Advancements in Free-Radical Pathologies and an Important Treatment Solution with a Free-Radical Inhibitor

Unsaturated carbon-carbon double bonds particularly at exposed end groups of nonsolid fluids are susceptible to free-radical covalent bonding on one carbon atom creating a new free radical on the opposite carbon atom. Subsequent reactive secondary sequence free-radical polymerization can then continue across extensive carbon-carbon double bonds to form progressively larger molecules with ever-increasing viscosity and eventually produce solids. In a fluid solution when carbon-carbon double bonds are replaced by carbon-carbon single bonds to decrease fluidity, increasing molecular organization can interfere with molecular oxygen (O) diffusion. During normal eukaryote cellular energy synthesis O is required by mitochondria to combine with electrons from the electron transport chain and hydrogen cations from the proton gradient to form water. When O is absent during periods of irregular hypoxia in mitochondrial energy synthesis, the generation of excess electrons can develop free radicals or excess protons can produce acid. Free radicals formed by limited O can damage lipids and proteins and greatly increase molecular sizes in growing vicious cycles to reduce oxygen availability even more for mitochondria during energy synthesis. Further, at adequate free-radical concentrations a reactive crosslinking unsaturated aldehyde lipid breakdown product can significantly support free-radical polymerization of lipid oils into rubbery gel-like solids and eventually even produce a crystalline lipid peroxidation with the double bond of O. Most importantly, free-radical inhibitor hydroquinone intended for medical treatments in much pathology such as cancer, atherosclerosis, diabetes, infection/inflammation and also ageing has proven extremely effective in sequestering free radicals to prevent chain-growth reactive secondary sequence polymerization.