Fat-Soluble Vitamins PDF

Dr. Ahmed M Issa  VITAMINS A vitamin is an organic molecule and is an essential micronutrient. The organism needs vitamins in small quantities for the proper functioning of its metabolism. These essential nutrients cannot be synthesized in the organism, either at all or not in suff...

Dr. Ahmed M Issa  VITAMINS A vitamin is an organic molecule and is an essential micronutrient. The organism needs vitamins in small quantities for the proper functioning of its metabolism. These essential nutrients cannot be synthesized in the organism, either at all or not in sufficient quantities, and therefore must be obtained through the diet. Most vitamins are precursors of A healthy diet usually covers average daily coenzymes; in some cases, they are also vitamin requirements. By contrast, precursors of hormones or act as malnutrition, malnourishment (e. g., an antioxidants. Vitamin requirements vary unbalanced diet in older people, from species to species and are influenced malnourishment in alcoholics, ready meals), by age, sex, and physiological conditions or resorption disturbances lead to an such as pregnancy, breast-feeding, physical inadequate supply of vitamins from which exercises, and nutrition. The vitamins are hypovitaminosis, or in extreme cases divided into two groups: water-soluble avitaminosis, can result. Medical vitamins and fat-soluble vitamins. treatments that kill the intestinal flora- e. g., antibiotics — can also lead to vitamin deficiencies (K,B12,biotin) due to the absence of bacterial vitamin synthesis. Since only a few vitamins can be stored (A, There are 13 essential vitamins that D, E, B12), a lack of vitamins quickly leads nutritionists divide into two groups: fat to deficiency diseases. These often affect soluble and water soluble. the skin, blood cells, and nervous system. The causes of vitamin deficiencies can be Fat soluble vitamins are: treated by improving nutrition and by vitamin A administering vitamins in tablet form. vitamin D An overdose of vitamins only leads to vitamin E hypervitaminoses, with toxic symptoms, in vitamin K the case of vitamins A and D. Normally, excess vitamins are rapidly excreted with the urine. Water soluble vitamins are: vitamin B-1 (thiamine) Most vitamins are precursors of vitamin B-2 (riboflavin) coenzymes; in some cases, they are also vitamin B-3 (niacin) precursors of hormones or act as vitamin B-5 (pantothenic acid) antioxidants. Vitamin requirements vary vitamin B-6 ( pyridoxal ) from species to species and are influenced vitamin B-7 (biotin) by age, sex, and physiological conditions vitamin B-9 (folate, folic acid) such as pregnancy, breast-feeding, physical vitamin B-12 (cyanocobalamin) exercises, and nutrition. vitamin C ( ascorbate )  Fat- soluble vitamins: Vitamin A (retinol): 1912y The lipid-soluble vitamins include vitamins A, D, E, Vit A is the parent substance of the and K, all of which belong to the isoprenoids. retinoid, which include retinal and retinoic acid. The retinoid also can be synthesized by cleavage from the provitamin (β- carotene). Retinoid are found in meat- containing diets, whereas β-carotene occurs in fruits and vegetables (particularly carrots). Retinal is involved in visual processes as the pigment of the chromo protein rhodopsin. Retinal function as both a visual pigment as well as a hormone. Retinoic acid, like the steroid hormones, Signaling substances and many proteins are influences the transcription of genes in the involved in visual processes. Initially, a cell nucleus. It acts as a differentiation light-induced cis–trans isomerization of the factor in growth and development pigment retinal triggers a conformational processes. change in the membrane protein rhodopsin. Vitamin A deficiency can result in night Via the G protein transducin, which is blindness, visual impairment, and growth associated with rhodopsin, an enzyme is disturbances. activated that breaks down the second messenger cGMP. Finally, the cGMP Vitamin A has many functions like deficiency leads to hyperpolarization of the 1. Detection of light in the eye light-sensitive cell, which is registered by 2. Activation of vitamin D receptors subsequent neurons as reduced 3. Activation of thyroid hormone neurotransmitter release. receptors 4. Regulation of gene expression and cell differentiation Two types of photoreceptor cell are found in the human retina—rods and cones. Rods are sensitive to low levels of light, while the cones are responsible for color vision at higher or bright light intensities  Photoreceptor The cell illustrated is a rod cell, which has a structure divided by membrane discs into which the 7-helix receptor rhodopsin is integrated.In contrast to other receptors in the 7-helix class ,rhodopsin is a light-sensitive chromoprotein. Its protein part is opsin, and contains the aldehyde retinal an isoprenoid which is bound to the ε-amino group of a lysine residue as an aldimine. The light absorption of rhodopsin is in the visible range, with a maximum at about 500 nm. The absorption properties of the visual pigment are thus optically adjusted to the spectral distribution of sunlight. Absorption of a photon triggers isomerization from the 11-cis form of retinal to alltrans- retinal. Within milliseconds, this photochemical process leads to an allosteric conformational change in rhodopsin. The active conformation (rhodopsin*) binds and activates the G protein transducin. The signal cascade that now follows causes the Rod cells to release less neurotransmitter (glutamate) at their synapses (In the nervous system, a synapse is a structure that permits a neuron to pass an electrical or chemical signal to another cell ) The adjoining bipolar neurons register this change and transmit it to the brain through the optical nerve as a signal for light.  Visual signal cascade In Dark Rod cells that are not exposed to light contain relatively high concentrations (70 µM) of the cyclic nucleotide cGMP (3_,5_-cycloGMP), which is synthesized by a guanylate cyclase. The cGMP binds to an ion channel in the rod membrane (bottom left) and thus keeps it open. The inflow of cations (Na+, Ca2+) depolarizes the membrane and leads to release of the...neurotransmitter glutamate at the synapse. IN LIGHT When the G protein transducin binds to light-activated rhodopsin* , it leads to the GDP that is bound to the transducin being exchanged for GTP. In transducin* that has been activated in this way, the GTP- containing α_subunit breaks off from the rest of the molecule and in turn activates a membrane cGMP phosphodiesterase. This hydrolyzes cGMP to GMP and thus reduces the level of free cGMP within milliseconds. As a consequence, the cGMP bound at the ion channel dissociates off and the channel closes. As cations are constantly being pumped out of the cell, the membrane potential falls and hyperpolarization of the cell occurs, which interrupts glutamate release.  Regeneration Vitamin A deficiency After exposure to light, several processes Deficiency of vitamin A results in restore the initial conditions: night blindness (rod cells are 1. The α_subunit of transducin* responsible for vision in low light), inactivates itself by GTP metaplasia (Metaplasia (Greek: hydrolysis and thus terminates "change in form") is the reversible the activation of cGMP esterase. replacement of one differentiated 2. The reduced Ca2+ concentration cell type with another mature causes activation of guanylate differentiated cell type )of the cyclase, which increases the corneal epithelium, dry eyes, cGMP level until the cation bronchitis, pneumonia, and follicular channels reopen. hyperkeratosis. 3. An isomerase transfers all- trans -retinal to the 11-cis - form, in which it is available for the next cycle. A dehydrogenase can also allow retinal to be supplied from vitamin A (retinol). Toxicity of vitamin A causes: red blood breakage, cessation of menstruation, nose bleeds, bone pain; growth retardation; increased pressure inside skull; headaches; possible bone mineral loss, abdominal pain, nausea, vomiting, diarrhea, weight loss, over-activity, blurred vision, muscle weakness, fatigue, irritability, loss of appetite, dry skin, rashes, loss of hair,cracking & bleeding lips, brittle nails, hair loss, liver enlargement & liver damage and birth defects. Vitamin D (calciol, cholecalciferol) Calcitriol and parathyroid hormone, on the Vitamin D (calciol, cholecalciferol) is one hand, and calcitonin on the other, ensure the precursor of the hormone calcitriol a more or less constant level of Ca2+ in the (1,25dihydroxycholecalciferol);Togethr blood plasma and in the extracellular with two other hormones regulates the space(80–110 mg/l or 2.0–2.6 mM ) calcium metabolism Ca2+ metabolism is balanced in healthy adults. Approximately 1g Ca2+ is taken up per day, about 300 mg of which is resorbed. The same amount is also excreted again. The amounts of Ca2+ ): released from bone and deposited in it per day are much smaller. Milk and milk products, especially cheese, are particularly rich in calcium.. The peptide parathyroid hormone (PTH ) and the steroid calcitriol. promote direct or indirect processes that raise the Ca2+ level in blood. Calcitriol increases Ca2+ resorption in the intestine and kidney by inducing transporters. Parathyroid hormone supports these processes by stimulating calcitriol biosynthesis in the kidneys In addition, it directly promotes resorption of Ca2+ in the kidneys and Ca2+ release from bone.The PTH antagonist calcitonin {Calcitonin is a 32-amino acid linear polypeptide hormone that is produced in humans primarily by the parafollicular cells (also known as C-cells) of the thyroid, It acts to reduce blood calcium (Ca2+), opposing the effects of parathyroid hormone or counteracts these processes. Calciol can be synthesized in the skin from 7-dehydrocholesterol, an endogenous steroid, by a photochemical reaction. Vitamin D deficiencies only occur when the skin receives insufficient exposure to ultraviolet light and vitamin D is lacking in the diet. Deficiency is observed in the form of rickets in children and osteomalacia in adults. In both cases, bone mineralization is disturbed.  Vitamin E (Tocopherol ) Vit E and related compounds only occur in plants (e. g., wheat germ). They contain what is known as a chromane ring. In the lipid phase, vitamin E is mainly located in biological membranes, where it acts as an antioxidant. it protects unsaturated lipids against ROS (reactive oxygen species) and other radicals.  Reactive oxygen species ROS A fourth electron transfer and subsequent The dioxygen molecule (O2) protonation also convert O– into water. contains two unpaired electrons, it is a diradical. Despite this, O2 is relatively stable due to its special electron arrangement. However, if the molecule takes up an extra electron (a), the highly reactive superoxide radical ( O2 – ) arises. Another reduction step (b) leads to the peroxide anion (O2 2–), which easily binds protons and thus becomes hydrogen peroxide (H2O2). Inclusion of a third electron (c) leads to cleavage of the molecule into the ions O2– and O–. While O2– can form water by taking up two protons, protonation of O– provides the extremely dangerous hydroxy radical ( OH). *Vit E prevents peroxidation of fatty acids in Vitamin E insufficiency induces red cell membranes, helping to maintain their blood cell fragility and neuron degeneration, especially in peripheral normal fluidity. Deficiency can lead to axons and posterior column neurons. hemolysis, neurologic problems, and retinitis These chemicals operate as pigmentosa. Vitamin E acts as a radical antioxidants, preventing polyunsaturated scavenger, delivering a hydrogen (H) atom to fatty acid lipid peroxidation in cellular free radicals. The O-H bond in tocopherols is membranes. Vegetable oils and nuts are good sources of vitamin E in the diet. about 10% weaker than in most other phenols. This weak bond allows the vitamin to donate a hydrogen atom to the peroxyl radical and other free radicals, minimizing their damaging effect. *It prevents oxidation of LDL particles. Oxidized LDLs are strongly associated with atherosclerosis and coronary artery disease.  Vitamin K ( phylloquinone) Vit K and similar substances with modified side chains are involved in the carboxylation of glutamate residues of coagulation factors of the liver. The form that acts as a cofactor for carboxylase is derived from the vitamin by enzymatic reduction. Vitamin K is required to introduce Ca2+ binding sites on several calcium-dependent proteins. The modification that introduces the Ca2+ binding site is a γ-carboxylation of glutamyl residue(s) in these proteins. Vitamin K antagonists (e. g., coumarin derivatives and warfarin). Warfarin is a prescription medication used to prevent harmful blood clots from forming or growing larger. Beneficial blood clots prevent or stop bleeding, but harmful blood clots can cause a heart attack, stroke, deep vein thrombosis or pulmonary embolism. Inhibit this reaction and consequently carboxylation is used to inhibit blood coagulation in prophylactic treatment against thrombosis. Vitamin K deficiency occurs only rarely, as the vitamin is formed by bacteria of the intestinal flora. THANKS