Co-enzyme Q10, a vitamin-like natural compound you can buy as a supplement from the drugstore, has a life extending effect. In 2004 researchers at Tokai University, Japan, reported in Mechanisms of Ageing and Development that microscopic roundworms live longer if Q10 is mixed with their food. The substance prevents aggressive molecules from being released during metabolic processes at cell level.
Q10 [chemical structure shown below] is produced by the body’s cells, but we also get it from eating animal products. A Q10 molecule looks like a thumbtack. The cell pushes the point into the membranes of the mitochondria, the cellular power packs that convert food into energy.
The head of the thumbtack collects electrical charges that are released during the processes of combustion and passes them on. In this way Q1 prevents the electrical charges – in the form of free radicals – from damaging the cell, and also makes sure that the mitochondria produce energy.
As cells age they produce less Q10. There are also signs that young organisms produce less Q10 when under conditions of stress.
The researchers added Q10 to food of the roundworms Caenorhabditis elegans, a favourite lab animal among fundamental researchers. The Japanese used ordinary roundworms [N2] and a variant in which the gene for an endogenous antioxidant system was not functioning properly [mev-1]. The defective gene stops the electrical charges from being transferred correctly to the Q10 thumbtacks. As a result, the mev-1 roundworms age prematurely.
If you add 150 mcg Q10 to 1 ml nutrient medium, the mev-1 roundworms live just as long as the non-defective roundworms. Actually, the ordinary roundworms also live longer.
The process of energy generation in the mitochondria takes four steps, each of which involves a complex of enzymes. In the mev-1 roundworms the problem occurs in step 2, or more exactly: in complex 2. When the researchers stimulated complex 1, they observed that Q10 supplementation had no effect. When they repeated the procedure with complex 2 [B], there was an effect.
The figure shows the production of superoxide anions. This increases in the mev-1 roundworms that got no Q10. Vitamin E supplementation does nothing to change this, but Q10 does. But the researchers do not know what the mechanism through which Q10 causes ordinary roundworms to live longer.
“CoQ supplementation can significantly extend the life span of Caenorhabditis elegans”, the Japanese conclude. “The reduction in superoxide anion levels with supplementation suggests that life span extension is the consequence of reduced oxidative stress in mitochondria.”
Researchers in Canada are experimenting with a mix of life-extending components, which has extended the lifespan of mice by 11 percent. That’s a lot. It’s more difficult to extend the lifespan of a mammal by adding substances to its diet, than it is with roundworms or fruit flies. The Canadian mixture includes Ginkgo biloba, ginseng, n-3 fatty acids, melatonin – and co-enzyme Q10.
Coenzyme Q10 can prolong C. elegans lifespan by lowering oxidative stress.
The mev-1 gene encodes cytochrome b, a large subunit of the Complex II enzyme succinate-CoQ oxidoreductase. The mev-1(kn1) mutants are hypersensitive to oxidative stress and age precociously, probably because of elevated superoxide anion production in mitochondria. Coenzyme Q (CoQ) is essential for the mitochondrial respiratory chain. Here, we show that CoQ(10) and Vitamin E extended the life span of wild-type Caenorhabditis elegans. Conversely, only CoQ(10) recovered the life shortening effects seen in mev-1. We also show that CoQ(10) but not Vitamin E reduced superoxide anion levels in wild type and mev-1. Another previously described phenotype of mev-1 animals is the presence of supernumerary apoptotic cells. We now demonstrate that CoQ(10) (but not Vitamin E) suppressed these supernumerary apoptoses. Collectively these data suggest that exogenously supplied CoQ(10) can play a significant anti-aging function. It may do so either by acting as an antioxidant to dismutate the free radical superoxide anion or by reducing the uncoupling of reactions during election transport that could otherwise result in superoxide anion production. The latter activity has not been ascribed to CoQ(10); however, it is known that conditions that uncouple electron transport reactions can lead to elevated superoxide anion production.
PMID: 14706236 [PubMed – indexed for MEDLINE]