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A metabolic model of the mitochondrion and its use in modelling diseases of the tricarboxylic acid cycle

Anthony C Smith and Alan J Robinson*

BMC Systems Biology 2011, 5:102  doi:10.1186/1752-0509-5-102

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Exogenous inhibitors of succinate dehydrogenase

Heikki Savolainen   (2011-07-25 17:45)  Dept. of Occup.Safety & Hlth., Tampere, Finland email

Dear Editor,

The model on mitochrondrial roles summarizes excellently the metabolic aspects (1). It may be added that inhibitors of succinate dehydrogenase activity can cause direct toxicity to highly oxygen dependent organs. The classical example is 3-niropropanoic acid with cerebral effects.

The alkoxyacetic acids, metabolites of ethylene glycol ethers, are another example. They inhibit in experimental (2) and clinical studies (3) the enzyme activity which should according to the current model contribute to the risk of malignant diseases associated with exposure to them.

1 Smith AC, Robinson AJ. A metabolic model of the mitochondrion and its use in modelling diseases of the tricarboxylic acid cycle. BMC Systems Biol 2011; 5: 102

2 Savolainen H. Glial cell toxicity of ethyleneglycol monomethylether vapor. Environ Res 1980; 22: 423

3 Laitinen J, Liesivuori J, Turunen T, Savolainen H. Urinary biochemistry in occupational exposure to glycol ethers. Chemosphere 1994; 29: 781

Competing interests

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