T. Miura et al., TEMPERATURE-DEPENDENT LIPID-PEROXIDATION OF RAT-BRAIN HOMOGENATE, Research communications in molecular pathology and pharmacology, 100(1), 1998, pp. 117-128
When rat brain homogenate was incubated without adding iron, lipid per
oxidation occurred temperature dependently between 27 degrees C and 42
degrees C. When homogenates of liver and heart were incubated under t
he same conditions, lipid peroxidation did not occur. The brain, compa
red with other organs, seems to be very vulnerable to oxidative damage
with fever. Catalase promoted lipid peroxidation. The ability of dihy
drolipoic acid and alpha-tocopherol to inhibit lipid peroxidation was
very weak. In contrast, iron chelators, such as bathophenanthroline, d
esferrioxamine and EDTA, strongly inhibited lipid peroxidation, indica
ting that endogenous iron is involved in lipid peroxidation, Dialysis
of brain homogenate depressed the temperature-dependent lipid peroxida
tion by about 30%. Then, the iron content of the homogenate decreased
by about 35%. On the other hand, dialysis of EDTA-treated homogenate c
ompletely depressed the lipid peroxidation and the iron content of the
homogenate decreased by about 87%. Adding iron to the homogenate dial
yzed after EDTA treatment remarkably increased the lipid peroxidation,
but the peroxidation reaction proceeded temperature independently. Ou
r results suggest that endogenous iron, which may bind to cell compone
nts, causes temperature dependent lipid peroxidation by a site-specifi
c mechanism.