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

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.

1981 ◽  
Vol 46 (2) ◽  
pp. 337-344 ◽  
Author(s):  
W. R. H. Duncan ◽  
E. Rona Morrison ◽  
G. A. Garton

1. Two groups of ewes were fed on a cobalt-deficient diet throughout pregnancy; one group (group A) was given the diet from the beginning of pregnancy, whilst the other (group B) received the diet for 16 weeks before mating. The ewes in group A continued to receive the diet for 12 weeks post-partum.2. The vitamin B12 content of serum was estimated on three occasions before parturition and, for group A ewes, at 12 weeks post partum. Urinary concentration of methylmalonic acid was also determined at intervals before the lambs were born.3. Serum values for vitamin B12 indicated that the ewes in both groups were depleted of the vitamin, though those in group B were more severely affected, as was evidenced by the high incidence of perinatal mortality among the lambs born to these ewes. Perinatal mortality appeared to be associated with abnormally-high values for urinary concentration of methylmalonic acid.4. Analysis of liver lipids and adipose tissue triacylglycerols of some of the vitamin B12-deprived lambs which died before, or within 1 d of, birth showed that, compared with the corresponding tissues of control lambs, these lipids contained unusually high proportions of odd-numbered fatty acids (mostly 15:0, 17:0 and 19:0). This observation is discussed in relation to the likelihood that, in vitmain B12-deprived lambs, propionate becomes available as a primer unit for fatty acid synthesis when the metabolism of its carboxylation product, methylmalonic acid, is impaired due to partlal lack of a vitamin B12-containing enzyme system.


1976 ◽  
Vol 160 (2) ◽  
pp. 287-294 ◽  
Author(s):  
T O Eloranta ◽  
E O Kajander ◽  
A M Raina

The hepatic synthesis and accumulation of S-adenosylhomocysteine, S-adenosylmethionine and polyamines were studied in normal and vitamin B-6-deficient male albino rats. A method involving a single chromatography on a phosphocellulose column was developed for the determination of S-adenosylhomocysteine and S-adenosylmethionine from tissue samples. Feeding the rat with pyridoxine-deficient diet for 3 or 6 weeks resulted in a four- to five-fold increase in the concentration of S-adenosylhomocysteine, whereas that of S-adenosylmethionine was only slighly elevated. The concentration of putrescine was decreased to half, that of spermidine was somewhat decreased and that of spermine remained fairly constant. The activities of L-ornithine decarboxylase, S-adenosyl-L-methionine decarboxylase, L-methionine adenosyltransferase and S-adenosyl-L-homocysteine hydrolase were moderately increased. S-Adenosylmethionine decarboxylase showed no requirement for pyridoxal 5′-phosphate. The major effect of pyridoxine deficiency of S-adenosylmethionine metabolism seems to be a block in the utilization of S-adenosylhomocysteine, resulting in the accumulation of this metabolite to a concentration that may inhibit biological methylation reactions.


2014 ◽  
Vol 39 (7) ◽  
pp. 793-800 ◽  
Author(s):  
Akshaya P. Meher ◽  
Asmita A. Joshi ◽  
Sadhana R. Joshi

An altered one-carbon cycle is known to influence placental and fetal development. We hypothesize that deficiency of maternal micronutrients such as folic acid and vitamin B12 will lead to increased oxidative stress, reduced long-chain polyunsaturated fatty acids, and altered expression of peroxisome proliferator activated receptor (PPARγ) in the placenta, and omega-3 fatty acid supplementation to these diets will increase the expression of PPARγ. Female rats were divided into 5 groups: control, folic acid deficient, vitamin B12 deficient, folic acid deficient + omega-3 fatty acid supplemented, and vitamin B12 deficient + omega-3 fatty acid supplemented. Dams were dissected on gestational day 20. Maternal micronutrient deficiency leads to lower (p < 0.05) levels of placental docosahexaenoic acid, arachidonic acid, PPARγ expression and higher (p < 0.05) levels of plasma malonidialdehyde, placental IL-6, and TNF-α. Omega-3 fatty acid supplementation to a vitamin B12 deficient diet normalized the expression of PPARγ and lowered the levels of placental TNF-α. In the case of supplementation to a folic acid deficient diet it lowered the levels of malonidialdehyde and placental IL-6 and TNF-α. This study has implications for fetal growth as oxidative stress, inflammation, and PPARγ are known to play a key role in the placental development.


2002 ◽  
Vol 227 (11) ◽  
pp. 998-1000 ◽  
Author(s):  
Jack M. Cooperman ◽  
Rafael Lopez

The amino acid histidine is metabolized to glutamic acid in mammalian tissue. Formiminoglutamic acid (FIGLU) is an intermediary in this reaction, and tetrahydrofolic acid is the coenzyme that converts it to glutamic acid. A test for folate deficiency concerns the measurement of urinary FIGLU excretion after a histidine load. It was observed that folate-deficient individuals receiving the histidine for the FIGLU test made hematological response that alleviated the anemia associated with this deficiency. This was unusual in that a biochemical test to determine the deficiency results in a beneficial effect for one aspect of the deficiency. The studies reported in this paper give a metabolic explanation for this phenomenon. Urine was collected for 24 hr from 25 folate-deficient subjects, 10 vitamin B12-deficient subjects, and 15 normal controls. Urinary excretion of histidine was a mean of 203 mg with a range of 130–360 mg for the folate-deficient subjects; 51.5 mg with a range of 30–76.6 mg for normal subjects; and 60.0 mg with a range of 32.3–93.0 mg for the vitamin B12-deficient subjects. All the folate-deficient subjects subsequently made a hematological response to the histidine administered for the FIGLU test. No hematological response was observed in the vitamin B12-deficient individuals. When folic acid was given to folate-deficient subjects who received no histidine, urinary histidine levels returned to normal levels rapidly and this was followed by a hematological response. Others have shown that volunteers fed a histidine-free diet developed anemia. In normal subjects, histidine is excreted much more in the urine than other essential amino acids are. Hemoglobin protein contains 10% histidine. Under normal conditions, dietary histidine can supply sufficient histidine to prevent anemia. When the dietary intake is diminished or the urinary excretion is greatly increased, anemia results. It is concluded that folate deficiency causes histidine depletion through increased urinary excretion of this amino acid. Feeding histidine replenishes tissue levels of histidine, resulting in hemoglobin regeneration. Folic acid administration results in return of histidine to normal urinary levels. Thus, a combination of folic acid histidine would be beneficial for folate deficient individuals.


Author(s):  
Michela Cirillo ◽  
Rossella Fucci ◽  
Sara Rubini ◽  
Maria Elisabetta Coccia ◽  
Cinzia Fatini

The homocysteine pathway in the preconception period should be evaluated to highlight micronutrient deficiencies and warrants optimal multivitamin supplementation, before Assisted Reproduction, as preconception care. We conducted a retrospective study aimed at investigating the role of vitamin B complex (5-methyltetrahydrofolate, vitamin B12, vitamin B6) supplement use compared with the role of only folic acid supplement use, in relation to clinical pregnancy and live birth in infertile women undergoing homologous ART. We investigated 269 Caucasian women referred to the Centre for Assisted Reproductive Technology for homologous ART. In these women, 111 (Group A) were daily supplemented with vitamin B complex and 158 (Group B) with only folic acid. In group A the mean number of Metaphase II oocytes and the 2PN Fertilization Rate were higher in comparison to group A (p = 0.04; p = 0.05, respectively). A higher percentage of women in group A had a clinical pregnancy and live birth in comparison to group B (p = 0.01; p = 0.02, respectively). Vitamin B complex supplementation remained independently associated, after multivariable adjustment, with clinical pregnancy (OR 2.03, p = 0.008) and live birth (OR 1.83, p = 0.03). Women supplemented with 5-MTHF and vitamin B12, have a higher chance of clinical pregnancy and live birth in comparison to those supplemented with only folic acid.


2015 ◽  
Vol 4 ◽  
Author(s):  
Marie-Édith Côté-Robitaille ◽  
Christiane L. Girard ◽  
Frédéric Guay ◽  
J. Jacques Matte

AbstractHomocysteine (Hcy) is an intermediary sulphur amino acid recognised for pro-oxidative properties in several species which may weaken immune competence in piglets. In this species, there is an acute 10-fold increase of concentrations of plasma Hcy (pHcy) during the first 2 weeks of life. The present experiment aimed to determine if pHcy in piglets can be regulated by oral supplementations of betaine as a methyl group supplier, creatine for reducing the demand for methyl groups, choline with both previous functions and vitamin B6 as enzymic co-factor for Hcy catabolism. A total of seventeen sows (second parity) were fed gestation and lactation diets supplemented with folic acid (10 mg/kg) and vitamin B12 (150 µg/kg). Eight piglets in each litter received daily one of the eight following oral treatments (mg/kg body weight): (1) control (saline); (2) betaine (50); (3) choline (70); (4) creatine (300); (5) pyridoxine (0·2); (6) treatments 2 and 5; (7) treatments 3 and 4; and (8) treatments 2, 3, 4 and 5. According to age, pHcy increased sharply from 2·48 µm at birth to 17·96 µm at 21 d of age (P < 0·01). Concentrations of pHcy tended to be lower (P = 0·09) in treated than in control piglets but the highest and sole pairwise significant decrease (23 %) was observed between treatments 1 and 8 (P = 0·03). Growth from birth to 21 d of age was not influenced by treatments (P > 0·70). Therefore, it appears possible to reduce pHcy concentrations in suckling piglets but a combination of all chosen nutrients is required.


1977 ◽  
Vol 55 (3) ◽  
pp. 427-433 ◽  
Author(s):  
I. F. Tagbo ◽  
D. C. Hill

Two groups of 63-day-old female Wistar rats were fed a folic acid deficient diet, based on 20% of vitamin-free casein and containing 1% of succinylsulfathiazole, for 5 weeks (group A) and 9 weeks (group B) before being bred, and the same diet was continued through pregnancy and lactation. Three out of eleven (21.3%) and three out of seven (42.9%) rats in groups A and B, respectively, resorbed completely, while no control rat resorbed. No pups from group B survived to weaning. Both groups (A and B) showed depressed feed consumption (although the effect in group A rats was small) and weight gains and increased formiminoglutamic acid excretion in the urine during gestation, and low serum folic acid by the end of lactation. A study of blood components in group A rats revealed leucopenia, granulocytopenia, and increased reticulocyte count. While no congenital deformities were observed in pups from deficient dams, group A and group B dams in contrast to controls produced smaller sized litters with lower birth weights and poor survival rate. Surviving pups from group A dams had decreased weaning weights with significantly lower brain weights and brain DNA per gram of tissue.


1992 ◽  
Vol 15 ◽  
pp. 169-171 ◽  
Author(s):  
G. E. J. Fisher ◽  
A. MacPherson

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.


2020 ◽  
Vol 16 (S3) ◽  
Author(s):  
Yvette Wilda Jyrwa ◽  
Ravindranadh Palika ◽  
Swetha Boddula ◽  
Naveen Kumar Boiroju ◽  
Radhika Madhari ◽  
...  

2017 ◽  
Vol 76 ◽  
pp. 743-751 ◽  
Author(s):  
Laura Jaimes-Aguirre ◽  
Enrique Morales-Avila ◽  
Blanca E. Ocampo-García ◽  
Luis Alberto Medina ◽  
Gustavo López-Téllez ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document