Coenzyme Q₁₀ Protects the Aging Heart against Stress

Abstract

With aging of the population, increasing numbers of elderly patients are presenting for cardiac surgery. However, the results in the elderly are inferior to those in the young. A likely contributing factor is an age-related reduction in cellular energy production in the myocardium during surgery, which is known to induce aerobic and ischemic stress. The lipophilic antioxidant and mitochondrial respiratory chain redox coupler, coenzyme Q10 (CoQ10), has the potential to improve energy production in mitochondria by bypassing defective components in the respiratory chain as well as by reducing the effects of oxidative stress. We hypothesized that CoQ10 pretreatment prior to stress could improve the recovery of the myocardium after stress.

Coenzyme Q10 Status as a Determinant of Muscular Strength in Two Independent Cohorts

“…The relationship of obesity and health and CoQ 10 as a major lipophilic antioxidant and mitochondrial respiratory chain redox coupler [39] is currently a matter of debate. Recently, the impact of aging, BMI and physical capacity on the CoQ 10 levels in human blood was investigated [8].…”

Age-related decline in mitochondrial bioenergetics: Does supercomplex destabilization determine lower oxidative capacity and higher superoxide production?

“…An age-related decline in coenzyme Q, a key isoprene-derivative that mediates electron transfer between several IMM protein complexes, has been observed in plasma [87] and also in cardiac muscle from human subjects [88, 89]. In addition, tissue levels of coenzyme Q appear to decline in heart, kidney, and skeletal muscle from aged rats [90].…”

Dietary supplementation with essential amino acids boosts the beneficial effects of rosuvastatin on mouse kidney

“…Mitochondrial mechanisms have been repeatedly implicated, particularly in muscle damage (Golomb and Evans 2008). Statins lead to dose-dependent reductions in coenzyme Q 10 (De Pinieux et al 1996), a key mitochondrial antioxidant and electron transport carrier that can bypass existing mitochondrial respiratory chain defects (Rosenfeldt et al 2002). Several studies demonstrate that statins predispose to mitochondrial defects (Gambelli et al 2004; Schick et al 2007) in all users and, to a greater degree, in vulnerable individuals.…”