Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.99.3 (acyl-CoA dehydrogenase)
 1,425 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A study was made of the biodegradation of alkylbenzene sulphonate homologues, one of the major components of commercially marketed detergents. A Bacillus species was elected for growth on alkylbenzene sulphonate homologues as the sole source of carbon and sulphur. 2. The results from both whole-cell and cell-free systems indicated that the alkyl, aryl and sulphonate moieties of alkylbenzene sulphonate homologues were all further metabolized by the Bacillus species. 3. The alkyl side chain, after a presumed initial oxidation of the terminal methyl group, was subsequently oxidized by a beta-oxidation pathway. Three enzymes of the beta-oxidation pathway, i.e. acyl-CoA synthetase, acyl-CoA dehydrogenase and beta-hydroxyacyl-CoA dehydrogenase, were identified in cell-free extracts of the detergent-grown Bacillus species. The substrate specificity of acyl-CoA synthetase indicated activity towards several alkylbenzene sulphonate homologues. 4. The sulphonate moiety was released as sulphite by a desulphonating enzyme. Some kinetic properties of this enzyme were determined. The sulphite was subsequently metabolized to either sulphate or adenosine 5'-sulphatophosphate. Two enzymes involved in sulphite metabolism, i.e. sulphite-cytochrome c reductase and adenosine 5'-sulphatophosphate-cytochrome c reductase were detected in cell-free extracts of undecylbenzene-p-sulphonate-grown Bacillus species. 5. The combined results of continuous sampling programmes monitored by both t.l.c. and sulphite appearance in the growth medium indicated that desulphonation of the aromatic moiety was the likely first step in the overall biodegradation of several alkylbenzene sulphonate homologues. 6. The presence of p-hydroxyphenylpropionate, p-hydroxybenzoate and 3,4-dihydroxybenzoate in cells after growth on several alkylbenzene sulphonate homologues containing an odd number of carbon atoms in the side chain was confirmed by g.l.c. and t.l.c. analysis. Cells grown on several homologues containing an even number of carbon atoms in the side chain were shown to contain p-hydroxyphenylacetate and 3,4-dihydroxyphenylacetate. 7. The aromatic nucleus obtained from undecylbenzene-p-sulphonate was further metabolized by an oxidation sequence involving an ;ortho-cleavage' route. 8. An overall metabolic pathway for the biodegradation of various alkylbenzene sulphonate homologues by this Bacillus species is proposed.
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PMID:Microbial metabolism of alkylbenzene sulphonates. Bacterial metabolism of undecylbenzene-p-sulphonate and dodecylbenzene-p-sulphonate. 434 74

1. Oxygen consumption was measured by means of an O2 electrode in mitochondrial suspensions from riboflavin-deficient and pair-fed control rats, using six different substrates. Whereas consumption of O2 by glutamate was only slightly depressed in mitochondria from deficient animals, the consumption of O2 by hexanoate and by palmitoyl-L-carnitine was depressed to approximately half the control value: a highly significant difference. A comparable magnitude of depression was observed for stearoyl-, oleoyl-, and linoleoyl-L-carnitine. There were no major or consistent differences between groups of animals receiving two different types, and two different levels, of fat in their diet. 2. The activity of acyl coenzyme A dehydrogenase (EC 1.3.99.3) in hepatic mitochondrial fragments, measured by cytochrome c reduction with palmitoyl-coenzyme A as substrate, and expressed as maximum velocity (Vmax) with respect to phenazine methosulphate, was also reduced to approximately half the control value in deficient animals. 3. In hepatic microsomes, cytochrome b5 reductase (EC 1.6.2.2) activity was unaffected by riboflavin deficiency, although NADPH-cytochrome c reductase (EC 1.6.2.4) and microsomal flavin content were diminished to approximately half the control values. Acyl CoA (delta 9) desaturase activity (EC 1.14.99.5) was virtually identical in deficient, pair-fed, and ad lib.-fed control groups. 4. It is concluded that the depression of mitochondrial beta-oxidation of fatty acids which is observed in riboflavin-deficient animals is not a secondary result of inanition, and may account for the observed changes in fatty acid profiles of triglycerides and phospholipids. Failure of the microsomal fatty acid desaturation system is less likely to be a major consequence of riboflavin deficiency.
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PMID:Lipid metabolism in riboflavin-deficient rats. 2. Mitochondrial fatty acid oxidation and the microsomal desaturation pathway. 708 27