C. Torri et al., SYNAPTOSOMAL IRON-DEPENDENT LIPID-PEROXIDATION INHIBITION AFTER SUBARACHNOID HEMORRHAGE BY LAZAROID IN-VIVO TREATMENT, Molecular and chemical neuropathology, 30(1-2), 1997, pp. 15-24
The production of oxygen-free radicals and their subsequent peroxidati
ve action on membrane unsaturated fatty acids could be enhanced after
subarachnoid hemorrhage (SAH). We have studied the effects of the in v
ivo pharmacological treatment with a lazaroid (U78517F) after experime
ntal SAH, on lipid peroxidative patterns in cortical synaptosomal prep
arations. U78517F is a lipid-soluble antioxidant with a potent action
to inhibit iron-dependent lipid peroxidation. Experimental SAH was ind
uced in anesthetized rats by slow injection of 0.3 mt of autologous ar
terial blood into cisterna magna. The hemorrhagic animals were treated
with 5 mg/kg iv of U78517F immediately after surgical operation. The
animals were sacrificed Id after the hemorrhage and the thiobarbituric
acid reactive material (TBAR) was assayed in basal conditions and aft
er. 1, 3, 5, 10, and 20 min of incubation at 37 degrees C with a pro-o
xidant mixture on three different rat groups: sham-operated (0.3 mt of
mock cerebrospinal fluid (CSF) into cisterna magna), hemorrhagic (0.3
mL of autologous arterial blood into cisterna magna), and hemorrhagic
-treated. The hemorrhagic event did not influence the membrane lipoper
oxidation levels in basal conditions, whereas peroxidative stimulation
in vitro caused significant increases in hemorrhagic animals compared
to the sham-operated, and in hemorrhagic-treated animals, the synapto
somal TBARs were similar to controls. The pharmacological treatment sh
owed its effectiveness only following incubations with pro-oxidants; t
herefore, U78517F seems to be protective for membranes in case of seve
re lipid peroxidative stress.