A telomere is a region of repetitive DNA at the end of a chromosome. Telomeres protect the ends of a given chromosome’s DNA from deterioration (although the shortening of chromosome telomeres normally occurs during chromosome replication). All cells that make up tissues undergo some degree of turnover (replication and apoptosis, i.e. programmed cell death). Cells are more easily destroyed when their telomeres are shortened, compromised, or defective. Some cells have ways, however, of evading normal programmed destruction and replacement. During replication, telomeres lose some of their genetic material but are repaired by an enzyme, telomerase. Some cancer cells maintain their telomeres and become so-called “immortalized” because of differences in telomere maintenance or the relative expression of telomerase levels.
Likewise, mitochondrial integrity is linked to apoptosis. There is little evidence, however, that directly links telomere integrity and telomerase activity to mitochondriogenesis or mitochondrial turnover. Telomere truncation and a reduction in cellular mitochondria, both contribute to apoptosis, but by separate, although coordinated by independent processes. Longer-lived cells often have more
With regard to PQQ, to the extent that pyrroloquinoline quinone can stimulate mitochondriogenesis, then one may speculate that PQQ may slow aging. If true, a likely mechanism is better control of maintaining reactive oxygen species (ROS), which can affect many aspects of cellular activity. Does PQQ affect telomere integrity? This question has not been specifically examined, but in one large gene array experiment using a rodent model (Biochem J.  429:515-26), no specific modulation of telomere-related proteins were detected. Mitochondria-related ROS modulation, however, might have an indirect
With regard to Coenzyme Q or ubiquinone, the primary effect is on the electron transport chain and aerobic cellular respiration. Ninety-five percent of the human body’s energy is generated this way and involves CoQ10. Tissues with high energy requirements usually have higher CoQ10 concentrations. It has been shown levels of CoQ10 seem to correlate with ROS production. Low dosages of CoQ10 reduce cellular ROS levels and DNA double-strand breaks (note – a different process than telomere maintenance). With this said, however, CoQ10 supplementation only has been associated with increased lifespan in mice or rats with very mixed results. The take-home message here is that for a defined response, if an organism has enough of a given substance taking more (of that substance) may not have an effect (and in some cases have an adverse adverse effect).
With regard to “feeling” better or worst in response to a supplement or change in a diet or activity – the answer is always a relative one. It is always important to ask – what are the thresholds that I am trying to achieve? If it is protection from disease or optimizing cellular maintenance, you may not know the answer until the end of life. Some times the best we can do is infer that the effects will be positive based on the scientific data available at the time.