normal, but in all examined tissues the proportions of pentadecanoate (C15 fatty acid) and heptadecanoate (C17 fatty acid) were considerably increased in vitamin B12 deficiency.4. 3H2O was incorporated to the same extent into the fatty acids of nervous tissue from vitamin B12-deficient and control rats after 48 h. Less 3H was found in the liver fatty acids of the vitamin B12-deficient rats.5. Neurological dysfunction can be demonstrated in the vitamin B12-deficient rat; the relation of the biochemical and neuropathological changes to the neurological signs needs further study.

Effect of a Vitamin B-12-Deficient Diet on Lipid and Fatty Acid Composition of Spinal Cord Myelin in the Fruit Bat

1983 ◽  
Vol 113 (3) ◽  
pp. 531-537 ◽  
Author(s):  
Justin van der Westhuyzen ◽  
Richard C. Cantrill ◽  
Francisco Fernandes-Costa ◽  
Jack Metz
Keyword(s):  
Spinal Cord ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Acid Composition ◽  
Vitamin B ◽  
Deficient Diet ◽  
Fruit Bat ◽  
Vitamin B 12

scholarly journals The experimental production of vitamin B12 deficiency in the baboon (Papio cynocephalus). A 2-year study

1974 ◽  
Vol 32 (2) ◽  
pp. 219-228 ◽  
Author(s):  
R. C Siddons
Keyword(s):  
Methylmalonic Acid ◽  
Daily Intake ◽  
Serum Vitamin ◽  
Vitamin B12 Deficiency ◽  
Vegetarian Diet ◽  
Vitamin B ◽  
Papio Cynocephalus ◽  
Experimental Production ◽  
Deficient Diet ◽  
Liver Vitamin

1. The development of vitamin B12 deficiency, as indicated by the serum and liver vitamin B12 levels and the excretion of methylmalonic acid, was studied over a 2-year period in baboons (Papio cynocephalus) given a diet deficient in vitamin B12. The effects of partial hepatectomy and the inclusion of either ampicillin or sodium propionate in the diet on the rate of development of the deficiency were also studied.2. The baboons had previously been fed on a mainly vegetarian diet. Their serum vitamin B12 levels were less than 100 ng/l and the mean liver vitamin B12 concentration was 0·56 μ/g. Similar serum and liver vitamin B12 levels were found in baboons given a purified diet supplemented with 1 μg vitamin B12/d, and marked increases in the serum and liver vitamin B12 levels occurred when the daily intake was increased to 2 μg.3. The serum vitamin B12 levels decreased to less than 20 ng/l in all baboons given a vitamin B12-deficient diet.4. The liver vitamin B12 concentration also decreased in all baboons given a deficient diet. At 9 months the lowest levels (0·20 μ/g) were found in partially hepatectomized baboons but subsequently baboons given the diet containing ampicillin had the lowest levels (0·11 μ/g).5. The excretion of methylmalonic acid after a valine load was found to be inversely related to the liver vitamin B12 concentration. In the early part of the study, partially hepatectomized baboons excreted the highest amount but subsequently baboons given a diet containing ampicillin excreted the highest amount.6. Increased formiminoglutamic acid excretion after a histidine load was observed in two baboons given a vitamin B12-deficient diet and in both baboons the liver folic acid concentration was low.7. No haematological or neurological symptoms of the vitamin B12 deficiency were observed.

scholarly journals Production within the rumen and removal from the blood-stream of volatile fatty acids in sheep given a diet deficient in cobalt

1972 ◽  
Vol 27 (1) ◽  
pp. 147-157 ◽  
Author(s):  
Hedeey R. Marston ◽  
Shirley H. Allex ◽  
R. M. SMITH
Keyword(s):  
Fatty Acids ◽  
Volatile Fatty Acids ◽  
Blood Stream ◽  
Acetate Metabolism ◽  
Vitamin B ◽  
Deficient Diet ◽  
Progressive Loss ◽  
Before And After ◽  
Loss Of Appetite ◽  
Oral Supplement

1. The production and metabolism of volatile fatty acids were studied in sheep offered a cobalt-deficient diet.2. The molar proportions of acetic (60%), propionic (26%) and butyric (14%) acids in the rumen fluids of sheep given the Co-deficient diet, but whose stores of vitamin B12 were adequate, were similar before and after administration of an oral supplement of Co.3. In pair-fed sheep, one member of which was vitamin B12-deficient and the other (control) treated with vitamin B12 parenterally, the concentrations after feeding of both total and individual volatile fatty acids in the blood tended to be higher in deficient than in control sheep.4. Following injection of the respective salts of individual volatile fatty acids into the blood-stream, formate clearance was apparently not affected, whereas that of acetate was slightly, and that of propionate very significantly, delayed in vitamin B12-deficient sheep compared with pair-fed control animals.5. Acetate metabolism was retarded in the presence of propionate; the effect was greater in deficient than in pair-fed control sheep.6. The hypothesis is advanced that it is the failure to metabolize propionate at the normal rate that leads to the progressive loss of appetite in vitamin B12-deficient sheep.

scholarly journals NUTRITIONAL CYTOPENIA (VITAMIN M DEFICIENCY) IN THE MONKEY

1938 ◽  
Vol 68 (6) ◽  
pp. 923-940 ◽  
Author(s):  
William C. Langston ◽  
William J. Darby ◽  
Carroll F. Shukers ◽  
Paul L. Day
Keyword(s):  
Nicotinic Acid ◽  
Liver Extract ◽  
Vitamin B ◽  
Good Growth ◽  
Deficient Diet ◽  
Polished Rice ◽  
Whole Wheat ◽  
Body Development ◽  
Loss Of Weight ◽  
Brewers Yeast

Young rhesus monkeys (Macaca mulatta) were given a diet containing casein, polished rice, whole wheat, salt mixture, sodium chloride, cod liver oil, and ascorbic acid. They developed a syndrome characterized by anemia, leukopenia, and loss of weight. Ulceration of the gums and diarrhea were common, and death occurred between the 26th and 100th day. 4 monkeys were given the deficient diet supplemented with 1 mg. of riboflavin daily, and these developed the characteristic signs and died. in periods of time similar to the survival of monkeys receiving the deficient diet alone. Nicotinic acid, either alone or in combination with riboflavin and thiamin chloride, failed to alter appreciably the course of the deficiency manifestations. Thus, it is evident that this nutritional cytopenia is not the result of a deficiency of vitamin B, riboflavin, or nicotinic acid. The deficient diet supplemented with either 10 gm. of dried brewers' yeast or 2 gm. of liver extract (Cohn fraction G) daily supported good growth, permitted normal body development, and maintained a normal blood picture over long periods. It is obvious that yeast and liver extract contain a substance essential to the nutrition of the monkey which is not identical with any of those factors of the vitamin B complex that have been chemically identified. We have proposed the term vitamin M for this factor which prevents nutritional cytopenia in the monkey.

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