alexa Molybdenum Cofactor and Sulfite Oxidase Deficiency
ISSN: 2153-0769

Metabolomics:Open Access
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Research Article

Molybdenum Cofactor and Sulfite Oxidase Deficiency

Jochen Reiss*

Institute of Human Genetics, University Medicine Göttingen, Germany

*Corresponding Author:
Jochen Reiss
Institute of Human Genetics, University Medicine Göttingen, Germany
Tel: 495513912926
E-mail: mailto:[email protected]

Received date: August 04, 2016; Accepted date: August 31, 2016; Published date: September 05, 2016

Citation: Reiss J (2016) Molybdenum Cofactor and Sulfite Oxidase Deficiency. Metabolomics (Los Angel) 6:184. doi: 10.4172/2153-0769.1000184

Copyright: © 2016 Reiss J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

A universal molybdenum-containing cofactor is necessary for the activity of all eukaryotic molybdoenzymes. In humans four such enzymes are known: Sulfite oxidase, xanthine oxidoreductase, aldehyde oxidase and a mitochondrial amidoxime reducing component. Of these, sulfite oxidase is the most important and clinically relevant one. Mutations in the genes MOCS1, MOCS2 or GPHN - all encoding cofactor biosynthesis proteins - lead to molybdenum cofactor deficiency type A, B or C, respectively. All three types plus mutations in the SUOX gene responsible for isolated sulfite oxidase deficiency lead to progressive neurological disease which untreated in most cases leads to death in early childhood. Currently, only for type A of the cofactor deficiency an experimental treatment is available.

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