A new method for the assay of tissue. S-adenosylhomocysteine and S-adenosylmethione. Effect of pyridoxine deficiency on the metabolism of S-adenosylhomocysteine, S-adenosylmethionine and polyamines in rat liver

T O Eloranta; E O Kajander; A M Raina

doi:10.1042/bj1600287

A new method for the assay of tissue. S-adenosylhomocysteine and S-adenosylmethione. Effect of pyridoxine deficiency on the metabolism of S-adenosylhomocysteine, S-adenosylmethionine and polyamines in rat liver

Biochemical Journal ◽

10.1042/bj1600287 ◽

1976 ◽

Vol 160 (2) ◽

pp. 287-294 ◽

Cited By ~ 75

Author(s):

T O Eloranta ◽

E O Kajander ◽

A M Raina

Keyword(s):

Fold Increase ◽

Major Effect ◽

Albino Rats ◽

Vitamin B ◽

Deficient Diet ◽

Tissue Samples ◽

Adenosylmethionine Decarboxylase ◽

Pyridoxine Deficiency ◽

Hepatic Synthesis

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.

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

Canadian Journal of Biochemistry ◽

10.1139/o65-152 ◽

1965 ◽

Vol 43 (8) ◽

pp. 1367-1374 ◽

Cited By ~ 12

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.

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

Biochemical Journal ◽

10.1042/bj1660081 ◽

1977 ◽

Vol 166 (1) ◽

pp. 81-88 ◽

Cited By ~ 19

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.

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Determination of Vitamin B6 Deficiency in Rainbow Trout (Salmo gairdneri) by Liver Enzyme Assay and HPLC Analysis

Canadian Journal of Fisheries and Aquatic Sciences ◽

10.1139/f87-030 ◽

1987 ◽

Vol 44 (1) ◽

pp. 219-222 ◽

Cited By ~ 7

Author(s):

Ronald W. Hardy ◽

Edmundo Casillas ◽

Toshiro Masumoto

Keyword(s):

Rainbow Trout ◽

Vitamin B6 ◽

Enzyme Assay ◽

Clinical Signs ◽

Salmo Gairdneri ◽

Vitamin B ◽

Deficient Diet ◽

Vitamin B6 Deficiency ◽

Stimulation Of

Rainbow trout (Salmo gairdneri), initially averaging 125 g, were fed a complete or a pyridoxine-deficient diet for 14 wk. Vitamin B6 status was evaluated biweekly by direct measurement of liver pyridoxine and pyridoxal levels by HPLC and by determining pyridoxal-5′-phosphate-enhanced liver aspartate aminotransferase (ASAT) activity. By 14 wk, mortality had severely reduced the number of fish remaining in the pyridoxine-deficient group. At 14 wk, no significant differences in liver pyridoxine and pyridoxal levels were detected between the trout fed the complete or pyridoxine-deficient diet. Significant differences between dietary groups are found in ASAT activity in liver and percent stimulation of liver ASAT by the addition of pyridoxal-5′-phosphate after 8 wk. Clinical signs of vitamin B6 deficiency including anorexia, listlessness, frantic and erratic swimming, and ataxia were observed after 11 wk of feeding a pyridoxine-deficient diet. This study shows that vitamin B6 deficiency in rainbow trout can be readily determined weeks before signs of clinical deficiency are apparent by measuring pyridoxine-enhanced liver ASAT activity. However, liver levels of pyridoxine and pyridoxal are not sensitive indicators of vitamin B6 status.

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

BSAP Occasional Publication ◽

10.1017/s0263967x00004201 ◽

1992 ◽

Vol 15 ◽

pp. 169-171 ◽

Cited By ~ 1

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.

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Hexagonal boron nitride nanoparticles trigger oxidative stress by modulating thiol/disulfide homeostasis

Human & Experimental Toxicology ◽

10.1177/09603271211002892 ◽

2021 ◽

pp. 096032712110028

Author(s):

F Kar ◽

İ Söğüt ◽

C Hacıoğlu ◽

Y Göncü ◽

H Şenturk ◽

...

Keyword(s):

Oxidative Stress ◽

Boron Nitride ◽

Hexagonal Boron Nitride ◽

Chemical Properties ◽

Heart Tissue ◽

Albino Rats ◽

Dependent Manner ◽

Tissue Samples ◽

Boron Nitride Nanoparticles

Background: Hexagonal boron nitride nanoparticles (hBN NPs) are encouraging nanomaterials with unique chemical properties in medicine and biomedical fields. Until now, the optimal hBN NP’s dosage and biochemical mechanism that can be used for in vivo systems has not been fully revealed. The main aim of this article is to reveal characteristics, serum and tissue interactions and any acute cytotoxic effect of different dose of hBN NPs for the first time. Methods: hBN NPs at concentrations varying between 50–3200 µg/kg was administered by intravenous injection to Wistar albino rats (n = 80) divided into seven dosage and control groups. Blood and tissue samples were taken after 24 hours. Results: Our findings suggested that higher doses hBN NPs caused oxidative stress on the serum of rats dose-dependently. However, hBN NPs did not affect thiol/disulfide homeostasis on kidney, liver, spleen, pancreas and heart tissue of rats. Furthermore, hBN NPs increased serum disulfide formation by disrupting the thiol/disulfide balance in rats. Also, LOOH and MPO levels increased at high doses, while CAT levels decreased statistically. Conclusion: The results revealed that hBN NPs induce oxidative stress in a dose-dependent manner by modulating thiol/disulfide homeostasis in rats at higher concentrations

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POLAROGRAPHIC DETERMINATION OF RIBOFLAVIN (VITAMIN B2) AND OTHER VITAMIN B FACTORS

Journal of Biological Chemistry ◽

10.1016/s0021-9258(19)56162-2 ◽

1941 ◽

Vol 137 (2) ◽

pp. 567-574

Author(s):

James J. Lingane ◽

Orris L. Davis

Keyword(s):

Polarographic Determination ◽

Vitamin B ◽

Vitamin B2

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On the robustness of inference of association with the gut microbiota in stool, rectal swab and mucosal tissue samples

Scientific Reports ◽

10.1038/s41598-021-94205-5 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Shan Sun ◽

Xiangzhu Zhu ◽

Xiang Huang ◽

Harvey J. Murff ◽

Reid M. Ness ◽

...

Keyword(s):

Gut Microbiota ◽

Rectal Swab ◽

Taxonomic Composition ◽

Mucosal Tissue ◽

Tissue Samples ◽

Health And Disease ◽

Inflammatory Drugs ◽

Metagenome Sequencing ◽

Functional Profiles

AbstractThe gut microbiota plays an important role in human health and disease. Stool, rectal swab and rectal mucosal tissue samples have been used in individual studies to survey the microbial community but the consequences of using these different sample types are not completely understood. In this study, we report differences in stool, rectal swab and rectal mucosal tissue microbial communities with shotgun metagenome sequencing of 1397 stool, swab and mucosal tissue samples from 240 participants. The taxonomic composition of stool and swab samples was distinct, but less different to each other than mucosal tissue samples. Functional profile differences between stool and swab samples are smaller, but mucosal tissue samples remained distinct from the other two types. When the taxonomic and functional profiles were used for inference in association with host phenotypes of age, sex, body mass index (BMI), antibiotics or non-steroidal anti-inflammatory drugs (NSAIDs) use, hypothesis testing using either stool or rectal swab gave broadly significantly correlated results, but inference performed on mucosal tissue samples gave results that were generally less consistent with either stool or swab. Our study represents an important resource for determination of how inference can change for taxa and pathways depending on the choice of where to sample within the human gut.

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Inhibition of carbon fixation as a function of zinc uptake in natural phytoplankton assemblages

Journal of the Marine Biological Association of the United Kingdom ◽

10.1017/s0025315400036936 ◽

1979 ◽

Vol 59 (4) ◽

pp. 937-949 ◽

Cited By ~ 13

Author(s):

Anthony G. Davies ◽

Jillian A. Sleep

Keyword(s):

Carbon Fixation ◽

Natural Populations ◽

Plant Cells ◽

Toxic Metal ◽

Vitamin B ◽

Phytoplankton Assemblages ◽

Metal Contents ◽

Rate Limiting ◽

Natural Phytoplankton

There is now a substantial body of evidence that the growth rates of phytoplankton in culture are more closely related to the cellular levels of the rate-limiting constituent, be it a nutrient, micronutrient or toxic metal, than to the concentrations in the supporting medium; nitrate, Caperon (1968); phosphate, Fuhs (1969); silicate, Paasche (1973); vitamin B12, Droop (1968); iron, Davies (1970); mercury, Davies (1974); cadmium, Davies (1978a). This has suggested the requirement for a technique which would allow the determination of comparable relationships for natural populations of phytoplankton - how, for instance, their carbon fixation rates depend upon the metal contents of the plant cells. Although the effects of metals upon carbon fixation in phytoplankton assemblages from several different sea areas have already been examined (Knauer & Martin, 1972; Patin et al. 1974; Zingmark & Miller, 1975; Ibragim & Patin, 1976) no data seem to have been obtained on the levels of the metals present in the phytoplankton at the time of the measurements.

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Thiamine (Vitamin B1)

Journal of Evidence-Based Complementary & Alternative Medicine ◽

10.1177/1533210110392941 ◽

2011 ◽

Vol 16 (1) ◽

pp. 12-20 ◽

Cited By ~ 28

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.

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