15678-54-3

Upstream product

• 7235-40-7 beta-carotene 
• 1923-89-3 5,6-epoxy-5,6-dihydro-β,β-carotene 

Downstream Products

• 7488-99-5 alpha-carotene 

Relevant academic research and scientific papers

Preparation and structure elucidation by NMR of the charge delocalised β,β-carotene dication

The β,β-carotene dication (λmax 985 nm at room temperature) prepared by treatment of β,β-carotene with BF3-etherate had considerable stability. The reaction, monitored by EPR studies at -25°C, occurred by free radical intermediates. EIMS further revealed a C40H56BF3 intermediate. The detailed structure of the charge delocalised β,β-carotene dication was established by COSY, HSQC, HMBC and 1D and 2D ROESY NMR techniques (600 MHz, CDCl3, -25°C) leading to complete assignments of 1H and 13C chemical shifts and 3JH,H coupling constants. Considerable downfield shifts were observed relative to β,β-carotene. The results are consistent with charge delocalisation mainly in the C-5-C-9 and C-5′-C-9′ regions and with retro shifted double bonds in the central C-13-C-13′ region. The effect of the two delocalised charges on chemical shift (charge distribution) and bond distance (3JH,H) is discussed.

Reactions of beta-carotene with cigarette smoke oxidants. Identification of carotenoid oxidation products and evaluation of the prooxidant/antioxidant effect.

Recent intervention trials reported that smokers given dietary beta-carotene supplementation exhibited an increased risk of lung cancer and overall mortality. beta-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 beta-carotene in model systems. Both whole smoke and gas-phase smoke oxidized beta-carotene in toluene to several products, including carbonyl-containing polyene chain cleavage products and beta-carotene epoxides. A major product of the reaction was identified as 4-nitro-beta-carotene, which was formed by nitrogen oxides in smoke. Both cis and all-trans isomers of 4-nitro-beta-carotene were detected. The hypothesis that smoke-driven beta-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 % beta-carotene. Both the lipid soluble antioxidant alpha-tocopherol and the water soluble antioxidant ascorbate were oxidized more slowly by gas-phase smoke exposure in liposomes containing beta-carotene. These data indicate that beta-carotene exerts weak antioxidant effects against smoke-induced oxidative damage in vitro. It is unlikely that a prooxidant effect of beta-carotene occurs under biologically relevant conditions or is responsible for an increased incidence of lung cancer observed in smokers who consume beta-carotene supplements.