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

1987 ◽  
Vol 44 (1) ◽  
pp. 219-222 ◽  
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.

Biochemical, Physiological, and Pathological Changes in Pyridoxine-Deficient Rainbow Trout (Salmo gairdneri)

1974 ◽  
Vol 31 (12) ◽  
pp. 1893-1898 ◽  
Author(s):  
Charlie E. Smith ◽  
Myron Brin ◽  
John E. Halver
Keyword(s):  
Rainbow Trout ◽  
Gastrointestinal Tract ◽  
Clinical Signs ◽  
Salmo Gairdneri ◽  
Glutamic Pyruvic Transaminase ◽  
Pathological Changes ◽  
Deficient Diet ◽  
Normochromic Anemia ◽  
Kidney Liver

Rainbow trout (Salmo gairdneri) fed a pyridoxine-deficient diet developed clinical signs of the deficiency after 8 wk of feeding. Erythrocyte and muscle glutamic pyruvic transaminase (GPT) concentrations were significantly depressed in deficient fish, while liver GPT was significantly elevated. Liver GPT was also elevated in starved trout suggesting the increase in enzyme concentrations was secondary to the deficiency. A normocyte, normochromic anemia, which responded favorably to pyridoxine, developed in pyridoxine-deficient trout. Microscopic lesions were found in gastrointestinal tract, kidney, liver, pancreas, and thymus of deficient fish.

BLOOD TRANSAMINASE ACTIVITIES IN VITAMIN B6 DEFICIENCY: SPECIFICITY AND SENSITIVITY

1965 ◽  
Vol 43 (4) ◽  
pp. 579-589 ◽  
Author(s):  
M. C. Cheney ◽  
D. M. Curry ◽  
G. H. Beaton
Keyword(s):  
Vitamin B6 ◽  
B Vitamins ◽  
Xanthurenic Acid ◽  
Vitamin B ◽  
Transaminase Activity ◽  
Liver Transaminase ◽  
Dietary Protein Level ◽  
Specificity And Sensitivity ◽  
Vitamin B6 Deficiency

The lowering of blood glutamic–oxaloacetic (GOT) and glutamic–pyruvic (GPT) transaminase activities was found to be specific for vitamin B6 deprivation among several B vitamins tested and in the presence of a simultaneous restriction of eight B vitamins, cortisone administration, or variation of dietary protein level. It was found that changes in blood transaminase activity did not always parallel those seen in liver transaminase activity. In the determination of vitamin B6 nutritional status, blood GPT activity appeared to be more sensitive than GOT activity and would seem to be as sensitive an indicator as xanthurenic acid excretion after a tryptophan load.

Roth-like Spot in an Adult With Vitamin B6 Deficiency and Nonepileptic Seizures

2021 ◽  
pp. 247412642110287
Author(s):  
Diana Driscoll ◽  
David Callanan
Keyword(s):  
Differential Diagnosis ◽  
Adult Patient ◽  
Vitamin B6 ◽  
Vitamin B ◽  
Case Review ◽  
Single Patient ◽  
Retinal Lesion ◽  
History Of ◽  
Nonepileptic Seizures ◽  
Vitamin B6 Deficiency

Purpose: This work reports retinal findings in an adult patient with vitamin B6 deficiency. Methods: A case review of a single patient is presented. Results: A patient with a Roth-type retinal lesion and a history of nonepileptic seizures was found to have lymphocytic colitis. She was treated with pyridoxine, which resolved her seizures and the white-centered hemorrhage. Conclusions: Vitamin B6 deficiency should be considered in the differential diagnosis of patients presenting with white-centered hemorrhages and a history of nonepileptic seizures.

VITAMIN B6 AND MENTAL DEFICIENCY: THE EFFECTS OF LARGE DOSES OF B6 (PYRIDOXINE) IN PHENYLKETONURIA

1959 ◽  
Vol 37 (3) ◽  
pp. 485-491 ◽  
Author(s):  
Edith G. McGeer ◽  
Bluma Tischler
Keyword(s):  
Ethyl Acetate ◽  
Vitamin B6 ◽  
Clinical Signs ◽  
Mental Deficiency ◽  
Vitamin B ◽  
Phenylpyruvic Acid ◽  
Serum Phenylalanine ◽  
Chromatographic Evidence

Vitamin B6 was given to 10 phenylketonuric patients in doses up to 150 mg/day for a period of 9 weeks. Their clinical signs, behavior, intelligence, E.E.G.('s), serum phenylalanine levels, urinary phenylpyruvic acid and phenol levels, and excretions of ethyl-acetate-soluble aromatic derivatives were followed serially. No changes of significance to phenylketonuria were found, although chromatographic evidence indicated some changes in excretion of a few aromatic derivatives, notably Nα-acetyltryptophan.

scholarly journals Some effects of vitamin E and selenium deprivation on tissue enzyme levels and indices of tissue peroxidation in rainbow trout (Salmo gairdneri)

1985 ◽  
Vol 53 (1) ◽  
pp. 149-157 ◽  
Author(s):  
J. G. Bell ◽  
C. B. Cowey ◽  
J. W. Adron ◽  
Aileen M. Shanks
Keyword(s):  
Rainbow Trout ◽  
Vitamin E ◽  
Peroxidase Activity ◽  
Cumene Hydroperoxide ◽  
Dietary Vitamin ◽  
Salmo Gairdneri ◽  
Deficient Diet ◽  
Exudative Diathesis ◽  
Malondialdehyde Formation

1. Duplicate groups of rainbow trout (Salrno gairdnert) (mean weight 11 g) were given for 40 weeks one of four partially purified diets that were either adequate or low in selenium or vitamin E or both.2. Weight gains of trout given the dually deficient diet were significantly lower than those of trout given a complete diet or a diet deficient in Se. No mortalities occurred and the only pathology seen was exudative diathesis in the dually deficient trout.3. There was significant interaction between the two nutrients both with respect to packed cell volume and to malondialdehyde formation in the in vitro NADPH-dependent microsomal lipid peroxidation system.4. Tissue levels of vitamin E and Se decreased to very low levels in trout given diets lacking these nutrients. For plasma there was a significant effect of dietary vitamin E on Se concentration.5. Glutathione (GSH) peroxidase (EC 1. 1 1. 1.9) activity in liver and plasma was significantly lower in trout receiving low dietary Se but was independent of vitamin E intake. The ratios of hepatic GSH peroxidase activity measured with cumene hydroperoxide and hydrogen peroxide were the same for all treatments. This confirms the absence of a Se-independent GSH peroxidase activity in trout liver.6. Se deficiency did not lead to any compensatory increase in hepatic GSH transferase (EC 2. 5. 1. 18) activity; values were essentially the same in all treatments.7. Plasma pyruvate kinase (EC 2. 7. 1.40) activity increased significantly in the trout deficient in both nutrients. This was thought to be due to leakage of the enzyme from the muscle and may be indicative of incipient (subclinical) muscle damage.

scholarly journals Effect of selenium deficiency on hydroperoxide-stimulated release of glutathione from isolated perfused liver of rainbow trout (Salmo gairdneri)

1986 ◽  
Vol 56 (2) ◽  
pp. 421-428 ◽  
Author(s):  
J. G. Bell ◽  
J. W. Adron ◽  
C. B. Cowey
Keyword(s):  
Hydrogen Peroxide ◽  
Rainbow Trout ◽  
Weight Gain ◽  
Peroxidase Activity ◽  
Selenium Deficiency ◽  
Salmo Gairdneri ◽  
Perfused Liver ◽  
Deficient Diet ◽  
Significant Difference ◽  
Glutathione Disulphide

1. Duplicate groups of rainbow trout (Salmo gairdneri) were each given partially purified diets which were either adequate or depleted in selenium for 40 weeks.2. Although there was no significant difference in weight gain, liver Se concentration was significantly lower in fish given the deficient diet.3. Glutathione (GSH) peroxidase (EC 1. 11. 1. 9) activity was significantly reduced in liver of Se-deficient fish but a differential assay did not indicate the presence of a non-Se-dependent GSH peroxidase activity, although liver GSH S-transferase (EC 2. 5. 1. 18) was significantly increased.4. Perfusion of livers from trout given Se-adequate diets with t-butyl hydroperoxide (BuOOH) or hydrogen peroxide caused an increase in the rate of release of glutathione disulphide (GSSG) into the perfusate.5. Perfusion of livers from Se-deficient trout with BuOOH or H2O2 did not result in any change in rate of release of GSSG into the perfusate.6. These findings confirm the absence of any compensatory non-Se-dependent peroxidase activity in Se-depleted trout.

scholarly journals 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

1976 ◽  
Vol 160 (2) ◽  
pp. 287-294 ◽  
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.

Zinc Influx Across the Isolated, Perfused Head Preparation of the Rainbow Trout (Salmo gairdneri) in Hard and Soft Water

1988 ◽  
Vol 45 (12) ◽  
pp. 2206-2215 ◽  
Author(s):  
Douglas J. Spry ◽  
Chris M. Wood
Keyword(s):  
Steady State ◽  
Rainbow Trout ◽  
Hard Water ◽  
Soft Water ◽  
Chloride Cells ◽  
Salmo Gairdneri ◽  
First Order ◽  
Scanning Electron Micrography ◽  
Primary Substrate ◽  
Stimulation Of

At a waterborne [Zn] of 1.9 mg∙L−1 in hard water (~1 mmol Ca∙L−1), Zn influx across an isolated, saline-perfused head preparation of rainbow trout (Salmo gairdneri) was about 1.5 nmol∙kg−1∙h−1 through the lamellar pathway and about 1 nmol∙kg−1∙h−1 through the filamental route. Flux rates came rapidly to steady state in both pathways. Trout preexposed to artificial soft water (~0.05 mmol Ca∙L−1) for 5 d showed differential stimulation of flux rates to about 42 and 5 nmol Zn∙kg−1∙h−1 through the lamellar and filamental pathways, respectively. Under these conditions, steady-state fluxes across the lamellae did not occur until 15–20 min after the start of perfusion. Preparations from hardwater-acclimated trout tested in soft water gave typical hardwater fluxes showing that these changes in influx were not simply due to acute exposure of the gill surface to low waterborne [Ca]. Influxes in softwater trout, studied over [Zn] from 0.4 to 7.5 mg Zn∙L−1, revealed a saturable, first-order uptake with apparent Jmax and Km of 150 nequiv∙kg−1∙h−1 and 1.5 mg Zn∙L−1 (23 μmol∙L−1), respectively. Because the apparent Km is in the toxic range, Zn is clearly not the primary substrate. Scanning electron micrography revealed hypertrophy and increased apical exposure of chloride cells; this stimulation, coupled with the increase in Zn influx, suggests that chloride cells may be the site of entry of Zn across the gill.

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