[Auto-oxidation or brain homogenate: research of oxidizing agent and targets. Comparison with liver homogenate]

The aim of this study was to determine: 1) the source of Thiobarbituric Reactive Substances (TBARS) spontaneously produced during rat brain homogenate incubation; 2) the cellular components involved; 3) the reason why brain and liver homogenates did not have the same behaviour. Measurements of TBARS, Polyunsaturated Fatty Acids (PUFAs), aldehydes coming from PUFAS breakdown, vitamin E and Schiff's bases levels were performed on brain and liver homogenates, membrane fractions (Mb) and medium containing soluble cytoplasmic components (CS). Mb and CS were prepared by differential centrifugation. Brain homogenate incubation, contrary to liver homogenate, led to an increase in TBARS amount, while PUFAS, aldehydes and vitamin E levels remained unchanged. No TBARS accumulation arose when Mb or CS were separately incubated. However, it was of interest to note that liver or brain incubation of Mb with CS led to an overproduction of TBARS. These results suggested that spontaneous oxidation of brain homogenate was not due to lipid peroxidation. On the other hand, the fact that, contrary to the liver homogenate, liver Mb incubated with CS led to an increase in TBARS level, supports the idea that a "protective agent" was eliminated during centrifugation. It can be speculated that this "agent" is not effective in the brain.