Antioxidant Treatment

Antioxidant treatments for mitochondrial diseases do look very promising, however, they are also rather confusing.

There is a strange irony in life in that one thing necessary for it - oxygen - also kills us. Oxidation reactions are required for life, but they also produce a thing called free radicals, which begin reactions that damage our cells. An antioxidant is a molecule that can either stop or slow down the rate at which this happens.

Most life, plant and animal alike, have systems with lots of antioxidants - vitim C and E, for example - that do this job. Low levels of any of these allow oxidate stress which damages our cells and, more imporantly for us, our mitochondria.

It is unfortunate, however, that we remain unsure as to whether oxidate damage is a cause or a symptom of mitochondrial disease.

This paradox (ie, that oxidation species are both required by life and also destroy it) leave us in a complicated position. Generally, antioxidant treatments stop these species forming, but because they also have useful functions as well, the treatment must be to keep them at an optimum level, which isn't nearly as simple as stopping them happening entirely.

The precise role of oxidate damage and anti-oxidants in mitochondrial diseases is very difficult to simplify, and is not really of great interest to anyone other than cell biologists - what matters, for our purposes, is that anti-oxidant treatments do appear to have some benefit.

While this area of research is still lacking, it appears that suppliments such as coenzyme Q, and vitamins C and E may have some benefit to many patients, helping to keep the level of oxidation at it's optimum level.

Do not take these suppliments without medical advice. As noted above, too much is just as bad as too little. Very importantly, taking these before proper diagnosis may mask your symptoms, and therefore make it harder to diagnose illness, which is already an exceptionally difficult task with mitochondrial diseases.

In short, a confusing, but promising line of research. If you have your mental climbing boots on, you may find the following links useful:

- A novel neurological phenotype in mice lacking mitochondrial manganese superoxide dismutase

- Calorie restriction induces mitochondrial biogenesis and bioenergetic efficiency

- Higher respiratory activity decreases mitochondrial reactive oxygen release and increases life span in Saccharomyces cerevisiae.