The radical cation generated during photobleaching of β-carotene is scavenged efficiently by the anion of methyl salicylate from wintergreen oil in a second-order reaction approaching the diffusion limit with k2 = 3.2 × 109 L mol−1 s−1 in 9:1 v/v chloroform–methanol at 23 °C, less efficiently by the anion of salicylic acid with 2.2 × 108 L mol−1 s−1, but still of possible importance for light-exposed tissue. Surprisingly, acetylsalicylate, the aspirin anion, reacts with an intermediate rate in a reaction assigned to the anion of the mixed acetic–salicylic acid anhydride formed through base induced rearrangements. The relative scavenging rate of the β-carotene radical cation by the three salicylates is supported by DFT-calculations.

Giant unilamellar vesicles of soy phosphatidylcholine are found to undergo budding when sensitized with chlorophyll a ([phosphatidylcholine] :[chlorophyll a] = 1500:1) under light irradiation (400–440 nm, 16 mW mm−2). ‘Entropy’ as a dimensionless image heterogeneity measurement is found to increase linearly with time during an initial budding process. For β-carotene addition ([phosphatidylcholine]:[β-carotene] = 500:1), a lag phase of 23 s is observed, followed by a budding process at an initial rate lowered by a factor of 3.8, whereas resveratrol ([phosphatidylcholine]:[resveratrol] = 500:1) has little if any protective effect against budding. However, resveratrol, when combined with β-carotene, is found to further reduce the initial budding rate by a total factor of 4.7, exhibiting synergistic antioxidation effects. It is also interesting that β-carotene alone determines the lag phase for the initiation of budding, while resveratrol supports β-carotene in reducing the rate of the budding process following the lag phase; however, it alone has no observable effect on the lag phase. Resveratrol is suggested to regenerate β-carotene following its sacrificial protection of unsaturated lipids from oxidative stress, modeling the synergistic effects in cell membranes by combinations of dietary antioxidants.

Green tea polyphenols, (−)-epicatechin (EC), (−)-epigallocatechin (EGC), (−)-epicatechin gallate (ECG), and (−)-epigallocatechin gallate (EGCG), all showed antioxidative effect in liposomes for lipid oxidation initiated in the lipid phase (antioxidant efficiency EC > EGCG > ECG > EGC) or in the aqueous phase (EC ≫ EGC > EGCG > ECG) as monitored by the formation of conjugated dienes. For initiation in the lipid phase, β-carotene, itself active as an antioxidant, showed antagonism with the polyphenols (EC > ECG > EGCG > EGC). The Trolox equivalent antioxidant capacity (TEAC EGC > EGCG > ECG > EC) correlates with the lowest phenol O–H bond dissociation enthalpy (BDE) as calculated by density functional theory (DFT). Surface-enhanced Raman spectroscopy (SERS) was used to assess the reducing power of the phenolic hydroxyls in corroboration with DFT calculations. For homogeneous (1:9 v/v methanol/chloroform) solution, the β-carotene radical cation reacted readily with each of the polyphenol monoanions (but not with the neutral polyphenols) with a rate approaching the diffusion limit for EC as studied by laser flash photolysis at 25 °C monitoring the radical cation at 950 nm. The rate constant did not correlate with polyphenol HOMO/LUMO energy gap (DFT calculations), and β-carotene was not regenerated by an electron transfer reaction (monitored at 500 nm). It is suggested that the β-carotene radical cation is rather reacting with the tea polyphenols through addition, as further evidenced by steady-state absorption spectroscopy and liquid chromatography–mass spectroscopy (LC-MS), in effect preventing regeneration of β-carotene as an active lipid phase antioxidant and leading to the observed antagonism.