doi:10.1093/qjmed/hch089 Commentary

Increased oxidative stress in diabetes mellitus may underlie the development of endothelial cell dys-function by decreasing the availability of nitric oxide (NO) as well as by activating pro-inflamma-tory pathways. In the arterial wall, redox imbalance and oxidation of tetrahydrobiopterin (BH4) uncou-ples endothelial nitric oxide synthase (eNOS). This results in decreased production and increased con-sumption of NO, and generation of free radicals, such as superoxide and peroxynitrite. In the mito-chondria, increased redox potential uncouples oxidative phosphorylation, resulting in inhibition of electron transport and increased transfer of electrons to molecular oxygen to form superoxide and other oxidant radicals. Coenzyme Q10 (CoQ), a potent antioxidant and a critical intermediate of the elec-tron transport chain, may improve endothelial dys-function by ‘recoupling ’ eNOS and mitochondrial oxidative phosphorylation. CoQ supplementation may also act synergistically with anti-atherogenic agents, such as fibrates and statins, to improve endotheliopathy in diabetes