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(2)) diffusion. During normal eukaryote cellular energy synthesis O(2) 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(2) 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(2) 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(2). 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.