ABSTRACT
Coenzyme Q10, an essential cofactor of mitochondrial ATP production, was discovered in 1957. Coenzyme Q10 is ubiquitously present in other biomembranes and even in lipoproteins. The reduced form of coenzyme Q10 (ubiquinol10) is believed to work as an antioxidant in these locations. When human plasma was incubated under aerobic conditions, ubiquinol-10 depleted after the depletion of ascorbate, but
α-tocopherol remained unchanged, indicating that ascorbate and ubiquinol-10 are frontline antioxidants against oxygen radicals. The redox status of plasma coenzyme Q10 is a good indicator of oxidative stress, oxidative stress being defined as a disturbance in the pro-oxidant-antioxidant balance in favor of the former. We, therefore, developed a simple and reliable method for the simultaneous detection of both oxidized and reduced forms of coenzyme Q10 and measured their plasma levels in nine patients who were treated with percutaneous transluminal coronary angioplasty (PTCA) after a heart attack. Plasma samples were collected on hospitalization and at various times (0, 4, 8, 12, 16, and 20 h; and 1, 2, 3, 4, and 7 d) after the PTCA. The percentage of the oxidized form of coenzyme Q10 in the total coenzyme Q10 (%CoQ10) before and immediately after PTCA were 9.9 ± 2.8 and 11.4 ± 2.0, respectively, reached a maximum (20 to 45) 1 or 2 d later, and decreased to 7.9 ± 2.7 at 7 d after PTCA, indicating an increase in oxidative stress in patients during coronary reperfusion.
