Many people have believed that mitochondrial biogenesis could only happen from strenuous exercise or extreme calorie restriction.
Researchers found in 2010 that PQQ could protect mitochondria from oxidative damage and also stimulate growth of new mitochondria.
Variations of the levels of PQQ in diets cause modulation in mitochondrial content.
PQQ also interacts with PGC-1alpha which regulates many of the mitochondrial-related events which regulate genes involved in energy metabolism, blood pressure and also muscle fibre type.
PGC-1alpha is also associated with a reduction in free radicals and acts as a protectant against various mitochondrial toxins.
PQQ has been shown to affect:
- Activity of ras gene (involved in cell signalling pathways that control cell growth & cell death
- Activates mitochondrial transcription factors which lead to increase mitochondrial biogenesis
- Activates other transcription factors (proteins involved in the process of converting, or transcribing DNA into RNA) such as NRF 1 & 2
Under the right conditions, PQQ can carry out the redox cycle continuously - capable of thousands of redox reactions.
Why is PQQ’s redox capabilities significant?
In comparison with other bioactive quinones such as epicatechin in green tea which tend to self-oxidise (run out of steam) or form polymers such as tannins making them redundant for further redox reactions, PQQ can keep going back for more.
Improving the number of mitochondria and their efficiency in our cells can have far-reaching benefits such as a longer life or better energy.
And it appears that PQQ plays a significant part in as an essential cofactor in one of the many protein subunits that make up Complex I of the ETC.
This is important to know because nearly all of the endogenous (growing or originating within the organism) free radicals are produced at Complex I.
A study in mice showed that a PQQ-free diet led to impaired reproductive and immune function with the growth of the mice being impaired.
More importantly, PQQ-deficient mice had 30% - 40% fewer mitochondria and the mitochondria they did have was abnormally small or appear to function properly.