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CoQ10 protects heart from age-related oxidative stress
Spanish researchers reported in the August 2005 issue of the Gerontological Society of America’s Journal of Gerontology: Biological Sciences that coenzyme Q10 (coQ10) protects against age-related oxidative stress and improves mitochondrial function in rats given diets rich in polyunsaturated fatty acids. Polyunsaturated fatty acids have been shown to benefit cardiovascular disease by improving lipid profiles and reducing arrhythmias, however they are highly susceptible to free radical attack, which increases oxidative damage in the bodies of those consuming them.
Julio Ochoa and colleagues from the University of Granada gave 120 rats a diet that provided 61 percent of its total fatty acid content as polyunsaturated fatty acids, and supplemented some of them with 0.7 milligrams per kilogram coQ10 per day. Twenty animals from each group were examined at 6, 12 and 24 months of age, which correspond to young adulthood, middle age and old age in the rat.
Dietary intake and body weight were similar for both groups at all age points examined. Not surprisingly, supplementation with coQ10 led to higher heart mitochondrial levels of the nutrient at 12 and 24 months of age. Heart mitochondrial hydroperoxide levels, a measure of lipid peroxidation, were lower in both groups at 6 months than at 12 and 24 months, which, according to the authors, is consistent with the free radical theory of aging, however, hydroperoxide levels were higher in the rats who did not receive coQ10 at all ages than in those who received the supplemented diets. While both groups had the highest hydroperoxide values at 12 months of age, in the nonsupplemented rats, the value stayed relatively the same until 24 months but in the supplemented older group the level dropped to almost that of the nonsupplemented rats at 6 months.
Cardiac mitochondrial vitamin E levels were higher in animals supplemented with coQ10 at 6 and 12 months than in those not supplemented. When the research team tested mitochondrial membranes derived from older animals by exposing them to a free radical generator in vitro, they found that those derived from supplemented animals were more resistant to oxidative damage.
In addition, the body’s naturally produced antioxidant enzyme glutathione peroxidase showed greater activity at 6 months, and another antioxidant enzyme, catalase, showed greater activity at 24 months in rats who received coQ10 than in animals who did not receive the supplement.
The authors suggest that “previously reported positive effects of coQ10 supplementation on mean and maximal life span of rats fed a PUFA-rich diet might be a consequence, at least in part, of a lower oxidative stress level and perhaps, to a minor extent, to a smaller decrease in mitochondrial function.”
The following examples exemplify the breadth of CoQ10's credits:
Coenzyme Q10: New applications for cancer therapy, by Christie Yerby, ND
Interest in CoQ10’s therapeutic uses can be traced as far back as 1957, when it was first identified by Frederick Crane, PhD. In the 1960s, Peter D. Mitchell, PhD, discovered that CoQ10 produces energy at the cellular level, work that would eventually earn him a Nobel Prize in Chemistry in 1978. In the early 1980s, Karl Folkers, PhD, director of the Institute for Biochemical Research at the University of Texas, and Peter H. Langsjoen, MD, FACC, began studying CoQ10. In 1983, seven years before Folkers received the National Medal of Science in recognition of his work, the Life Extension Foundation announced CoQ10’s potential benefits for health disorders ranging from neurological aging to heart disease, and drew attention to numerous clinical studies demonstrating its safety.
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