Pantothenic acid, oxidation

Rice bran is the richest natural source of B-complex vitamins. Considerable amounts of thiamin (Bl), riboflavin (B2), niacin (B3), pantothenic acid (B5) and pyridoxin (B6) are available in rice bran (Table 17.1). Thiamin (Bl) is central to carbohydrate metabolism and kreb s cycle function. Niacin (B3) also plays a key role in carbohydrate metabolism for the synthesis of GTF (Glucose Tolerance Factor). As a pre-cursor to NAD (nicotinamide adenine dinucleotide-oxidized form), it is an important metabolite concerned with intracellular energy production. It prevents the depletion of NAD in the pancreatic beta cells. It also promotes healthy cholesterol levels not only by decreasing LDL-C but also by improving HDL-C. It is the safest nutritional approach to normalizing cholesterol levels. Pyridoxine (B6) helps to regulate blood glucose levels, prevents peripheral neuropathy in diabetics and improves the immune function. 

ATP and magnesium were required for the activation of acetate. Acetylations were inhibited by mercuric chloride suggesting an SH group was involved in the reaction either on the enzyme or, like lipoic acid, as a cofactor. Experiments from Lipmann s laboratory then demonstrated that a relatively heat-stable coenzyme was needed—a coenzyme for acetylation—coenzyme A (1945). The thiol-dependence appeared to be associated with the coenzyme. There was also a strong correlation between active coenzyme preparations and the presence in them of pantothenic acid—a widely distributed molecule which was a growth factor for some microorganisms and which, by 1942-1943, had been shown to be required for the oxidation of pyruvate. 

Note that this overall reaction requires three coenzymes that we encountered as metabolites of vitamins in chapter 15 NAD+, derived from lucotiiuc acid or nicotinamide FAD, derived from riboflavin and coenzyme A(CoASH), derived from pantothenic acid. In the overall process, acetyl-SCoA is oxidized to two molecules of carbon dioxide with the release of CoASH. Both NAD+ and FAD are reduced to, respectively, NADH and FADH2. Note that one molecule of guanosine triphosphate, GTP, functionally equivalent to ATP, is generated in the process. 

The synthetic form is the alcohol, panthenol, which can be oxidized in vivo to pantothenic acid. It is included in the list of substances that may be added in foods and in food supplements [403], Pantothenic acid is part of the coenzyme A (CoA) molecule therefore it is involved in acylation reactions, such as in fatty acid and carbohydrate metabolism. 

Reactions of the TCA cycle Enzyme that oxidatively decarboxylates pyruvate, its coenzymes, activators, and inhibitors REACTIONS OF THE TRICARBOXYLIC ACID CYCLE (p. 107) Pyruvate is oxidatively decarboxylated by pyruvate dehydrogenase complex producing acetyl CoA, which is the major fuel for the tricarboxylic acid cycle (TCA cycle). The irreversible set of reactions catalyzed by this enzyme complex requires five coenzymes thiamine pyrophosphate, lipoic acid, coenzyme A (which contains the vitamin pantothenic acid), FAD, and NAD. The reaction is activated by NAD, coenzyme A, and pyruvate, and inhibited by ATP, acetyl CoA, and NADH. 

Vitamins folic acid, ascorbic acid (reduced and oxidized species), biotin, cholin, pantothenic acid Amino acids Di- and tripeptides Bile acids... 

The oxidation of pantothenic acid (PA) by CAT in acid solution is first order in CAT and exhibits a frational order with respect to PA. The reaction is retarded by an increase... 

Panthenol is absorbed via passive diffusion after topical or oral application and then enzymatically oxidized to pantothenic acid. This is a component of coenzyme A and acyl carrier protein, and as such of great importance in fatty acid, carbohydrate, and amino acid metabolism. Deficiency leads to uncharacteristic symptoms such as headaches, apathy, gastrointestinal disturbances, palpitations, and paraesthesia typically in the feet, also known as burning feet syndrome. Wound healing is impaired. The recommended daily allowance is 5 to 7 mg.112... 

Product Glycidylbutyrate Butyl glucosides Styrene oxides Oligosaccharides D-pantothenic acid L-malic acid L-methionine L-valine R-mandelic acid L-Camitine Aspartame L-aspartate Cyclodextrins (S)-CPA 6-APA Cocoa Butter Acrylamide HFCS... 

Nicotinic acid was discovered and named as a product of the chemical oxidation of nicotine in 1867. When it was later discovered to he the pellagra-preventing vitamin, it was not assigned a number among the B vitamins because its chemistry was already known. Niacin is generally placed between vitamins B2 and Bg, although it is incorrect to call it vitamin B3, which was at one time assigned to pantothenic acid (Section 12.1). 

Pantothenol, the alcohol ofpantothenic acid (see Figure 12.1), is frequently used in pharmaceutical preparations. Although it is a substrate for pantothenate kinase in vitro, it is more likely that it first undergoes oxidation to pantothenic acid, catalyzed by liver alcohol dehydrogenase, rather than phosphorylation to phosphopantothenol followed by oxidation. 

Expression of the pantothenate kinase gene is induced by glucagon (which is secreted under conditions when there is an increased need for CoA for fatty acid oxidation) and repressed by insulin (Kirschbaum et al., 1990 Yun et al., 2000). 

The major functions of pantothenic acid are in CoA (Section 12.2.1) and as the prosthetic group for AGP in fatty acid synthesis (Section 12.2.3). In addition to its role in fatty acid oxidation, CoA is the major carrier of acyl groups for a wide variety of acyl transfer reactions. It is noteworthy that a wide variety of metabolic diseases in which there is defective metabolism of an acyl CoA derivative (e.g., the biotin-dependent carboxylase deficiencies Sections 11.2.2.1 and 11.2.3.1), CoA is spared by formation and excretion of acyl carnitine derivatives, possibly to such an extent that the capacity to synthesize carnitine is exceeded, resulting in functional carnitine deficiency (Section 14.1.2). 

In pantothenic acid-deficient rats, tissue CoA is depleted, affecting mainly the peroxisomal oxidation of fatty acids, which is mainly concerned with detoxication mitochondrial /3 -oxidation, which is an essential energy-yielding pathway, is spared to a great extent (Youssef et al., 1997). However, relatively moderate deficiency in animals results in increased plasma triacylglycerol and nonesterifled fatty acids, suggesting some impairment of lipid metabolism (Wittwer et al., 1990). 

S-Oxidation of cysteamine released by the catabolism of pantothenic acid (Section 12.2.2) or formed by the decarboxylation of cysteine. 

Mustard exposure causes depletion of ATP in cells. Better outcomes after exposure have been demonstrated when mitochondrial substrates were provided to offset this depletion. CEES-exposed rabbit corneas have been treated after exposure with a mix of taurine, pyruvate, a-keto glu-tarate, and pantothenic acid. Analysis showed reduced necrosis of the cornea. Electron microscopic and other analyses showed protection against membrane damage and oxidative damage (Varma et al, 1998a, b). 

The coenzyme form of pantothenic acid is coenzyme A and is represented as CoASH. The thiol group acts as a carrier of acyl group. It is an important coenzyme involved in fatty acid oxidation, pyruvate oxidation and is also biosynthesis of terpenes. The epsilon amino group of lysine in carboxylase enzymes combines with the carboxyl carrier protein (BCCP or biocytin) and serve as an intermediate carrier of C02. Acetyl CoA pyruvate and propionyl carboxylayse require the participation of BCCP. The coenzyme form of folic acid is tetrahydro folic acid. It is associated with one carbon metabolism. The oxidised and reduced forms of lipoic acid function as coenzyme in pyruvate and a-ketoglutarate dehydrogenase complexes. The 5-deoxy adenosyl and methyl cobalamins function as coenzyme forms of vitamin B12. Methyl cobalamin is involved in the conversion of homocysteine to methionine. 

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