Previously, we demonstrated an inverse correlation between CoenzymeQ10 (CoQ10) and thyroid hormones, suggesting its usefulness as index of thyroid hormone tissue effect. A low-T3 syndrome, observed in chronic diseases, is considered an adaptive mechanism and its treatment is still debated. To evaluate the metabolic status of these patients and antioxidant vs energetic role of CoQ10, we studied 32 patients, with chronic obstructive pulmonary disease (COPD), comparing respiratory indexes, thyroid hormones, CoQ10 (also corrected for cholesterol levels) and Total Antioxidant Capacity (TAC) in patients with low (n=12) or normal (n=20) fT3 concentrations. Another low-T3 model was represented by five patients studied after major heart surgery (HS). Twenty-one normal subjects were studied as controls. CoQ10 were assayed by HPLC; TAC was determined using the system metmyoglobin-H2O2, which interacting with the chromogen ABTS generates a radical spectroscopically revealed; the latency time (Lag) in the appearance of radical species is proportional to the antioxidant content. CoQ10/Cholesterol ratio values were significantly higher in COPD with low- vs normal-fT3 (CoQ10: 0.88±0.06 vs 0.83±0.07 μg/ml; CoQ10/Cholesterol 239.7±28.5 vs 185.1±14.0 nmol/mmol, P<0.05); TAC showed opposite pattern (54±6 vs 64±2 s). Similarly in post-surgical cardiac patients, all exhibiting low values of fT3, CoQ10 levels were in the hypothyroid range (CoQ10: 0.97±0.01 μg/ml; CoQ10/Cholesterol: 216.6±3.85 nmol/mmol) despite the fact cardiac diseases are well known to be associated with low CoQ10.
These data suggest that low fT3 levels are accompanied by indexes of true hypothyroidism in COPD and HS, supporting the need for replacement therapy. The different TAC pattern suggests that elevated CoQ10, despite oxidative stress, expresses a reduced tissue utilization.