SOME PREVALENT BIOMOLECULES AS DEFENSES AGAINST SINGLET OXYGEN DAMAGE

Abstract— We have compared the relative abilities of some putative biological protectors to block oxidation of 2,5‐bis(hydroxymethyl)furan (BHMF)† in illuminated solutions containing the photosensitizer rose bengal and in the separated‐surface‐sensitizer (S‐S‐S) system involving pure singlet oxygen ( 1 ΔA g O 2 ). While L‐histidine is a well‐known quencher of singlet oxygen, free L‐histidine is not commonly found in high concentrations in nature. L‐Carnosine (β‐alanyl‐L‐histidine), however, is present in the striated muscles of many organisms, most notably mammals, in concentrations up to 40 m M . At neutral pH, carnosine quenched singlet oxygen more effectively than did equimolar histidine, both in solubilized sensitizer studies and in the S‐S‐S system. In the pure singlet oxygen system, 1 m M carnosine reduced the rate of BHMF oxidation as effectively as 3 m M histidine alone, or a mixture of 3 mM histidine and 3 m M β‐alanine. The fungal product L‐ergothioneine (2‐thiol‐L.‐histidine betaine) and its synthetic analogue, 2‐thiolhistidine, at 1 m M blocked photosensitized BHMF oxidation using solubilized rose bengal, as did urate at 0.5 m M . All three compounds failed to reduce the rate of BHMF oxidation by singlet oxygen in the S‐S‐S system, however. Homocarnosine (‐γ‐aminobutyryl‐L‐histidine) gave levels of protection against BHMF oxidation identical to histidine, but is present in the central nervous system only at micromolar concentrations. Neither 1 m M imidazole nor 5 m M urea reduced BHMF oxidation in either system. We conclude that some prevalent biomolecules may afford protection either by preventing singlet oxygen production (urate, L‐ergothioneine) or by intercepting singlet oxygen once formed (L‐carnosine). Such protective devices may be of importance in natural systems.