B vitamins: key players in energy metabolism
Most water-soluble vitamins serve as precursors to coenzymes, without which enzyme system function is impossible.
Thiamine (vitamin $B_1$) The daily requirement is 1.5–2.5 mg. Main sources: pork, grains, legumes, and whole grain bread. In the body, thiamine is phosphorylated to form the active coenzyme thiamine diphosphate (TDP), also known as thiamine pyrophosphate (TPP). Its deficiency leads to beriberi (severe polyneuritis), as well as Wernicke-Korsakoff specific encephalopathy.
Riboflavin (vitamin $B_2$) Required in amounts of 1.5–2.5 mg per day. Found in liver, cheese, milk, and eggs. It serves as the basis for the formation of flavin coenzymes — FMN (flavin mononucleotide) and FAD (flavin adenine dinucleotide). Hypovitaminosis leads to ariboflavinosis, which manifests as angular stomatitis ("soress"), glossitis, and corneal vascularization.
Nicotinic acid (vitamin PP, $B_3$, niacin) The body needs 15–25 mg daily. It can be obtained from meat, fish, liver, and legumes. Niacin is part of the structure of vital electron carriers — $NAD^+$ (NAD) and $NADP^+$ (NADP). Acute deficiency causes pellagra, a disease characterized by the classic triad of symptoms: dermatitis, diarrhea, and dementia.
Vitamins regulating protein metabolism and hematopoiesis
A distinct group of water-soluble compounds is critically important for the synthesis of amino acids, nucleic acids, and proper blood cell maturation.
Pyridoxine (vitamin $B_6$) The normal intake is 2–3 mg. Sources are similar to other B vitamins: grains, legumes, meat, and fish. The active form is pyridoxal phosphate (PLP). A decrease in its level in the body leads to peripheral neuritis, dermatitis, the development of microcytic anemia, and can provoke seizures in infants.
Folic acid (vitamin $B_9$, $B_c$, folacin) The daily dose is small—only 400 mcg (0.4 mg). Leafy green vegetables, yeast, and liver are rich in this vitamin. In cells, it is converted into tetrahydrofolic acid (THFA). Hypovitaminosis is extremely dangerous for dividing cells: leukopenia and megaloblastic (macrocytic) anemia develop.
Pantothenic acid (vitamin $B_5$) Found almost everywhere (yolk, yeast, liver), the daily norm is 10–15 mg. It is a structural component of Coenzyme A (HS-CoA) and 4-phosphopantetheine. Deficiency causes paresthesia ("burning feet" syndrome), hair depigmentation, and pellagra-like dermatitis.
Specific cofactors: biotin, vitamin C, and lipoamide
Some water-soluble compounds have unique mechanisms of action and pathways into the body.
Biotin (vitamin $H$, $B_7$) Required in microdoses (150–300 mcg). In addition to liver and egg yolk, a significant portion of the vitamin is synthesized by the intestinal microflora itself. It forms the coenzyme biocytin (carboxybiotin). Deficiency manifests as alopecia, muscle pain, and seborrheic dermatitis (often occurring as "raw egg white-eating syndrome").
Lipoic acid (vitamin N, lipoamide) The requirement is about 30 mg, and the substance can be synthesized in the body. Sources: heart, kidneys, liver. It functions in the form of the lipoamide coenzyme. Specific avitaminosis is not clinically described, but deficiency may lead to impaired cellular energy metabolism.
Ascorbic acid (vitamin C) The norm is 75–100 mg per day. Main sources: rosehip, peppers, black currant, and citrus fruits. Unlike other vitamins in this group, ascorbic acid does not form a true coenzyme, but acts as a potent reducing cofactor. Profound deficiency leads to scurvy, characterized by petechiae, loose teeth, and pronounced bleeding gums.
Briefly: answers to topical questions
Which specific protein in raw egg white binds biotin and causes its deficiency?
The biotin-binding protein in raw egg white is called avidin.
- Avidin is a glycoprotein that converts biotin into an insoluble and unabsorbable state. It is destroyed (denatured) by heat treatment, so the negative effect only manifests when consuming raw egg white.
In which biochemical reactions does thiamine diphosphate (TDP) participate?
Thiamine diphosphate (TDP) participates in the following biochemical reactions:
- Oxidative decarboxylation of pyruvate: TDP is a coenzyme of pyruvate decarboxylase as part of the pyruvate dehydrogenase complex and participates in the transfer of the acetyl (hydroxyethyl) residue to lipoic acid.
- Non-oxidative stage of the pentose phosphate pathway: TDP is a coenzyme of transketolase, which transfers a two-carbon fragment.
In which amino acid metabolism reactions does pyridoxal phosphate participate?
Pyridoxal phosphate participates in the following amino acid metabolism reactions:
- Transamination — the transfer of an amino group from an amino acid to an α-keto acid. Examples: synthesis of alanine from pyruvate, aspartate from oxaloacetate, and glutamate from α-ketoglutarate.
- Decarboxylation — the removal of $CO_2$ from the α-carboxyl group of amino acids with the formation of biogenic amines (serotonin, histamine, GABA, etc.).
What reaction does vitamin C catalyze as a cofactor in collagen synthesis?
Vitamin C acts as a reducing cofactor in proline and lysine hydroxylation reactions (formation of hydroxyproline and hydroxylysine) during post-translational modification of collagen.
Specific hydroxylase enzymes (prolyl hydroxylase and lysyl hydroxylase) participate in these reactions. The role of ascorbic acid is to maintain the iron ion in the active center of the enzyme in its reduced form ($Fe^{2+}$). This reaction is necessary for the formation of hydrogen bonds that stabilize the triple helix of the tropocollagen molecule.
To memorize the classic manifestations of pellagra (vitamin PP deficiency), use the rule of the "three D's": Dermatitis, Diarrhea, Dementia.
Class and exam questions
Which water-soluble vitamin does not form a coenzyme form?
Ascorbic acid (vitamin C). It does not form a true coenzyme, but functions in biochemical reactions as a reducing cofactor.
What is the difference between anemias in vitamin B6 and B9 deficiencies?
Pyridoxine (B6) deficiency leads to microcytic anemia. Folic acid (B9) deficiency disrupts cell maturation, leading to megaloblastic (macrocytic) anemia.
Why does biotin deficiency occur if it is synthesized in the body?
Biotin hypovitaminosis can develop due to the suppression of intestinal microflora or frequent consumption of raw egg white, the components of which tightly bind this vitamin, preventing its absorption.
What else to study on this topic
- Mechanisms of TDP action in decarboxylation reactions
- Redox reactions involving NAD and NADP
- Structure of Coenzyme A and its role in lipid metabolism
- Involvement of tetrahydrofolic acid in nucleotide synthesis
- Biochemical basis of Wernicke-Korsakoff encephalopathy development
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