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quenched effectively by the in vitro addition of free radical scavengers, e.g. butyl hydroxytoluene, d-ƒ¿-tocopherol and 2, 5-diphenylfuran, while super oxide dismutase, catalase and D-manmtol gave only negligible inhibitions on AOLO-induced liver CL. The luminescence spectrum recorded by a filter spectral analyzing method gave definitive two emission peaks at 585 and 635 nm and broad emission band around 500-560nm. The spectrum was similar to that reported for a singlet molecular oxygen. In the experiment of successive AOLO administration (0.3ml/rat/day) for 10 days, a large increase in CL intensities and TBA reactants in various tissues was observed, especially on the 2nd day to the 6th day of feeding. Among them, the enhancement of CL and the accumulation of TBA reactants in liver and kidney were inhibited significantly by the oral administration of supplemental d-ƒ¿-tocopherol (5mg/rat/day). These re sults suggest that AOLO-induced tissue spontaneous CL originated in the occurrence of free radical species which are possibly derived from chain reactions of tissue lipid peroxidation caused by the AOLO administration to rats.

Characteristics of tissue ultraweak chemiluminescence in rats fed with autoxidized linseed oil.