A. History. Thiamine was the first member of the vitamin
B group to be identified and hence given the name vitamin B1. Thiamine was first isolated by Jansen (1949) in Holland and Adolf Windaus in Germany. On account of its curing action against beriberi, it is commonly known as antiberiberi factor. It is also known as antineuritic factor or heat-labile factor. In Europe, it is also designated aneurin.
B. Occurrence. Thiamine is found practically in all plant and animal foods. Cereals, heart, liver and kidney are excellent sources of it. In cereals, the outer layers of seeds are especially rich in the In yeasts and animal tissues, however, it is present mainly as its coenzyme, thiamine pyrophosphate (TPP). Milk also contains thiamine, although in relatively low amounts. The milling of wheat flour lowers the thiamine content considerably, sometimes to the extent of even 80%. Consequently, wheat flour is usually enriched with thiamine at many places. Furthermore, improper cooking (esp., when the water in which foods are cooked is discarded) loses thiamine content. This is because of the
solubility of thiamine in water. Therefore, it is desirable to use the “cook water” for soups and sauces. Thiamine is easily destroyed by heat in neutral or alkaline media. Because the covering of the grains of cereals contains most of the vitamin, polishing
reduces its availability. Canning processes are, however, not particularly destructive.
C. Structure. The chemical structure of
thiamine (in Fig. ) was determined in 1935 by Robert R. Williams and his associates in the United States and its chemical synthesis was achieved soon thereafter. Thiamine (C12H17N4OS) is 2,5-dimethyl-6- aminopyrimidine bonded through a methylene linkage to 4-methyl-5-hydroxyethyl-thiazole. Thus, pyrimidine and thiazole are the two moieties present in its molecule. The pyrimidine is unique in that it is the only natural pyrimidine containing an alkyl group at C2. Also, with the possible exception of penicillin, thiamine is the only
natural compound which contains a thiazole group. It is interesting to note that plants can use a mixture of pyrimidine and thiazole compounds in place of thiamine itself. On the other hand, all the animals except pigeon require the complete vitamin.
D. Properties. Thiamine is a white crystalline substance, readily soluble in water, slightly so in ethyl alcohol but insoluble in ether and chloroform. Its odour resembles that of a yeast. The aqueous solution is optically inactive. Thiamine is destroyed at elevated temperature, unless the pH is low. It can stand short boiling up to 100°C. Hence, it is only partly lost in cooking or canning processes. Long boiling or boiling with alkali destroys it. But it is stable in acid medium. On oxidation, it produces thiochrome, which gives fluorescence.
E. Metabolism. The requirement of this vitamin is increased under high metabolic conditions such as fever, increased muscular activity, pregnancy and lactation and also under surgery and stress. A correlation also exists between the type of food taken and the vitamin B1 requirement. Fats and proteins reduce while carbohydrates increase the amount of this vitamin required in the daily diet. Thiamine absorption decreases with gastrointestinal or liver disease. Raw seafoods (e.g., fishes and molluscs) contain an enzyme, thiaminase which destroys thiamine in the body. People consuming such foods may, therefore, reveal symptoms of thiamine deficiency. Thiaminase cleaves the thiamine molecule between the pyrimidine and thiazole rings. If thiamine is administered in human body, a part of it is excreted or recovered in the urine and a part is converted to pyramin by the enzyme, thiaminase. Besides thiaminase, certain flavonoids of nonenzymic nature also work against thiamine. These have been shown to be present in ferns and certain higher plants. Thiamine is phosphorylated with ATP to form thiamine pyrophosphate (TPP),
which is also called diphosphothiamine (DPT). TPP, in association with lipoic acid, forms the prosthetic group, cocarboxylase for the enzyme carboxylase. TPP participates in many reactions, such as decarboxylation of α-keto acids, notably pyruvic and α-ketoglutaric and transketolation.
F. Deficiency. Vitamin B1 deficiency leads to polyneuritis in animals and beriberi in human beings.
Polyneuritis in birds renders them unable to fly, walk or even stand. Rats develop, among other symptoms, a brachycardia (slowing of the heart rate).
Beriberi (berisinghalese = weakness, which here means I cannot, symbolizing the incapacitated condition created by thiamine deficiency) has been and continues to be a serious health problem
in Far East where polished or refined rice (rice from which husk has been removed) is eaten. The rice has a rather low content of thiamine. The problem is aggravated if the rice is polished because the husk contains nearly all the thiamine of rice. Beriberi is also occasionally seen in alcoholics who are severely malnourished. Even before the concept of vitamins was developed, beriberi was described as a deficiency disease. It is a disease of the nervous system and is characterized by polyneuritis (degeneration of the peripheral nerves) leading to partial paralysis of the extremities, muscular atrophy, cardiovascular changes and gastrointestinal disorders.
At first, there is fatigue, apathy, irritability, depression, drowsiness, anorexia (loss of appetite), insomnia (sleeplessness), nausea and abdominal discomfort. This is followed by symptoms like peripheral neuritis with tingling, burning paresthesias of the toes and feet; decreased tendon reflexes; loss of vibration sense; tenderness and cramping of leg muscles; congestive heart failure and psychic disturbances. There may be ptosis of the eyelids and atrophy of the optic nerve. Hoarseness due to paralysis of the laryngeal nerve is a typical sign. Muscular atrophy and tenderness of the nerve trunks are followed by ataxia, loss of coordination, and loss of deep sensation. Paralytic symptoms are more common in adults than in children. Finally, the major symptoms may follow one of the following 3 courses (and accordingly beriberi is of 3 types) :
(a) Symptoms involving nervous system, causing dry beriberi : In it, the child may appear plump but is pale, flabby, listless and dyspneic; the heart beat is rapid and the liver enlarged.
(b) Symptoms associated with edema and effusions, leading to wet beriberi : In it, the child is undernourished, pale and edematous and has dyspnea, vomiting and tachycardia. The skin appears waxy. The urine may contain albumin and casts.
(c) Symptoms involving heart, resulting in acute pernicious beriberi : In it, the lesions may be found principally in the heart, peripheral nerves, subcutaneous tissue and serous cavities. The heart is enlarged, especially to the right and there is fatty degeneration of the myocardium. Generally edema or edema of the legs, serous effusions, and venous engorgement may be seen. Lesions in the brain include vascular dilatation and hemorrhage. Finally, death ensues due to heart failure. Often the symptoms characteristic of more than one of these 3 types of beriberi appear simultaneously in individuals causing mixed beriberi. Although beriberi is caused due to thiamine avitaminosis, it is usually associated with deficiencies of other vitamins. This is true of all vitamin B complex-deficiency conditions in man.
G. Human requirements. The daily recommended dietary allowances are 1.2–1.4 mg for men and 1.0 mg for women. Pregnant and lactating mothers, however, require up to 1.5 mg daily. The thiamine requirement for infants is between 0.2 and 0.5 mg daily.
H. Treatment : If beriberi occurs in breast-fed infant, both the mother and child should be treated with thiamine. In such cases, the daily dose for adults is 50 mg and for children 10 mg or more. Oral administration is effective until gastrointestinal disturbances prevent absorption. Thiamine should be instilled intramuscularly or intravenously to children with cardiac failure
several animal speces. Some of the coenzymes alsoparticipate in electron transport and/or oxidative phosphorylation. Various homologues of coenzyme Q, containing 6 to 10 isoprene units, have been isolated from various microbes, chloroplasts of green plants and mitochondria of animals. These have the same quinonoid nucleus (in Fig.) but differ in the number of isoprenoid units in the side chain. For example, coenzyme Q from animal source has 10 isoprene units and is, henceforth, called coenzyme Q10 or ubiquinone50 (50 carbon atoms, i.e., 10 isoprene units, in the side chain), where as the one from bacteria has less than 10 isoprene units. Mycobacteria, however, contain no coenzyme Q.
several animal speces. Some of the coenzymes alsoparticipate in electron transport and/or oxidative phosphorylation. Various homologues of coenzyme Q, containing 6 to 10 isoprene units, have been isolated from various microbes, chloroplasts of green plants and mitochondria of animals. These have the same quinonoid nucleus (in Fig.) but differ in the number of isoprenoid units in the side chain. For example, coenzyme Q from animal source has 10 isoprene units and is, henceforth, called coenzyme Q10 or ubiquinone50 (50 carbon atoms, i.e., 10 isoprene units, in the side chain), where as the one from bacteria has less than 10 isoprene units. Mycobacteria, however, contain no coenzyme Q.
It is a plant sterol and has been isolated from soybean and wheat germ oils. It in present in alfalfa and fresh cream. Chemically, it resembles ergosterol closely and contains only 2 double bonds at carbon postitons 5—6 and 22—23 (in fig). The absence of stigmasterol causes stiffness of the wrists and elbows of the guinea pigs. For this reason, it is commonly called as ‘antistiffness factor’.The muscles atrophy and become streaked.
It is a plant sterol and has been isolated from soybean and wheat germ oils. It in present in alfalfa and fresh cream. Chemically, it resembles ergosterol closely and contains only 2 double bonds at carbon postitons 5—6 and 22—23 (in fig). The absence of stigmasterol causes stiffness of the wrists and elbows of the guinea pigs. For this reason, it is commonly called as ‘antistiffness factor’.The muscles atrophy and become streaked.
