Effects of vitamin C and vitamin E on lipid peroxidation, blood serum metabolites, and mineral concentrations of laying hens reared at high ambient temperature

This study was conducted to determine the effects of vitamin C (L-ascorbic acid) and vitamin E (alpha-tocopherol acetate) on serum concentrations of lipid peroxidation (MDA) and triiodothyronine (T3), thyroxine (T4), adrenocorticotropic hormone (ACTH), and some metabolite and mineral in laying hens reared at high ambient temperatures ranging from 25 degrees C to 35 degrees C. One hundred twenty laying hens (18 wk old; Hy-Line) were divided into 4 groups, 30 hens per group. The laying hens were fed either a basal diet (control) or the basal diet supplemented with either 250 mg of L-ascorbic acid/kg of diet (vitamin C), 250 mg of alpha-tocopherol acetate/kg of diet (vitamin E), or 250 mg of L-ascorbic acid plus 250 mg alpha-tocopherol acetate/kg of diet (combination). Separately or as a combination vitamins C and E increased serum vitamin C and vitamin E concentrations (p < 0.001) but decreased serum MDA concentration (p < 0.05). Serum concentrations of vitamin E and vitamin C were found highest but serum MDA concentration was lowest in the combination group. Supplemental vitamins C and E either separately or in a combination increased serum T3 and T4 concentrations (p < 0.05), whereas decreased serum ACTH concentration (p < 0.01). Serum glucose and cholesterol concentrations decreased, whereas serum protein concentration increased (p < 0.05) when vitamins C and E singly or together were added to the diet. Vitamin C and vitamin E supplementation resulted in an increase in serum concentrations of Ca, P, and K (p < 0.01) but a decrease in serum concentration of Na (p < 0.05). The results of the present study suggest that supplemental vitamin C and vitamin E alter serum lipid peroxidation, vitamin C, vitamin E and metabolite status, and diets supplemented with a combination of these two vitamins offer a good management practice in laying hens reared at high temperatures. In addition, the results suggest that dietary vitamin C and vitamin E act synergistically.     

Leaf aging and lipid peroxidation: The role of the antioxidants vitamin C and E

To study age-related peroxidation in annual beech ( Fagus silvatica Mill.) leaves and perennial fir ( Abies alba Mill.) needles, the concentration changes of the antioxidants vitamin C (ascorbic acid) and vitamin E (α-tocopherol) present in leaves and needles were determined, and the formation of thiobarbituric acid reactants was measured as an index of age-related lipid peroxidation. With age, the content of the lipid-soluble antioxidant vitamin E increased, and the increase was higher in beech leaves than in fir needles. A comparable age-dependent increase of the vitamin C content was found neither in leaves nor in needles. The concentration ratio of the vitamin C to the vitamin E present in leaves and needles, which determines the potency of the anti oxidative system consisting of both vitamins, declined with age. This decline was directly related to a higher peroxidation of lipids. The extent of age-related peroxidative damage of cells seems to be controlled by the potency of anti oxidative systems.     

Effects of dietary chromium and ascorbic acid supplementation on digestion of nutrients,serum antioxidant status,and mineral concentrations in laying hens reared at a low ambient temperature

This experiment was conducted to evaluate the effects of chromium (chromium picolinate, CrPic) and vitamin C (l-ascorbic acid) supplementation on the digestion of nutrients and serum concentration of some antioxidant vitamins and minerals of laying hens (Hy-Line) reared at a low ambient temperature (6.8°C). One hundred twenty laying hens (32 wk old) were divided into 4 groups, 30 hens per group. The laying hens were fed either a basal diet or the basal diet supplemented with either 400 μg of Cr/kg diet, 250 mg of l-ascorbic acid/kg diet, or 400 μg of Cr plus 250 mg l-ascorbic acid/kg diet. The digestibility of nutrients (DM, OM, CP, and EE) increased by the supplementation of chromium and vitamin C (p<0.05). Supplemental chromium and vitamin C also increased serum vitamin C and E but decreased malondialdehyde concentrations (p<0.05). Additionally, supplemental chromium and vitamin C caused an increase in the serum concentrations of Fe, Zn, Mn, and Cr (p<0.05) but a decrease in Cu concentration. The results of the present study showed that each dietary supplement influenced most of the parameters measured in a similar way. Also, a combination of the two supplements resulted in an additive effect, and supplementing a combination of vitamin C (250 mg/kg of diet) and chromium (400 μg Cr/kg diet) may offer a potential protective management practice in preventing cold-stress-related depression in the performance of laying hens.     

Early effects of feeding excess vitamin A: mechanism of fatty liver production in rats

Oral administration of vitamin A (30,000 IU daily for 2 days) to young rats caused a marked increase in hepatic glycogen, cholesterol, and glycerides, while hepatic phospholipid content remained almost unaltered. In an examination of the pathogenesis of the lipid accumulation, it was found that more glucose-(14)C was incorporated into liver lipids in vitamin A-fed rats, whereas incorporation of glucose-(14)C and dl-glycine-(14)C into liver protein remained unaltered. The increase in glucose-(14)C incorporation was confined to the glyceride-glycerol portion of the lipids; incorporation into liver fatty acids was inhibited. Plasma free fatty acid concentrations were elevated. It is postulated that in the vitamin A-fed rats, increased accumulation of lipids in the liver is caused by a stimulation of fatty acid mobilization from adipose tissue and enhanced formation of glycerophosphate through glycolysis, with consequent increase in the glyceride synthesis in the liver. The weight of the adrenals was increased, whereas cholesterol concentration in the gland was decreased, after administration of vitamin A to rats. This indicates adrenocortical stimulation. Interestingly enough, vitamin A feeding did not affect either the level of liver lipids or of plasma FFA in adrenalectomized rats.     

In vitro differentiation of human monocytes to macrophages results in depletion of antioxidants and increase in n-3 fatty acids levels

The lipid composition and alpha-tocopherol content of human monocytes were investigated before and after their differentiation to macrophages. The total lipid and protein content per number of cells increased after the differentiation of monocytes by approximately four-fold; a two-fold increase in docosahexaenoic and docosapentaenoic acids and a two-fold decrease in linoleic acid were also noted. As opposed to an initial monocytic vitamin E content of 4.75 pmol/10(6) cells, macrophagic vitamin E levels were undetectable. Changes in vitamin E and fatty acids contents in macrophages, with respect to monocytes, appear to reflect the lipid composition of fetal calf serum, that is low in vitamin E and has a proportionally higher docosahexaenoic acid content than adult human serum.     

Effect of tannic acid on liver levels of vitamin A in rats maintained on balanced diets or deprived of this vitamin]

A 6 month study in rats fed a balanced diet containing 3,2 p. 100 tannic acid resulted in a marked decrease of the hepatic concentration of vitamin A. In an other study, rats were fed vitamin A deficient diets containing 0, 0,8, 1,6 and 3,2 p. 100 tannic acid. There was no effect of tannic acid on the hepatic concentrations of vitamin A determined on days 20, 40 and 60.     

Effect of oat by-product antioxidants and vitamin E on the oxidative stability of pork from pigs fed diets supplemented with linseed oil

The aim of the experiment was to compare the antioxidative potential of an oat by-product with the effect of vitamin E on the oxidative stability of pork from pigs fed a diet enriched with linseed oil. Thirty-four crossbreed barrows were fed individually from 39 to 109 kg body weight (BW) on one of four diets: a control diet based on barley-triticale-soybean (Diet C), a diet containing an oat byproduct (Diet O), and the same diets supplemented with vitamin E (100 mg/kg diet) (Diets CE and OE, respectively). The oat by-product, comprising oat hulls and bran, was included at 10 and 20% in the grower and finisher diets, respectively. To Diets O and OE, refined rapeseed oil was added to equalise their energy content to Diets C and CE. Compared to Diets C and CE, the inclusion of the oat by-product in Diets O and OE increased the antioxidative capacity of water-soluble and lipid soluble compounds in these diets. Dietary treatment did not influence growth performance, slaughter value, longissimus dorsi (LD) muscle quality measured by nutrient contents, pH, drip loss or colour. Vitamin E supplementation increased the alpha-tocopherol concentration in serum and meat (p < 0.01), and decreased the formation of thiobarbituric acid reactive substances (TBARS) in the fresh and stored LD (p < 0.01). In addition, diets with the oat by-product increased serum alpha-tocopherol concentration (p < 0.01) and decreased the TBARS levels in the fresh and stored LD (p < 0.05), without increasing muscle alpha-tocopherol concentration. The obtained results indicate that the phenolic compounds present in oat by-products have a considerable antioxidant potential and a beneficial effect on the pig organism and oxidative stability of meat. However, dietary inclusion with the oat by-product was not as efficient as supplementation with vitamin E.     

Effect of vitamin C administration on serum and egg-yolk cholesterol level of the chicken

Ascorbic acid (vitamin C) was given to 144-days-old layer chickens mixed with their ration at three concentrations: 30, 60 and 90 p.p.m. for 6 months. Cholesterol levels in blood serum (CS) and egg yolk (CE) were measured every 6 weeks (four periods); there was a marked decrease in CS in most treated birds, especially those receiving the highest concentration of vitamin C. There was also a slight decrease in CE in most treated birds. Thyroidal weight showed a significant increase in most treated groups, especially those receiving the highest concentration of vitamin C.     

Effect of exercise training on tissue vitamin E and ubiquinone content

Endurance exercise training led to an adaptive increase in the ubiquinone content and cytochrome c reductase activity of red quadriceps and soleus muscles and adipose tissues, but not of cardiac or white quadriceps muscle. These findings are consistent with the well-known positive adaptation of skeletal muscle mitochondria to endurance training. However, there was no concomitant increase in the vitamin E content of tissues, which showed an increase in mitochondrial content. Since ubiquinone is located in the mitochondrial inner membrane and the major pool of vitamin E is also associated with mitochondrial membranes, the results suggest that training causes a substantial decrease in vitamin E concentration in the proliferating muscle mitochondrial membranes, thus depleting muscle mitochondria of their major lipid antioxidant. Since vitamin E is the major cellular, lipid-soluble, chain-breaking antioxidant, these findings indicate increased free radical reactions in the tissues of exercising animals.     

The effects of vitamin A deficiency on hepatic folate metabolism in rats

The effects of severe vitamin A deficiency (liver retinol less than 2 micrograms/g) on hepatic folate metabolism in rats were studied. The oxidation of a [ring-2-14C] histidine load or a [14C]formate load to 14CO2 was significantly depressed in vitamin A-deficient rats and those given histidine also excreted more urinary formiminoglutamic acid (FiGlu) than pair-fed controls. The increase in FiGlu excretion was not due to augmented production from histidine, implicating an impairment of FiGlu catabolism. FiGlu formiminotransferase activity was unaltered in vitamin A-deficient rats, but hepatic tetrahydrofolic acid (THF) concentration was decreased by 58% in vitamin A-deficient rats given a histidine load while 5-methyl-THF concentration was increased by 39%. Formyl-THF and total folate levels were similar to controls. A redistribution of folate coenzymes was not found in vitamin A-deficient rats not force fed histidine. A 43% decrease in 10-formyl-THF dehydrogenase activity, which generates both THF and the 14CO2 from the labeled substrates, and an 81% increase in 5,10-methylene-THF reductase activity, which generates 5-methyl-THF, were found in vitamin A-deficient rats. It appears that the production of severe vitamin A deficiency results in selective changes in the activities of hepatic folate-dependent enzymes, so that when a load of a one-carbon donor is given, THF concentration decreases and metabolism of the load is impaired.     

增大罐压提高脱氮假单胞菌发酵生产维生素B12的产量

【目的】提高发酵罐的罐压,增加维生素B12的产率。【方法】利用常规代谢通量分析(MFA)方法,对脱氮假单胞菌生产维生素B12的发酵过程进行研究。【结果】发现随着VB12合成速率的加快,磷酸烯醇式丙酮酸(PEP)羧化生成草酰乙酸(OAA)的通量明显加大,以满足维生素B12合成对前体的需求。根据该分析结果,对发酵工艺进行了改进,即在脱氮假单胞菌进入合成维生素B12阶段时,提高发酵罐的罐压,增加发酵液中二氧化碳的溶解度,从而强化了羧化回补途径。维生素B12的产率明显增加,发酵160 h的产物浓度为176 mg/L,比对照批次终浓度147 mg/L高出了19.7%。【结论】通过增大罐压提高了脱氮假单胞菌进入合成维生素B12的产量。     

Metabolism of vitamin A in the heart increases after a myocardial infarction

The supply of vitamin A to the myocardium by storage organs during increased oxidative stress subsequent to myocardial infarction (MI) was examined in hemodynamically assessed rats using compartment analysis of a radio-labeled vitamin A. 3H-Vitamin A was injected into two groups of rats: an MI group and a control group. There were no differences in the plasma or myocardial content of total vitamin A (unlabeled + labeled) between the two groups. However, the proportion of 3H-vitamin A was greater in the myocardium as well as plasma of MI rats. Rats with MI also had significantly lower 3H-vitamin A levels in liver and kidney than sham controls. The greatest difference in vitamin A content was in the concentrations of 3H-labeled storage forms of vitamin A in the liver of MI animals. Activity of bile salt-dependent retinyl ester hydrolase, an enzyme responsible for hydrolyzing vitamin A storage forms, was significantly increased in the liver of MI animals. These data indicate that analysis of plasma concentrations of vitamin A to ascertain links to cardiac conditions may be inappropriate. Specifically, during MI, increased amounts of vitamin A are mobilized from the liver to the heart without changing plasma concentrations. This is facilitated by an increase in the activity of an enzyme that hydrolyzes vitamin A storage forms.     

Dietary fatty acid composition rather than vitamin E supplementation influence ex vivo cytokine and eicosanoid response of porcine alveolar macrophages

This study examined the influence of different dietary fat sources (animal fat, sunflower oil, and fish oil) and supplementation of vitamin E (85, 150 and 300 mg all-rac-alpha-tocopheryl acetate/kg diet) on the ex vivo synthesis of eicosanoids and cytokines by porcine alveolar macrophages. Supplementation of vitamin E provoked an increase in the concentration of alpha-tocopherol of the macrophages irrespective of fat sources. Fish oil increased the macrophage n-3 content with 100% and 40%, and reduced the n-6 with 60% and 53% in comparison with sunflower oil and animal fat, respectively. Fish oil decreased the production of TNF-alpha, IL-8, LTB4, and PGE2 (but not IL-6) relative to the other dietary fat sources, and no difference was observed between sunflower oil and animal fat. Positive correlations were found between the n-6 fatty acid content and the production of PGE2, and the PGE2 production was positively correlated with TNF-alpha and IL-8. Negative correlations were found between the n-3 PUFA content and the concentration of PGE2, TNF-alpha and IL-8. In conclusion, dietary fish oil supplemented at a level of 5%, but not supplemental vitamin E, influenced the inflammatory responses of alveolar macrophages isolated from weaned pigs relatively to animal fat and sunflower oil.     

Alteration of α-Tocopherol Content in the Developing and Aging Peripheral Nervous System: Persistence of High Correlations with Total and Specific (n-6) Polyunsaturated Fatty Acids

In contrast to brain, the sciatic nerve concentration of vitamin E in rats increased rapidly during the postnatal period (approximately fivefold between days 1 and 8), then decreased dramatically (about twofold between days 8 and 30), and further decreased slowly between days 30 and 60 and remained constant up to 2 years. Although the sciatic nerve concentration of vitamin E decreased by 58% between days 8 and 30, the concentration of vitamin E in serum presented a marked decrease (approximately 75%). The vitamin E concentrations varied in a similar pattern in whole sciatic nerve and in endoneurium and showed a very close correlation (r = 0.94). The age-related changes in fatty acid concentration of the endoneurial fraction of the sciatic nerve were characterized by a large increase in content of saturated and monounsaturated fatty acids up to 6 months (twofold for saturated and fourfold for monounsaturated fatty acids). Then, up to 24 months, the amount of these fatty acids decreased very slowly. The content of (n-6) polyunsaturated fatty acids (PUFAs) decreased rapidly up to 1 year and slowly afterward. In contrast, during development the amount of (n-3) PUFA was relatively stable and decreased during aging. A highly significant correlation between vitamin E and (n-6) PUFA [18:2(n-6), 20:4(n-6), and total (n-6)] was observed but not between (n-3) PUFA and vitamin E. It is suggested that there may be a relationship between vitamin E and (n-6) PUFA in the PNS membranes during development and aging.     

Effects of Spray Application of Lanthanum and Cerium on Yield and Quality of Chinese Cabbage (Brassica chinensis L) Based on Different Seasons

The use of single light rare earth elements in agriculture was studied using the application of single rare earth elements (La and Ce) to Chinese cabbage (Brassica chinensis L.) in field plot experiments where the soil conditions remained the same but the season (spring or autumn) in which application occurred was altered. The results showed that the Chinese cabbage’s nutrition quality between the two seasons had obvious differences. When planted in the autumn, the soluble sugar and vitamin C content was higher, the titratable acid and nitrate content was lower, and the ratio of sugar to acid was higher, while when planted in spring, the situation was opposite. La or Ce treatments in spring and autumn promoted the growth of the Chinese cabbage, the fresh and dry weight of the stems and leaves increased, the ratio of dry to fresh weight increased, and the observed effects were greater in the Ce treatments than the La treatments. Moreover, the soluble sugar content increased and the titratable acid content decreased, which meant that the ratio of sugar to acid increased. There was an increase in the vitamin C and nitrate content in the spring Chinese cabbage, while there was a decrease in the vitamin C and nitrate content in the autumn. The levels of the heavy metals Cu, Zn, Cd, Pb, and Ni decreased. The La treatment had greater effects on the spring Chinese cabbage, while the Ce affected the autumn Chinese cabbage more.     

Protective role of vitamin E on mefenamic acid-induced alterations in erythrocytes

Erythrocyte osmotic fragility (O.F.), acetylcholinesterase (AChE) activity,and the level of malonyl dialdehyde (MDA) of control, mefenamic acid treated, and mefenamic acid with vitamin E treated rats were investigated. Administration of mefenamic acid to albino rats brought about a significant increase in the osmotic fragility of red cells and a significant (p<0.01) decrease in the activity of AChE. We have also observed increased red cell level of MDA and decreased cholesterol (Chl), hemoglobin (Hb), and reduced glutathione (GSH) content. Supplementation of vitamin E to the mefenamic acid treated rats restored the O.F., AChE activity, level of MDA, and Chl, Hb, and GSH content almost to normal. These observations suggest that mefenamic acid causes functional impairment of red cell membrane, while vitamin E shows its protective role in maintaining normal red cell functions.     

In vivo studies of altered expression patterns of p53 and proliferative control genes in chronic vitamin A deficiency and hypervitaminosis.

Several clinical trials have revealed that individuals who were given beta-carotene and vitamin A did not have a reduced risk of cancer compared to those given placebo; rather, vitamin A could actually have caused an adverse effect in the lungs of smokers [Omenn, G.S., Goodman, G.E., Thornquist, M.D., Balmes, J., Cullen, M.R., Glass, A., Keogh, J.P., Meyskens, F.L., Valanis, B., Williams, J.H., Barnhart, S. & Hammar, S. N. Engl. J. Med (1996) 334, 1150-1155; Hennekens, C.H., Buring, J.E., Manson, J.E., Stampfer, M., Rosner, B., Cook, N.R., Belanger, C., LaMotte, F., Gaziano, J.M., Ridker, P.M., Willet, W. & Peto, R. (1996) N. Engl. J. Med. 334, 1145-1149]. Using differential display techniques, an initial survey using rats showed that liver RNA expression of c-H-Ras was decreased and p53 increased in rats with chronic vitamin A deficiency. These findings prompted us to evaluate the expression of c-Jun, p53 and p21WAF1/CIF1 (by RT-PCR) in liver and lung of rats. This study showed that c-Jun levels were lower and that p53 and p21WAF1/CIF1 levels were higher in chronic vitamin A deficiency. Vitamin A supplementation increased expression of c-Jun, while decreasing the expression of p53 and p21WAF1/CIF1. Western-blot analysis demonstrated that c-Jun and p53 showed a similar pattern to that found in the RT-PCR analyses. Binding of retinoic acid receptors (RAR) to the c-Jun promoter was decreased in chronic vitamin A deficiency when compared to control hepatocytes, but contrasting results were found with acute vitamin A supplementated cells. DNA fragmentation and cytochrome c release from mitochondria were analyzed and no changes were found. In lung, an increase in the expression of c-Jun produced a significant increase in cyclin D1 expression. These results may explain, at least in part, the conflicting results found in patients supplemented with vitamin A and illustrate that the changes are not restricted to lung. Furthermore, these results suggest that pharmacological vitamin A supplementation may increase the risk of adverse effects including the risk of oncogenesis.     

Dose of 3-methylcholanthrene enhances vitamin C accumulation and mRNA expression of its transporter in the liver of ODS rats and in HepG2 cells

Polycyclic aromatic hydrocarbon (PAH) compounds including 3-methylcholanthrene induce harmful reactive intermediates and reactive oxygen species. This study reports the effect of 3-methylcholanthrene on the accumulation of vitamin C and the expression of vitamin C transporters. ODS rats were given l-ascorbic acid daily and intraperitoneal injections of 10 mg 3-methylcholanthrene in total. On day 10, vitamin C concentrations and the expression of vitamin C transporter in the tissues were measured. As a result, the levels of sodium-dependent vitamin C transporter (SVCTs) 1 and the l-ascorbic acid concentration in 3-methylcholanthrene-treated livers and hepatocytes have increased significantly. However, the content of vitamin C in the urine and TBARS in the liver have not changed. These results suggest that the administration of 3-methylcholanthrene elevates the requirement for vitamin C via (SVCTs) 1 due to xenobitics-metabolizing, such as the induction of cytochrome P450 family.     

Tempe fermentation: some aspects of formation of gamma-linolenic acid, proteases and vitamins

During a tempe fermentation the concentrations of linoleic, and alpha-linolenic acids (ALA) decreased while the concentration of oleic acid increased. During fatty acid synthesis Rhizopus sp. produced only gamma-linolenic acid (GLA) instead of ALA. The amount of GLA in tempe were influenced by varying external parameters.The proteolytic capacity of 36 strains of the genus Rhizopus isolated from Indonesian tempe or tempe inocula was examined. There was a distinct increase in the amount of free amino acids during tempe fermentation. Fermentations with mixed populations of bacteria and Rhizopus yielded a lower level of free amino acids, but an increase in total amount of amino acids. In comparison to intracellular, and extracellular proteases the proteases of the cell wall fraction are most responsible for proteolytic capacity of the different Rhizopus strains.Two isolated strains of Citrobacter freundii were found to be the best vitamin B(12) producers during the soaking of soybeans. In the solid substrate fermentation the Rhizopus molds formed vitamin B(6), riboflavin, and nicotinic acid. The addition of bacteria to the solid substrate fermentation resulted in a strong increase of active vitamin B(12) in tempe. In the presence of the Rhizopus mold, the vitamin B(12) formation by C. freundii was three times higher than that of a fermentation without the mold.     

Regulation of coenzyme A biosynthesis.

Coenzyme A (CoA) and acyl carrier protein are two cofactors in fatty acid metabolism, and both possess a 4'-phosphopantetheine moiety that is metabolically derived from the vitamin pantothenate. We studied the regulation of the metabolic pathway that gives rise to these two cofactors in an Escherichia coli beta-alanine auxotroph, strain SJ16. Identification and quantitation of the intracellular and extracellular beta-alanine-derived metabolites from cells grown on increasing beta-alanine concentrations were performed. The intracellular content of acyl carrier protein was relatively insensitive to beta-alanine input, whereas the CoA content increased as a function of external beta-alanine concentration, reaching a maximum at 8 microM beta-alanine. Further increase in the beta-alanine concentration led to the excretion of pantothenate into the medium. Comparing the amount of pantothenate found outside the cell to the level of intracellular metabolites demonstrates that E. coli is capable of producing 15-fold more pantoic acid than is required to maintain the intracellular CoA content. Therefore, the supply of pantoic acid is not a limiting factor in CoA biosynthesis. Wild-type cells also excreted pantothenate into the medium, showing that the beta-alanine supply is also not rate limiting in CoA biogenesis. Taken together, the results point to pantothenate kinase as the primary enzymatic step that regulates the CoA content of E. coli.