The regulatory effects of pyridoxine deficiency on the grass carp (Ctenopharyngodon idella) gill barriers immunity, apoptosis, antioxidant, and tight junction challenged with Flavobacterium columnar.

The effects of dietary pyridoxine (PN) on the gill immunity, apoptosis, antioxidant and tight junction of grass cap (Ctenopharyngodon idella) were investigated in this study. Fish were fed semi-purified diets containing graded levels of PN for 10 weeks, and then challenged with Flavobacterium columnare by bath immersion exposure for 3 days. The results indicated that compared with the optimal PN level, PN deficiency resulted in a decline in the antimicrobial compound production of gill. In addition, PN deficiency up-regulated the pro-inflammatory cytokines and down-regulated the anti-inflammatory cytokines gene expression, which might be associated with the enhanced nuclear factor κB p65 and the inhibited target of rapamycin signalling pathways, respectively, suggesting that PN deficiency could impair gill immune barrier function. Furthermore, PN deficiency (1) induced cell apoptosis, which may be partly associated with the (apoptotic protease activating factor-1, Bcl-2 associated X protein)/caspase-9 and c-Rel/tumor necrosis factor α (rather than FasL)/caspase-8 mediated apoptosis pathway. (2) Inhibited Kelch-like ECH-associating protein 1a/NF-E2-related factor 2 mRNA expression, decreased the mRNA expression and activities of antioxidant enzymes, increased the levels of reactive oxygen species, protein carbonyl and malondialdehyde. (3) Increased the mRNA expression level of myosin light chain kinase, which may be result in the down-regulation of tight junction complexes such as zonula occludens 1, occludin and claudins (expect claudin-12 and claudin-15). These results suggest that PN deficiency could impair gill physical barrier function. In summary, dietary PN deficiency could cause the impairment of gill barrier function associated with immunity, apoptosis, antioxidant and tight junction, which may result in the increased the susceptibility of fish to pathogenic bacteria. Moreover, based on the gill rot morbidity, LZ activity and MDA content, the dietary PN requirements for grass cap were estimated to be 4.85, 4.78 and 4.77 mg kg-1 diet, respectively.

Activities of glycogen phosphorylase, alanine aminotransferase and aspartate aminotransferase in adult worms of Litomosoides carinii recovered from pyridoxine deficient cotton rats (Sigmodon hispidus).

This paper demonstrates that the activities of glycogen phosphorylase (GP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are reduced in adult worms of the filarial nematode Litomosoides carinii recovered from pyridoxine-deficient cotton rats when compared to worms recovered from pyridoxine-sufficient controls. GP, ALT and AST activities were determined in adult worms L. carinii recovered from cotton rat hosts over a 20-week experimental period. Activities of GP, ALT and AST in the parasite showed a direct correlation with the dietary pyridoxine intake of their host. Throughout the experiment, enzyme activities were significantly lower (P < 0.001) in worms from rats fed a pyridoxine-free diet ad libitum that in worms from rats fed either a stock colony diet, a pyridoxine-free diet ad libitum with daily supplementation of 100 micrograms pyridoxine or limited amounts of pyridoxine-free diet with daily supplementation of 100 micrograms pyridoxine. The lower than normal activity of GP, ALT, AST and other enzymes dependent on the biologically active derivative of pyridoxine, the coenzyme pyridoxal-5-phosphate (PLP), interferes with the protein, carbohydrate and lipid metabolism of L. carinii and may in part cause the reduced establishment, development and growth of the parasite in pyridoxine-deficient hosts.

Vitamin B6 deficiency experimentally-induced bone and joint disorder: microscopic, radiographic and biochemical evidence.

In the present study the effect of pyridoxine deficiency on the ultrastructure and morphology of bone and its metabolism was examined in the rapidly growing chick. Pyridoxine-deficient animals had tibias of reduced dry weight and cortical thickness. Histomorphometry demonstrated a disproportionately high eroded surface, lower amount of osteoid tissue and reduced mineralized trabecular width. Anterior-posterior radiographs of the tibiotarsometatarsal joint showed reduced secondary ossification centres and coarse trabeculation. Decalcified metaphyseal cartilage showed irregular trabeculas and a markedly reduced amount of Fast-green counterstain matrix suggesting that there is less collagen present and in turn less availability for matrix to be laid down for later calcification. Plasma activity of the bone alkaline phosphatase isoenzyme (EC 3.1.3.1) was decreased. Plasma Ca and PO4 levels did not vary. The present bone study referring to a pseudo-lathyritic state in which collagen maturation is not completely achieved supports the hypothesis that pyridoxine is an essential nutrient for the connective tissue matrix.

Effects of dietary proteins and yeast Saccharomyces cerevisiae on vitamin B6 status during growth.

Male rapidly growing broiler chicks were fed a moderate (22%) or a high protein (30%) well-balanced diet containing yeast Saccharomyces cerevisiae (2%) and consisting of soy protein isolate (Soyamin) or a purified amino acid mixture. The vitamin B6 status was assessed according to the in vitro stimulated activity of aspartic aminotransferase (activation coefficient; AC) and pyridoxal phosphate concentrations in plasma and erythrocytes. No weight difference was found between age-matched control and B6-deficient animals fed the Soyamin diet containing yeast. None of the deficient animals presented signs of malfunctions of the central nervous system. These animals grew well and their skeletal development was normal after 6 weeks of age. Due to the presence of yeast, increasing dietary protein intake did not augment the metabolic requirement for pyridoxine. The removal of yeast from the Soyamin diet provoked a severe symptomatic deficiency (AC 1.5). It seemed that yeast did more than promoting growth. It also protected against a lack of vitamin B6: feed utilization was not impaired. The present study showed that a low level of 0.6 mg vitamin B6/kg in a corn-Soyamin diet containing yeast was adequate to maintain normal growth and to avoid neurological symptoms. The pyridoxine requirement for normal growth and absence of convulsions has been reported to be approximately 3 mg/kg diet.

Embryogenesis in Litomosoides carinii from pyridoxine deficient cotton rats.

Pyridoxine (vitamin B6) deficiency was induced in cotton rats which were then infected with the filarial parasite Litomosoides carinii. Embryogenesis was assessed microscopically in worms taken from pyridoxine deficient cotton rats and from various categories of control animals. Embryogenesis was retarded in worms from pyridoxine deficient hosts and more abnormal embryos were present in such worms than in those from control animals.

Vitamin B-6 requirement of growing kittens.

Two experiments were conducted to determine the vitamin B-6 requirement for growing kittens. Ten kittens were divided into two groups and given a purified diet containing 8.0 mg pyridoxine (PN)/kg diet (+PN) or a PN-free diet (-PN) for 11 wk. Daily body weight gain, food intake, weekly plasma free amino acids, plasma B-6 vitamers, urinary oxalate excretion, hemoglobin (Hb) and hematocrit were measured. Kittens fed a -PN diet had depressed body weight gain, food intake, plasma pyridoxal phosphate (PLP) and pyridoxal (PL), Hb and hematocrit, and had elevated urinary oxalate, plasma tyrosine and plasma cystathionine. In a second experiment, 24 kittens were given a -PN diet for 45 d to deplete their body reserves. The kittens were then divided into six groups of four kittens each and given a purified diet containing either 0.5, 1.0, 2.0, 3.0, 4.0 or 8.0 mg PN/kg diet for 46 d. Following supplementation, positive responses in body weight gain, PLP, Hb and hematocrit, and decreased urinary oxalate excretion, plasma tyrosine and plasma cystathionine occurred in all groups except those fed 0.5 mg PN/kg diet. At the end of the repletion period, kittens fed 1.0 mg PN/kg diet had lower body weight gain, higher plasma tyrosine and cystathionine, slower rate of decrease in urinary oxalate, and lower values for Hb, hematocrit and PLP than did the kittens from groups fed 2.0-8.0 mg PN/kg diet. These findings indicate that the dietary requirement for PN is greater than 1.0 mg/kg diet, but 2.0 mg PN/kg diet is adequate for growing kittens given a 35% casein diet.

Nutritional deficiency anemias in nonhuman primates.

The purpose of this report is to review past studies in which anemias, occurred spontaneously in nonhuman primates due to feeding inadequate diets or were induced by feeding diets deficient in a nutrient. Included is a review of anemias induced by deficiencies of iron, niacin, pyridoxine, pantothenic acid, protein, riboflavin, cyanocobalamin, folic acid, ascorbic acid and alpha-tocopherol. The anemia induced by deficiency of each nutrient is discussed with emphasis on the major clinical signs as well as peripheral blood and bone marrow pathology. Results of supplementation of the diet following induction of deficiency states are discussed also. Whenever applicable, a discussion is included of the use of nonhuman primates as animal models for studies simulating parallel nutritional deficiencies in man.

Evaluation of the erythrocyte aspartate aminotransferase activity coefficient as an indicator of the vitamin B-6 status of postpubertal gilts.

In two experiments, postpubertal gilts, individually housed in gestation stalls, were fed daily 1.9 kg of a purified diet providing 0.45, 1.5, 2.1 or 83 mg of vitamin B-6/d. The erythrocyte aspartate aminotransferase (more commonly known as glutamic-oxaloacetic transaminase) activity coefficient (EGOT-Ac) of gilts fed the low vitamin B-6 diet (0.45 mg vitamin B-6/d) for 121 d increased 200%, while the EGOT-Ac of gilts fed the high vitamin B-6 diet (83 mg vitamin B-6/d) remained unchanged. Two gilts were fed the low vitamin B-6 diet for 241 d at which time hair loss was observed. Muscle glutamic-oxaloacetic transaminase activity was reduced 75% in vitamin B-6-deficient gilts. The EGOT-Ac of gilts consuming 2.1 mg vitamin B-6/d was 100% greater than that of control animals (83 mg vitamin B-6/d). These findings indicate that the current NRC estimated vitamin B-6 requirement for mature swine (1.8 mg vitamin B-6/d) is inadequate. Prior intake of excess vitamin B-6 did not prevent the subsequent development of a vitamin B-6 deficiency.

Effect of deficient and excess dietary vitamin B-6 on amino transaminase and glycogen phosphorylase activity and pyridoxal phosphate content in two muscles from postpubertal gilts.

Postpubertal gilts averaging 111 kg and gaining 2.7 kg/wk were fed daily 1.9 kg/d of a diet providing 0.45, 2.1 or 83 mg of vitamin B-6/d. An additional group of animals were fed the high vitamin B-6 diet providing 83 mg of vitamin B-6/d for the initial 57 d of the experiment and then switched to 0.45 mg of vitamin B-6/d for the remainder of the 121-d experiment (61 gilts total). On d 0, 57 and 121, animals from each treatment were killed, and samples of the semitendinosus (ST) and semimembranosus (SM) were removed. Glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT), glycogen phosphorylase and pyridoxal phosphate (PLP) were measured in muscle tissues. The erythrocyte GOT activity coefficient indicated that gilts consuming 0.45 or 2.1 mg of vitamin B-6/d developed a vitamin B-6 deficiency. A vitamin B-6 deficiency resulted in the loss of whole-muscle transaminase activity (enzyme activity X muscle weight) with little effect on whole-muscle total phosphorylase or total PLP content. Excess dietary vitamin B-6 increased whole-muscle total PLP and total phosphorylase content with small decreases in whole-muscle transaminase. Under these conditions, muscle tissue acts as a nonmobile reservoir of PLP. Sixty to 95% of muscle PLP was bound to muscle glycogen phosphorylase.

Involvement of water-soluble vitamins in diseases of swine.

The various roles of the water-soluble vitamins (including choline and vitamin C) in diseases of swine are outlined. The most important role is in the prevention of deficiency disease; another important role is in relation to the immune response. Deficiency signs relating to each vitamin are described and the metabolism of each vitamin is outlined. Recent estimates of requirements are set out, together with suggestions on supplementation of practical diets for swine.

Hematology of chicks experiencing marginal vitamin B6 deficiency.

An economical vitamin B6-deficient ration, which was palatable to broiler chickens, was prepared and fed to 1-day-old broiler chicks. The experimental ration was a glucose-soybean meal diet. Vitamin B6 was removed by washing the soybean meal with water. Microbiological analysis revealed that the washed ration contained .45 mg vitamin B6 activity/kg. Experimental rations were formulated to contain .5, 1.0, and 3.0 mg added pyridoxine HCl/kg of ration. These supplemental levels produced total pyridoxine concentrations, as assayed, of .95, 1.48, and 3.18 mg pyridoxine HCl activity/kg of diet. Chicks were grown to 7 weeks of age and characteristic B6 deficiency traits, including increased mortality, decreased body weight gain, and increased incidence of abnormal leg conformation, were quantitated or observed. An extensive hematological evaluation at 4 weeks of age indicated that this marginal B6 deficiency resulted in increased erythrocyte numbers, decreased mean corpuscular hemoglobin levels, and increased erythrocyte fragility. No changes in hematocrits, total hemoglobin level, intracellular hemoglobin concentration, or reticulocyte number were found. These results indicate that anemia did not occur in broilers experiencing a moderate vitamin B6 deficiency. The hematological condition is described as microcytic, normochromic polycythemia.

Vitamin B6 in the etiology of gizzard erosion in growing chickens.

Six experiments have been completed on day-old male cross-bred chicks for periods of up to 2 and 4 weeks to learn more about the role of pyridoxine in the etiology of gizzard erosion. At the end of each experiment, chicks were sacrificed and their gizzards removed and scored for the severity and incidence of erosion. The results of these experiments confirm the previous finding that the severity and incidence of gizzard erosion is increased by B6 deficiency. They further show that taurocholic acid, at 1% of the diet, had a protective effect against this erosion. Feeding B6-adequate rations to chicks that previously had been fed a B6-deficient diet led to partial healing of gizzard erosions. Results also indicate that the feeding of purified diets to growing chickens produces a higher incidence of erosion than that of practical-type diets. Texture of the diet did nt influence the incidence of the erosion, because grinding a practical diet to the same fineness as a purified diet did not increase gizzard erosion. Pair-feeding experiments showed that gizzard erosion in partially starved chicks was not a specific result of anorexia but of deficiencies in certain nutrients, one of which is vitamin B6.

Influence of vitamin B-6 upon reproduction and upon plasma and egg cholesterol in chickens.

Vitamin B-6 deficiency in the laying hen causes an immediate anorexia, loss of body weight, greatly reduced body fat stores and severe effects upon primary and secondary sex characteristics resulting in severely reduced hatchability culminating in complete cessation of egg production. While inanition may have been largely responsible for involution of the ovaries and oviducts in the vitamin B-6 deficient hens, regression of combs and wattles appears to be a more specific sign of vitamin B-6 deficiency. Serum cholesterol levels of vitamin B-6-deficient hens were lower than those of hens receiving an adequate diet. Egg cholesterol values remained relatively constant regardless of dietary B-6 levels or of alterations in serum cholesterol. No ataxia or mortality was observed in vitamin B-6-deficient hens or roosters. The effects of vitamin B-6 deficiency were almost completely reversed upon repletion of the hens with adequate dietary vitamin B-6.

[Influence of vitamin B 6 deficiency in early weaned piglets on the digestibility and conversion of protein and energy]. / Zum Einfluss eines Vitamin-B6-mangels frühentwöhnter Ferkel auf die Verdaulichkeit und Verwertung von Eiweiss und Energie.

Early-weaned piglets were subjected during 2 metabolic periods (11th-18th and 32nd-39th days of the experiment) to conversion experiments to study the influence of vitamin B6 depletion on the digestibility of the crude nutrients, metabolizable energy and on nitrogen conversion using the difference procedure. The depleted piglets (0.4 mg vitamin B6/kh diet) and the pair-fed control animals raised under equal conditions (6.5 mg vitamin B6/kh diet) were first fed a pre-starter ration, and from the 24th experimental day, a starter feed. As the period of depletion increased, the vitamin B6 sub-provided piglets revealed deficiency symptoms such as reduced appetite, lethargic behaviour and less movement. Whilst in the first half of the experiment the control animals reached significantly higher weight gains at lower expenditure of dry matter and digestible energy per kg of weight gain, no differences were observed between both groups in the second period. On the other hand, during the 1st metabolic period the digestibility of all crude nutrients and energy in the depleted piglets proved slightly, but significantly higher than in the pair-fed control animals. In the second half of the experiment ther were just casual differences. After a 2-week vitamin B6 deficient nutrition, the piglets had a 4.1% lower nitrogen retention as compared with the pair-fed control. After a depletion period of 5 weeks, this difference reached 14.4%. As nitrogen excretion in the urine increased, a higher renal energy excretion was observed. Thus the vitamin B6 deficient animals had available less metabolizable energy (in % of digestible energy) than the control piglets.