A general and efficient copper catalyst for the amidation of aryl halides
Abstract
Recent intervention trials reported that smokers given dietary β-carotene supplementation exhibited an increased risk of lung cancer and overall mortality. β-Carotene has been hypothesized to promote lung carcinogenesis by acting as a prooxidant in the smoke-exposed lung. We have examined the interactions of cigarette smoke with β-carotene in model systems. Both whole smoke and gas-phase smoke oxidized β-carotene in toluene to several products, including carbonyl-containing polyene chain cleavage products and β-carotene epoxides. A major product of the reaction was identified as 4-nitro-β-carotene, which was formed by nitrogen oxides in smoke. Both cis and all-trans isomers of 4-nitro-β-carotene were detected. The hypothesis that smoke-driven β-carotene autoxidation exerts prooxidant effects was tested in a liposome system. Lipid peroxidation in dilinoleoylphosphatidylcholine liposomes exposed to gas-phase smoke was modestly inhibited by the incorporation of 0.1 mol % β-carotene. Both the lipid soluble antioxidant a-tocopherol and the water soluble antioxidant ascorbate were oxidized more slowly by gas-phase smoke exposure in liposomes containing β-carotene. These data indicate that β-carotene exerts weak antioxidant effects against smoke-induced oxidative damage in vitro. It is unlikely that a prooxidant effect of β-carotene occurs under biologically relevent conditions or is responsible for an increased incidence of lung cancer observed in smokers who consume β-carotene supplements. © 1999 American Chemical Society.
Publication Title
Journal of the American Chemical Society
Recommended Citation
Baker, D., Krol, E., Jacobsen, N., & Liebler, D. (2002). A general and efficient copper catalyst for the amidation of aryl halides. Journal of the American Chemical Society, 124 (25), 7421-7428. https://doi.org/10.1021/ja0260465
