Glyoxylic acid metabolism

Various aldehydes are encountered in wine. The most abundant is acetaldehyde which is both a product of yeast metabolism and an oxidation product of ethanol. Glyoxylic acid, resulting from oxidation of tartaric acid, especially catalyzed by metal ions (Fe, Cu) or ascorbic acid, can also be present. Other aldehydes reported to participate in these reactions include furfural and 5-hydroxymethylfurfural that are degradation products of sugar and can be extracted from barrels (Es-Safi et al. 2000), vanillin which also results from oak toasting, isovaleraldehyde, benzaldehyde, pro-pionaldehyde, isobutyraldehyde, formaldehyde and 2-methylbutyraldehyde which are present in the spirits used to produce fortified wines (Pissara et al. 2003). 

Ethyl benzene distributes to the adipose tissues. It is metabolized to mandelic acid (64%) and phenyl-glyoxylic acid (25%). The percentage of metabolites may vary according to the route of exposure with mandelic acid formation being favored with inhalation. The primary route of excretion is via the urine. Experimental evidence indicates that the percutaneous absorption rate of ethyl benzene is 37 pgcm... 

Although the mitochondria are the primary site of oxidation for dietary and storage fats, the peroxisomal oxidation pathway is responsible for the oxidation of very long-chain fatty acids, jS-methyl branched fatty acids, and bile acid precursors. The peroxisomal pathway also plays a role in the oxidation of dicarboxylic acids. In addition, it plays a role in isoprenoid biosynthesis and amino acid metabolism. Peroxisomes are also involved in bile acid biosynthesis, a part of plasmalogen synthesis and glyoxylate transamination. Furthermore, the literature indicates that peroxisomes participate in cholesterol biosynthesis, hydrogen peroxide-based cellular respiration, purine, fatty acid, long-chain... 

When introduced via the oral or inhalation routes, tetrachloroethane is metabolized primarily to tri-chloroethanol, trichloroacetic acids that are subsequently broken down to glyoxylic acid, oxalic acid and carbon dioxide and are excreted chiefly as metabolites in the breath and urine. A small amount is expired in the breath as carbon dioxide and as the parent compound. 

Many aroma compounds in fruits and plant materials are derived from lipid metabolism. Fatty acid biosynthesis and degradation and their connections with glycolysis, gluconeogenesis, TCA cycle, glyoxylate cycle and terpene metabolism have been described by Lynen (2) and Stumpf ( ). During fatty acid biosynthesis in the cytoplasm acetyl-CoA is transformed into malonyl-CoA. The de novo synthesis of palmitic acid by palmitoyl-ACP synthetase involves the sequential addition of C2-units by a series of reactions which have been well characterized. Palmitoyl-ACP is transformed into stearoyl-ACP and oleoyl-CoA in chloroplasts and plastides. During B-oxi-dation in mitochondria and microsomes the fatty acids are bound to CoASH. The B-oxidation pathway shows a similar reaction sequence compared to that of de novo synthesis. B-Oxidation and de novo synthesis possess differences in activation, coenzymes, enzymes and the intermediates (SM+)-3-hydroxyacyl-S-CoA (B-oxidation) and (R)-(-)-3-hydroxyacyl-ACP (de novo synthesis). The key enzyme for de novo synthesis (acetyl-CoA carboxylase) is inhibited by palmitoyl-S-CoA and plays an important role in fatty acid metabolism. 

Glyoxylic acid a naturally occurring compound, a metabolic intermediate or product of the metaboli m of certain bacteria, algae, and plants... 

Besides ascorbic acid, glycine is the most important source of oxalic acid (W5). The metabolic pathway leading from glycine to oxalic acid via glyoxylic acid (which can be readily converted to glycolic acid) and the enzyme systems involved in that pathway have been recently... 

Fig. 4. Scheme showing the pathway leading from glycine to oxalic acid and the other metabolic transformations of glyoxylic acid. 

OAA is an intermediate in several important pathways, including gluconeogenesis, citric acid cycle, glyoxylate cycle, urea cycle, and amino acid metabolism (see here). 

L-malate is an intermediate in the citric acid cycle, urea cycle, amino acid metabolism, the glyoxylate cycle, and shuttles across membranes of the cell (Figure 18.31). 

Administer pyridoxins (see p 499), folate (p 447), and thiamine (p 505), cofactors required tor the metabolism of ethylene glycol that may alleviate toxicity by enhancing metabolism of glyoxylic acid to nontoxic metabolites. 

I. Pharmacology. Thiamine (vitamin B ) is a water-soluble vitamin that acts as an essential cofactor for various pathways of carbohydrate metabolism. Thiamine also acts as a cofactor in the metabolism of glyoxylic acid (produced in ethylene glycol intoxication). Thiamine deficiency may result in beriberi and Wemicke-Korsakoff syndrome. Thiamine is rapidly absorbed after oral, intramuscular, or intravenous administration. However, parenteral administration is recommended for initial management of thiamine deficiency syndromes. 

Fig.2. Oxalic acid. Metabolic sources of oxalate. 2-Hydroxy-3-oxoadipate is a normal excretory product in humans, which diverts glyoxylate from oxalate production (see Inborn errors of metabolism. Oxalosis).

Oxalate is a terminal product of normal metabolism. When [ " C]oxalate is injected, most of the labeled compound is excreted, and only a small fraction of the radioactivity is recovered in bone and muscle. There are only two immediate precursors of oxalic acid in normal metabolic pathways glyoxylic acid and 2,3-diketo-L-gulonic acid. The first of these compounds is the product of amino acid oxidation (serine and glycine), and the second is derived from the oxidation of ascorbic acid (see Fig. 3-25). 

A carboxylic acid, normally excreted in the urine in small amounts. It is a constituent of many urinary tract stones. High levels of oxalic acid are excreted in the urine in the rare inborn error of metabolism, primary hyperoxaluria. In this disorder renal stones composed of oxalate are formed and death results from progressive renal failure. The increase in the urinary excretion of oxalic acid appears to be derived from glycine as a result of deficient glyoxylic acid-glycine transamination. 

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