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PQQ Effects on Cell Growth and New Mitochondria

Mitochondria can produce damaging reactive oxygen species (ROS) as a by-product of normal function. Over time, ROS degrade mitochondrial DNA (mtDNA), interfering with cellular energy production. When a cell loses mitochondria, eventually apoptosis or cell death can occur. Most cell’s strategy for dealing with damage is to “recycle” or turnover mitochondria on a regular basis.

Mitochondria replicate more often than the cells in which they live. In small animals, this occurs between one and a half to three days in liver cells, and two to four weeks in mature brain cells. Generally, the faster the mitochondria turn over, the better. In other words, it is better to replace mitochondria before too much mtDNA damage accumulates. Regarding turnover, the best data science has is related to caloric restriction. Studies have shown that calorie restriction speeds mitochondrial turnover (e.g., if calories are not used, less need fo mitochondria). In contrast, exercise slows mitochondrial turnover and appears to promote mitochondriogenesis. Appreciate, however, that these changes are not huge. A change as little as 5 to15 percent can be dramatic from a normal energy perspective.

So what are the effects from PQQ supplementation and withdrawal?

The only data that we have are from animal studies. Giving rats a supplement of pyrroloquinoline quinone that were previously fed diets devoid of PQQ, increases muscle and liver mitochondria about 10 to 20 percent somewhere between half a day to one and a half days. In contrast, methoxatin depletion causes reversal and multiple gene changes in about one to two days.

With regard to humans, there are ways of scaling data from rats to humans. Using those procedures, our best guess is that the withdrawal response in humans from a typical pyrroloquinoline quinone supplement (e.g., 10 milligrams) is somewhat rapid, probably within a week. Assuming circumstances short of starvation, the mitochondrial amounts will return to their relative basal levels. We need to clarify this as “relative basal levels” because the level may depend on the degree to which the respective person is exercising or taking other mitochondria stimulating substances.

Comments

John C

The base in the rat experiment was a diet devoid of PQQ. The result is an increase in mitochondria followed by a return to previous levels when pyrroloquinoline quinone is withdrawn. Can these levels be sustained absent PQQ? Is a devoid diet the presumed base of the human analogy or is it a normal diet? Wouldn’t dietary PQQ factor in here somewhere?

Michael Rucker

Dear John C, to be frank it remains to be proven that PQQ is essential in a nutritional context, but what can be said is that relative to very low pyrroloquinoline quinone exposure, PQQ supplementation in animal studies increases mitochondriogenesis. The effect may be exaggerated because of the initially lowered basal mitochondrial levels. However, the exaggeration or amplified response is useful when one is trying to sort out biological mechanisms. From an experimental perspective, the basal levels seemed to be sustained, but whatever happens can be eventually associated with decreased reproductive performance, a weaker immune defense system, and increased susceptibility to inflammation. This is obviously not a “real” life situation wherein there is always some PQQ dietary exposure. What the data tells us is that pyrroloquinoline quinone at very low levels (relative to the pristine background of feeding a nutritional complete, albeit a highly refined, diet) promotes presumably healthful responses.

As it relates to complex diets composed of mixed food ingredients, most of what we know about PQQ and improvements in cognitive functions, immune and antioxidant functions, as well as protecting against cardiac and neurological ischemic events has not involved the use of a truly PQQ-deficient diet for the base line measurements. Thus, one can infer that dietary supplementation (e.g. 3-5 mg PQQ/day or more) should have some kind of positive response.