The Mitochondria in Heart Failure: A Target for Coenzyme Q10 Therapy?

The developmental effects of pentachlorophenol on zebrafish embryos during segmentation: A systematic view

“…We noticed that in complex II, an alternative of complex I that shares part of the ETC and the citric acid cycle, two hydrophobic subunits, sdhc and sdhd , which transferred the electrons to ubiquinone (coenzyme Q10), were downregulated after exposure, while two hydrophilic subunits, sdha and sdhb , which have no Q10 pool, were unaffected. The extensive therapeutic roles of Q10 in cancer, male infertility, heart failure, and other pathologies have been highlighted recently 15 16 17 , findings that may indicate underlying correlations between metabolism and chemical toxicity/diseases. OXPHOS often opposes glycolysis and hypoxia/HIF1α, particularly in cancer studies 18 19 ; however, in our experiments, they were not strongly correlated.…”

Should Administration of Coenzyme Q10 Be Recommended to Patients with Congestive Heart Failure?

“…Although the hypothesis was not confirmed in a systematic review, 12 preliminary studies have shown improvements in pain scores after taking CoQ 10 In their Point piece, Mortensen and Mortensen conclude that future official society guidelines for treating patients with congestive heart failure (CHF) should recommend the administration of coenzyme Q10 (CoQ 10 ). 1 Presumably this means a dose of 100 mg three times a day, the dose in the Q-SYMBIO study by Mortensen et al 2 I agree with the Mortensens that numerous inadequately controlled clinical studies have claimed efficacy and safety of CoQ 10 in heart failure. In addition, two double-blind randomized placebo-controlled studies have shown remarkable efficacy for this supplement.…”

“…In their Point piece, Mortensen and Mortensen conclude that future official society guidelines for treating patients with congestive heart failure (CHF) should recommend the administration of coenzyme Q10 (CoQ 10 ) 1 . Presumably this means a dose of 100 mg three times a day, the dose in the Q‐SYMBIO study by Mortensen et al 2…”

Mitochondria-Accessing Ratiometric Fluorescent Probe for Imaging Endogenous Superoxide Anion in Live Cells and Daphnia magna

“…Superoxide anion radical (O 2 •– ) is one of the potent effector molecules and intracellular messengers. , Generally, only considerably less than 1–2% of consumed oxygen molecules undergo the conversion to superoxide anion at two discrete points (Complex I and Complex III) in mitochondrial respiratory chain. − And the diffusing superoxide anion in biological systems is typically converted to other ROS like hydrogen peroxide, , peroxynitrite as well as perhydroxyl redical , within a few tens of micrometers after leaving its generation sites. , Accordingly, superoxide anion can directly or indirectly regulate innate immune defense against invading organisms and trigger various signaling pathways in cellular growth and metabolism. , Despite the low concentration and short diffusion distance (or short lifetime), superoxide anion at excessive levels was suggested to induce increasing oxidative stress and mitochondrial dysfunction implicated in Alzheimer’s disease, rheumatoid arthritis, heart disease, diabetes mellitus, and even cancer. − Hence, in suit specific tracking and measurement of superoxide anion in complex biological systems can be meaningful for elucidating the exact pathogenesis of related diseases.…”