Vitamin B2, B7 and B5

A. Clinical indications for thiamine
The oxidative decarboxylation of pyruvate and ?-ketoglutarate, which plays a key role in energy metabolism of most cells, is particularly important in tissues of the nervous system. In thiamine deficiency, the activity of these two dehydrogenase-catalyzed reactions is decreased, resulting in a decreased production of ATP and, thus, impaired cellular function. [Note: Thiamine deficiency is diagnosed by an increase in erythrocyte transketolase activity observed on addition of thiamine pyrophosphate.]
1. Beriberi: Beriberi literally means "I can t, I can t" in Singhalese (one of the three official languages used in Sri Lanka) .This is a severe thiamine-deficiency syndrome found in areas where polished rice is the major component of the diet. Signs of infantile beriberi include tachycardia, vomiting, convulsions, and, if not treated, death. The deficiency syndrome can have a rapid onset in nursing infants whose mothers are deficient in thiamine. Adult beriberi (dry beriberi) is characterized by dry skin, irritability, disordered thinking and progressive paralysis resulting from damaged peripheral nerves. Wet beriberi affects the heart and circulatory system. It is sometimes fatal, as it causes a combination of heart failure and weakening of the capillary walls, which causes the peripheral tissues to become edematous.
2. Wernicke-Korsakoff Syndrome: In the United States, thiamine deficiency, which is seen primarily in association with chronic alcoholism, is due to dietary insufficiency or impaired intestinal absorption of the vitamin B1. Some alcoholics develop Wernicke-Korsakoff syndrome- a thiamine deficiency state characterized by apathy, loss of memory, ataxia, and a rhythmic to-and-fro motion of the eyeballs (nystagmus). The neurologic consequences of Wernicke s syndrome are treatable with thiamine supplementation.

B. Sources of Thiamine (Vitamin B1)
Whole grains (unpolished rice and wheat), legumes (beans and peas), meat ,bananas and soybeans.
C. Recommended Dietary Allowance of Thiamine (Vitamin B1)
Adults 1.5 mg/day.
Children 1.2 mg/day.
Pregnancy and lactation 2.0 mg/day.
6. NIACIN or (NICOTINIC ACID) VITAMIN B3
Niacin, or nicotinic acid, is a substituted pyridine derivative. The biologically active coenzyme forms are nicotinamide adenine dinucleotide (NAD+) and its phosphorylated derivative, nicotinamide adenine dinucleotide phosphate (NADP+, Figure 28.13).
Nicotinamide, a derivative of nicotinic acid that contains an amide instead of a carboxyl group, also occurs in the diet. Nicotinamide is readily deaminated in the body and, therefore, is nutritionally equivalent to nicotinic acid. NAD+ and NADP+ serve as coenzymes in oxidation-reduction reactions in which the coenzyme undergoes reduction of the pyridine ring by accepting a hydride ion (hydrogen atom plus one electron, Figure 28.14). The reduced forms of NAD+ and NADP+ are NADH and NADPH, respectively.
A. Distribution of Niacin (VITAMIN B3)
Niacin is found in unrefined and enriched grains, milk, and lean meats, especially liver. [Note: Corn is low in both niacin and tryptophan. Corn-based diets can cause pellagra].
B. Clinical Indications for Niacin (VITAMIN B3)
1. Deficiency of Niacin: A deficiency of niacin causes pellagra, a disease involving the skin, gastrointestinal tract, and CNS. The symptoms of pellagra progress through the three Ds: dermatitis diarrhea, dementia-and, if untreated, death.
2. Treatment of Hyperlipidemia: Niacin (at doses of 1.5 g/day or 100 times the recommended dietary allowance or RDA) strongly inhibits lipolysis in adipose tissue-the primary producer of circulating free fatty acids. The liver normally uses these circulating fatty acids as a major precursor for triacylglycerol synthesis. Thus, niacin causes a decrease in liver triacylglycerol synthesis, which is required for very-low-density lipoprotein (VLDL) production. Low-density lipoprotein (LDL, the cholesterol rich lipoprotein) is derived from VLDL in the plasma. Thus, both plasma triacylglycerol (in VLDL) and cholesterol (in VLDL and LDL) are lowered. Therefore, niacin is particularly useful in the treatment of Type llb hyperlipoproteinemia, in which both VLDL and LDL are elevated. [Note: Niacin raises HDL levels.]
Recommended Dietary Allowance of Niacin (VITAMIN B3)
Adults: 16-20 mg/ day
Children: 9-16 mg/ day
Infants: 5-8 mg/ day
7. RIBOFLAVIN (VITAMIN B2)
The two biologically active forms are flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), formed by the transfer of an adenosine monophosphate moiety from ATP to FMN (Figure 28.15). FMN and FAD are each capable of reversibly accepting two hydrogen atoms, forming FMNH2 or FADH2. FMN and FAD are bound tightly-sometimes covalently-to flavoenzymes that catalyze the oxidation or reduction of a substrate.
Functions of FMN and FAD
They take part in oxidation reactions.
FMN is required for:
L-amino acid oxidase
Cytochrome C reductase.
FAD is required as coenzyme for:
Succinate dehydrogenase
Pyruvate dehydrogenase complex
?-ketoglutarate dehydrogenase complex
Xanthine oxidase
Riboflavin deficiency
Riboflavin deficiency is not associated with a major human disease, although it frequently accompanies other vitamin deficiencies. Deficiency symptoms include dermatitis, cheilosis (fissuring at the corners of the mouth), and glossitis (the tongue appearing smooth and purplish).











Glossitis Cheilosis
Sources of Riboflavin (Vitamin B2)
Animal liver, yeast, green leafy vegetables, milk and eggs.
Recommended Dietary Allowance of Riboflavin (Vitamin B2)
Adults: 2.0 mg/ day
Children: 1.2 mg/ day
Pregnancy and lactation: 2.0 mg/day.
8. BIOTIN (Vitamin B7)
Biotin also known as vitamin H or coenzyme R, is a water-soluble B-vitamin (vitamin B7), is a coenzyme in carboxylation reactions, in which it serves as a carrier of activated carbon dioxide (Figure 10.3, for the mechanism of biotin-dependent carboxylations). Biotin is covalently bound to the ?-amino groups of lysine residues in biotin-dependent enzymes (Figure 28.16). Biotin deficiency does not occur naturally because the vitamin is widely distributed in food. Also, a large percentage of the biotin requirement in humans is supplied by intestinal bacteria. However, the addition of raw egg white to the diet as a source of protein induces symptoms of biotin deficiency, namely, hair loss (alopecia), dermatitis, glossitis, loss of appetite, and nausea. Raw egg white contains a glycoprotein, avidin, which tightly binds biotin and prevents its absorption from the intestine. With a normal diet. however, it has been estimated that 20 eggs/day would be required to induce a deficiency syndrome.
Thus, inclusion of an occasional raw egg in the diet does not lead to biotin deficiency, although eating raw eggs is generally not recommended due to the possibility of salmonella infection.
Multiple carboxylase deficiency results from a defect in the ability to link biotin to carboxylases or to remove it from carboxylases during their degradation. Treatment is biotin supplementation.
Sources of Biotin
Egg yolk, organ meats (liver, kidney), milk, legumes and nuts.
Recommended Dietary Allowance of Biotin
Adults: 0.3 mg/day
9. PANTOTHENIC ACID (VITAMIN B5)
Pantothenic acid or some time called vitamin B5 is a component of coenzyme A (CoA), which functions in the transfer of acyl groups (Figure 28.17). Pantothenic acid consists of a dihydroxy dimethyl butyric acid joined to ?-alanine by a peptide bond. The coenzyme form is Coenzyme A (CoASH). Its reactive group is sulfhydryl group (SH). CoASH or CoA is required to carries acyl compounds as activated thiol esters. Examples of such structures are:

Pantothenic acid is also a component of the acyl carrier protein (ACP) domain of fatty acid synthase. Pantothenic acid deficiency is not well characterized in humans. However, deficiency of pantothenic acid is rare. When it is produced experimentally have the symptoms, fatigue, sleep disorders, weakness, abdominal cramp and a burning sensation of the feet.
Sources of Pantothenic acid
Eggs, animal liver, yeast, meat, milk, vegetables and grains.
Recommended Dietary Allowance of Pantothenic acid
Adults: 5-10 mg/day
Children: 4-5 mg/day
Infants: 1-2 mg/day.