Vitamin accumulation

Estigmene acrea dietary requirement, vitamin accumulated in tissues during development 41,43... 

Micronutrients (vitamins and minerals) are also listed on food packaging. The vitamins we require are compounds that are necessary for metahohc processes either our bodies cannot synthesize them, or they cannot synthesize them in amounts sufficient for our needs. As a result, we must obtain vitamins from dietary sources. DVs are listed for the fat-soluble vitamins—vitamins A, D, and E (Section 8.7)—but care must be taken to avoid overdoses of these vitamins. Excesses can be toxic when lai e amounts of fat-soluble vitamins accumulate in adipose tissue. Excess vitamin A is especially toxic. With water-soluble vitamins, turnover is frequent enough that the danger of excess is not normally a problem. 

Lipid-soluble vitamins accumulate in fatty tissue, leading to toxic effects. Water-soluble vitamins are excreted, drastically reducing the chances of an overdose. 

Water-soluble vitamins can be excreted in water-based fluids much more readily than fat-soluble vitamins. Thus, large doses of fat-soluble vitamins accumulate in the body. 

Some vitamins (A, D, E, and K) have very nonpolar molecnlar strnctnres and therefore dissolve only in nonpolar solvents. In the body, the nonpolar solvents are the lipids we have classified as fats, so these vitamins are called fat-solnble. The fat-soluble vitamins have diverse functions in the body, and they act somewhat like hormones (Table 22.3). Care must be taken to avoid overdoses of the fat-solnble vitamins. Toxic effects are known to occur, especially with vitamin A, when excess amounts of these vitamins accumulate in body tissue. Excesses of water-soluble vitamins are excreted readily through the kidneys and are not normally a problem. 

Certain factors and product precursors are occasionally added to various fermentation media to iacrease product formation rates, the amount of product formed, or the type of product formed. Examples iaclude the addition of cobalt salts ia the vitamin fermentation, and phenylacetic acid and phenoxyacetic acid for the penicillin G (hen ylpenicillin) and penicillin V (phenoxymethylpenicillin) fermentations, respectively. Biotin is often added to the citric acid fermentation to enhance productivity and the addition of P-ionone vastly iacreases beta-carotene fermentation yields. Also, iaducers play an important role ia some enzyme production fermentations, and specific metaboHc inhibitors often block certain enzymatic steps that result in product accumulation. 

Reported cases of vitamin toxicity owing to overdose are usually associated with increased over-the-counter availabiHty of supplemental vitamins and indiscriminate supplementation. The misconception that if a Httle is good a lot is better has compounded toxicological problems with the vitamins. Eat-soluble vitamins tend to accumulate in the body with relatively inactive mechanism for excretion and cause greater toxicological difficulties than do water-soluble vitamins. 

The hver of sharks and other oily fishes sometimes accumulate toxic levels of vitamin A, and cases of acute poisoning have been reported both among Eskimos and the Japanese. 

Many kinds of amino acids (eg, L-lysine, L-omithine, t-phenylalanine, L-threonine, L-tyrosine, L-valine) are accumulated by auxotrophic mutant strains (which are altered to require some growth factors such as vitamins and amino acids) (Table 6, Primary mutation) (22). In these mutants, the formation of regulatory effector(s) on the amino acid biosynthesis is genetically blocked and the concentration of the effector(s) is kept low enough to release the regulation and iaduce the overproduction of the corresponding amino acid and its accumulation outside the cells (22). 

The age pigments (lipofuscin), which accumulate with age, aie largely made up of these precipitated Hpid-proteia complexes resultiag from such cross-linking. Vitamin E may function to help prevent formation of these complexes. The metaboHc role of antioxidants (qv) such as vitamin E in animal tissues, however, remains quite controversial. 

Many carotenoids function in humans as vitamin A precursors however, not all carotenoids have provitamin A activity (Table 3). Of the biologically active carotenoids, -carotene has the greatest activity. Despite the fact that theoretically one molecule of -carotene is a biological source of two molecules of vitamin A, this relationship is not observed and 6 p.g -carotene is equivalent to 1 p. vitamin A. Although -carotene and vitamin A have complementary activities, they caimot totally replace each other. Because the conversion of -carotene to vitamin A is highly regulated, toxic quantities of vitamin A cannot accumulate and -carotene can be considered as a safe form of vitamin A (8). 

Vitamin Bjg is not synthesized by animals or by plants. Only a few species of bacteria synthesize this complex substance. Carnivorous animals easily acquire sufficient amounts of Bjg from meat in their diet, but herbivorous creatures typically depend on intestinal bacteria to synthesize Bjg for them. This is sometimes not sufficient, and certain animals, including rabbits, occasionally eat their feces in order to accumulate the necessary quantities of Big. 

What would be the consequences of a deficiency in vitamin Bi2 for fatty acid oxidation What metabolic intermediates might accumulate ... 

Camitine deficiency can occur particularly in the newborn—and especially in preterm infants—owing to inadequate biosynthesis or renal leakage. Losses can also occur in hemodialysis. This suggests a vitamin-fike dietary requirement for carnitine in some individuals. Symptoms of deficiency include hypoglycemia, which is a consequence of impaired fatty acid oxidation and hpid accumulation with muscular weakness. Treatment is by oral supplementation with carnitine. 

Hypolipoproteinemias Abetaiipoproteinemia No chylomicrons, VLDL, or LDL are formed because of defect in the loading of apo B with lipid. Rare blood acylglycerols low intestine and liver accumulate acylglycerols. Intestinal malabsorption. Early death avoidable by administration of large doses of fat-soluble vitamins, particularly vitamin E. 

There is only a limited capacity to metabolize vitamin A, and excessive intakes lead to accumulation beyond the capacity of binding proteins, so that unbound vitamin A causes tissue damage. Symptoms of toxicity affect the central nervous system (headache, nausea. 

When acting as a methyl donor, 5-adenosylmethionine forms homocysteine, which may be remethylated by methyltetrahydrofolate catalyzed by methionine synthase, a vitamin Bj2-dependent enzyme (Figure 45-14). The reduction of methylene-tetrahydrofolate to methyltetrahydrofolate is irreversible, and since the major source of tetrahydrofolate for tissues is methyl-tetrahydrofolate, the role of methionine synthase is vital and provides a link between the functions of folate and vitamin B,2. Impairment of methionine synthase in Bj2 deficiency results in the accumulation of methyl-tetrahydrofolate—the folate trap. There is therefore functional deficiency of folate secondary to the deficiency of vitamin B,2. 

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