Temperature-dependent lipid peroxidation of rat brain homogenate.

When rat brain homogenate was incubated without adding iron, lipid peroxidation occurred temperature dependently between 27 degrees C and 42 degrees C. When homogenates of liver and heart were incubated under the same conditions, lipid peroxidation did not occur. The brain, compared with other organs, seems to be very vulnerable to oxidative damage with fever. Catalase promoted lipid peroxidation. The ability of dihydrolipoic acid and alpha-tocopherol to inhibit lipid peroxidation was very weak. In contrast, iron chelators, such as bathophenanthroline, desferrioxamine and EDTA, strongly inhibited lipid peroxidation, indicating that endogenous iron is involved in lipid peroxidation. Dialysis of brain homogenate depressed the temperature-dependent lipid peroxidation by about 30%. Then, the iron content of the homogenate decreased by about 35%. On the other hand, dialysis of EDTA-treated homogenate completely depressed the lipid peroxidation and the iron content of the homogenate decreased by about 87%. Adding iron to the homogenate dialyzed after EDTA treatment remarkably increased the lipid peroxidation, but the peroxidation reaction proceeded temperature independently. Our results suggest that endogenous iron, which may bind to cell components, causes temperature dependent lipid peroxidation by a site-specific mechanism.