Biology 3466B Lecture 3: CELL-L3
Document Summary
Antioxidants: protect cells/tissues from oxidative stress: catalases, glutathione peroxidase, peroxidase, peroxiredoxins, superoxide, thioredoxin. Oxidative stress: disturbance in pro-oxidant antioxidant balance leading to damage: excess ros, depleted aox (reduce antioxidant activity) Chemistry of hydroxyl in vitro, hydroxyl radicals produced non-enzymatically by radiation induced hemolytic fission (photolytic cleavage) of h20/h2o2 in vivo, hydroxyl radical generated non-enzymatically, in rxn of metal ions. Lipid peroxidation: proceeds by free radical chain rxn lipid peroxides toxic: membrane integrity, fluidity, permeability. Propagation: addition of o2 to generate unstable lipid peroxyl radical that reacts w/another free lipid (produce lipid peroxide) Termination: radical rxn stops when 2 radicals react and produce nonradical species or inactivated by antioxidants. Oxidative damage of nucleic acid: ros/radiation can modify bases producing many products, also induce fragmentation of deoxyribose. Point mutations change in gene expression single/double breaks. Oxidative damage to proteins: modification of aa and functional groups, protein aggregation due to cross-linked reaction fragmentation of peptide chain.