Oxidation Of Homogentisic Acid Research Articles

New insights and advances on pyomelanin production: from microbial synthesis to applications.

Pyomelanin is a brown-black phenolic polymer and results from the oxidation of homogentisic acid (HGA) in the L-tyrosine pathway. As part of the research for natural and active ingredients issued from realistic bioprocesses, this work re-evaluates the HGA pigment and makes an updated inventory of its syntheses, microbial pathways, and properties, with tracks and recent advances for its large-scale production. The mechanism of the HGA polymerization is also well documented. In alkaptonuria, pyomelanin formation leads to connective tissue damage and arthritis, most probably due to the ROS issued from HGA oxidation. While UV radiation on human melanin may generate degradation products, pyomelanin is not photodegradable, is hyperthermostable, and has other properties better than L-Dopa melanin. This review aims to raise awareness about the potential of this pigment for various applications, not only for skin coloring and protection but also for other cells, materials, and as a promising (semi)conductor for bioelectronics and energy.

SP0220 Peer and Research Support in Rare Diseases – A CASE Study from the AKU Society

Alkaptonuria (AKU) is an ultra-rare inheritable metabolic disease resulting in a 2000-fold accumulation of the intermediate product homogentisic acid (HGA). Oxidation of HGA by air or within the connective tissue...

Chemiluminescence during the oxidation of homogentisic acid

Chemiluminescence (CL) that accompanies the autooxidation of homogentisic acid in the presence of an alkali was studied. Data on the red shift of the CL spectrum at increased medium polarity and the dependence of the luminescence intensity and light efficiency on the reagent concentration were obtained. A CL emitter is supposed to be an excimer formed by two radical dianion molecules of homogentisic acid. Chemiluminescence of an excimer occurs during coproportionation.

Studies on Catalytic Activity of Chelating Resins. I. The Catalytic Activity of Resin–Metal Chelates for the Oxidation of 2,6-Dihydroxyphenylacetic Acid and Hydroquinone

Abstract Some crosslinked chelating resins were prepared and the catalytic activity of the resin-rnetal chelates for the oxidation; of 2,6-dihydroxyphenylacetic acid(homogentisic acid) and hydroquinone was investigated. The resin–Cu(II), resin–Au(III), and resin–Ag(I) chelates had a high catalytic activity. Especially resin–Cu(II) chelate had the highest catalytic activity for these oxidation reactions, and its activity did not decrease even after repeated use. The chelating resins having hydrazide or polyethylenepolyamine side chains had a high catalytic activity. In order to have a high catalytic activity, the resin–metal chelates must leave coordination places open for the substrate to coordinate to metal in the chelates. In the oxidation of homogentisic acid, the catalytic activity of gel type resin increased with the increase of crosslinking degree in the range from 0.5% to 7.5%. However, the catalytic activity of the macroreticular chelating reins was scarcely affected by the degree of crosslinking. The oxidation reaction of homogentisic acid showed a kinetic behavior of a typical Michaelis-Menten type.

Inborn Errors of Metabolism

Around the turn of the century Garrard established the concept of an inborn error of metabolism using his study on alcaptonuria to exemplify his hypothesis that a considerable number of metabolic disorders with clearly defined clinical, pathologic, and biochemical abnormalities arise because an enzyme governing a single metabolic step is either reduced in activity or missing altogether. He pointed out the familial distribution of alcaptonuria and later showed that the inheritance could be explained on mendelian principles, ie, the affected individual was homozygous for the abnormal gene and that the inheritance was recessive, both parents being heterozygous for the disorder. He suggested that the accumulation of homogentisic acid in alcaptonuria was evidence that this substance is a normal metabolite in the degradation of tyrosine and attributed this accumulation to a failure of oxidation of homogentisic acid. In addition to alcaptonuria he described cystinunia, pentosuria, and albinism. This work was the forerunner of the classic studies of Beadle and Tatum on mutants of Neurospora crassa which led to the one gene-one enzyme concept. DETECTION Different groups require special attention: the family at risk because of previously affected individuals, those with unusual features suggestive of metabolic disorders, and sick newborns. Screening of normal newborns requires a different approach.

Oxidation of homogentisic acid catalyzed by horse-radish peroxidase

Oxidation of homogentisic acid catalyzed by horse-radish peroxidase

Effects of protein availability on resting or induced activities of enzymes in the tyrosine oxidase system

Abstract 1. 1. Depletion of available exogenous protein results in decreases in the activities of liver tyrosine oxidation and liver p-hydroxyphenylpyruvate oxidation without a concomitant decrease in the oxidation of homogentisic acid. 2. 2. The depression in overall oxidation rates of tyrosine or p-hydroxyphenylpyruvate is due to reductions in the activities of tyrosine-α-ketoglutarate transaminase and p-hydroxyphenylpyruvate oxidase. The latter enzyme appears to be nearly twice as sensitive to protein restriction. 3. 3. Induction of tyrosine-α-ketoglutarate transaminase either by injection of tyrosine or hydrocortisone acetate is sensitive to restricted protein. Tyrosine induction is more sensitive to protein supply than is hydrocortisone induction. 4. 4. All of the above changes are reversible by restoring the original supply of exogenous protein.

Observations on the oxidation of homogentisic acid in urine.

Observations on the oxidation of homogentisic acid in urine.