Metabolite damage and its repair or pre-emption
Metabolite damage can occur through enzyme promiscuity or spontaneous chemical reactions. Many metabolites are chemically reactive and unstable and can react with other cell components or undergo unwanted modifications. Enzymatically or chemically damaged metabolites are always useless and often toxic. To prevent toxicity that can occur from the accumulation of damaged metabolites, organisms have damage-control systems that:
Damage-control systems can involve one or more specific enzymes.
Similarly to DNA and proteins, metabolites are prone to damage, which can occur chemically or through enzyme promiscuity. Much less is known about metabolite damage than about DNA and protein damage, in part due to the huge variety and number of damage-prone metabolites.
Many metabolites are chemically reactive and unstable, and thus prone to chemical damage. In general, any reaction that occurs in vitro under physiological conditions can also occur in vivo. Some metabolites are so reactive that their half-life in a cell is measured in minutes. For example, the glycolytic intermediate 1,3-bisphosphoglyceric acid has a half-life of 27 minutes in vivo. Typical types of chemical damage reactions that can occur to metabolites are racemization, rearrangement, elimination, photodissociation, addition, and condensation.
Although enzymes are generally specific towards their substrate, enzymatic side activities (enzyme promiscuity) can lead to toxic or useless products. These side reactions proceed at much lower rates than their normal physiological reactions, but build-up of damaged metabolites can still be significant over time. For example, the mitochondrial malate dehydrogenase reduces alpha-ketoglutarate to L-2-hydroxyglutarate 107 times less efficiently than its regular substrate oxaloacetate, but L-2-hydroxyglutarate can still accumulate to several grams per day in a human adult.
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