Oxygen- or organic hydroperoxide-induced chemiluminescence of brain and liver homogenates

Abstract

Oxygenation and anaerobically isolated [rat] brain and liver homogenates is associated with chemiluminescence and formation of lipid hydroperoxides, the latter determined by the thiobarbituric acid assay. Light emission and formation of malonaldehyde are 20-fold higher in brain than in liver; chemiluminescence of both decays when accumulation of malonaldehyde ceases. Exogenous organic peroxides, such as tert-butyl hydroperoxide, inhibit the light-emission response to oxygenation by brain homogenate, whereas they enhance that of liver homogenate. tert-Butyl hydroperoxide-induced photoemission of liver homogenate shows a polyphasic kinetic pattern that is O2-dependent. The spectral analysis of chemiluminescence arising from brain and liver homogenates on oxygenation shows a spectrum with 5 emission bands at 420-450, 475-485, 510-540, 560-580 and 625-640 nm. These bands are subjected to intensity changes or shifts of the wavelength whenever tert-butyl hydroperoxide is present, either inhibiting or stimulating light emission. The blue-band chemiluminescence, around 435 nm, is possibly due to the weak light emission arising from excited carbonyl compounds, whereas the presence of other bands suggests generation of singlet molecular oxygen either in the process triggered on oxygenation (lipid peroxidation) or after supplementation with organic hydroperoxides. Several explanations are presented for the spectral analysis presented here.