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Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
The phenomenon caused by vitamin deficiency in the body is called avitaminosis, and is easily cured by vitamin supply through food or supplements. In contrast, an excess of vitamins in human body, called hypervitaminosis, is toxic for the organism and can also cause ailments. It would be interesting to emphasize the difference and the similarity between vitamin and vitamer. Essentially all vitamins exist with multiple nutritionally active chemical species, often called vitamers (34). Vitamer is a member of vitamin. The term vitamin is generally designed for natural compounds found in nature (plants, animals), while different derivatives, artificial synthetic compounds or chemical names of the vitamin are called vitamer. For example, vitamin D has several vitamers which are all fat-soluble, including vitamin D2 or ergocalciferol found in mushrooms, vitamin D3 or cholecalciferol present in the human or animal body, three other vitamers rarely occuring in nature, and four synthetic analogs. Among 13 essential vitamins, there are only three vitamins endowed with antioxidant properties: vitamins A, C, and E. Some vitamins act specifically as coenzymes. The 13 vitamins will be described as follows.
Fat-Soluble Vitamins
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
The vitamin E requirements for humans are expressed as tocopherol equivalents (TE). Table 7 lists the various forms of vitamin E vitamers with their relative biological activity (TE). 1 TE = 1 mg RRR-α-d-tocopherol. Whenever possible, units of vitamin E amounts should be expressed as mg or TE (or μmol for specific vitamers), rather than IU. There has been a good deal of confusion and ambiguity in the literature concerning what type of vitamin E was used in studies. The differences between vitamers is not trivial and may have affected numerous conclusions of numerous studies.
Clinical Studies in Humans
Published in Stephen P. Coburn, The Chemistry and Metabolism of 4′-Deoxypyridoxine, 2018
Yamada and Tsuji557,558 studied the transport of vitamin B6 in human erythrocytes. Potassium fluoride inhibited the uptake of pyridoxal, pyridoxine, pyridoxamine, and pyridoxal phosphate by 0, 20, 15, and 60% respectively. Even under control conditions, uptake of pyridoxal phosphate was much less than uptake of the free forms. The authors felt that uptake of pyridoxine and pyridoxamine was more susceptible to potassium fluoride than the uptake of pyridoxal. However, we feel that the very rapid uptake of pyridoxal and pyridoxal phosphate during the first five minutes suggests that this may represent Schiff-base binding on the cell wall rather than true uptake. Equirnolar amounts of deoxypyridoxine inhibited the uptake of pyridoxine and pyridoxamine but not of pyridoxal or pyridoxal phosphate. Deoxypyridoxine phosphate had little effect on the uptake of any vitamers.
From pathogenesis to novel therapies in primary hyperoxaluria
Published in Expert Opinion on Orphan Drugs, 2019
Gill Rumsby, Sally-Anne Hulton
Pyridoxine, in the form of pyridoxal phosphate, as well as being a prosthetic group for AGT is also a molecular chaperone promoting correct folding and dimerization of the AGT protein and therefore promoting uptake into the peroxisomes. At least three pathological variants of AGT have been shown to be responsive to pyridoxine in vitro with successful retargeting of protein from the mitochondrion to the peroxisome [5]. There is further evidence that other B6 vitamers, including pyridoxamine, may be more effective as they do not lead to an accumulation of inhibitory pyridoxine phosphate [65].
Helicobacter pylori antibiotic eradication coupled with a chemically defined diet in INS-GAS mice triggers dysbiosis and vitamin K deficiency resulting in gastric hemorrhage
Published in Gut Microbes, 2020
Lisa Quinn, Alexander Sheh, Jessie L Ellis, Donald E Smith, Sarah L Booth, Xueyan Fu, Sureshkumar Muthupalani, Zhongming Ge, Dylan A Puglisi, Timothy C Wang, Tamas A Gonda, Hilda Holcombe, James G Fox
During the course of the study evaluating the effects of increased dietary folate and antibiotics on gastric disease, unexpected morbidities, and mortalities related to extensive gastric hemorrhage occurred within days of oral administration of H. pylori antibiotic eradication therapy. As our previous studies using the AAD diet or antibiotic therapy alone did not elicit gastric hemorrhage or clinical signs of blood loss anemia, we investigated the cause of the coagulopathy and hypothesized that marginal vitamin K levels in the AAD diet in conjunction with antibiotic-induced dysbiosis resulted in morbidity and mortality. Vitamin K refers to a family of structurally related fat-soluble vitamers involved in blood coagulation. Phylloquinone (PK or vitamin K1) is produced by plants, while menaquinones (MKn where n = numberof sidechain prenyl units collectively called vitamin K2) are predominantly produced by bacteria and play a role in vitamin K homeostasis in animals.19–22 Menadione (MD or vitamin K3) is a synthetic provitamin lacking vitamin K activity that can be converted to biologically active MK4 in the liver. Along with variable levels of PK derived from plant-based components, MD is the predominant source of vitamin K in conventional rodent diets. However, in AAD diets, the substitution of grain-based products for chemically defined materials makes MD the sole dietary source of vitamin K. While antibiotics are known to disrupt microbe-regulated physiologic functions and intestinal homeostasis,23,24 we report that antibiotic-mediated dysbiosis can lead to gastric hemorrhage and blood loss anemia in mice fed defined diets with suboptimal vitamin K levels. Eradication of menaquinone-producing bacteria by antibiotics altered the enteric vitamin K reservoir leading to clinical disease, which was reversible with parenteral supplementation with PK.
Inhibition of platelet activation using vitamins
Published in Platelets, 2020
Epidemiological data and studies of supplementation showed that some vitamins have a beneficial effect on CVD and prevent thrombosis. At least partly, these effects are caused by the inhibition of platelet activation by these compounds. Vitamins are weak inhibitors of platelet aggregation; the values of IC50 varying between 0.1 mM and 1 mM. The exception is 9-cis-retinoic acid, the 50% inhibitory concentrations for platelet aggregation with this vitamin are 3–20 µM. Vitamins inhibit platelet aggregation induced by both strong and weak agonists. There is no difference in the activity of α-tocopherol measured in PRP or in the suspension of platelets. The effectiveness of some vitamins depends on the agonist used for platelet activation. Thus, the activity of riboflavin was ten times higher for AA- compared to ADP-induced aggregation. On the other hand, the activity of ascorbic acid was the same with the five different agonists used. The effect of vitamins may depend on the incubation time with platelets. The concentration of vitamins in human blood after oral supplementation may be lower than the effective one in in vitro experiments. The effect of vitamins may depend on their levels in platelets rather than in plasma. The discrepancy between low effective concentrations in blood after the supplementation of vitamins and their higher effective concentration in vitro might also be explained by the combined effect of compounds in blood. Several antiplatelet compounds such as vitamins, nitric oxide and anti-platelet prostaglandins can be present in blood in sub-threshold concentrations before supplementation. In addition, exogenous anti-platelet compounds can induce the formation of endogenous anti-platelet factors in platelets, in other blood cells or in the endothelium. An anti-platelet vitamin can interact with these compounds. Effects from the combination of two or more agents may be significantly greater than the sum of the effects of each agent administrated alone, or the concurrent action of an agent at a concentration that is not effective may increase the effect of another agent. Thus, although an effective concentration of an anti-platelet vitamin in vitro may be essentially higher than its concentration in plasma after supplementation; this does not exclude its physiological relevance. The use of a mixture of vitamers and a combination of vitamins with other anti-platelet drugs may be preferable in the clinical application to prevent thrombosis. At present, the main interest in the field is concentrated on the anti-platelet activity of vitamins A and D.