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1 Department of Pharmacology and Neuroscience, Health Science Center at Fort Worth, University of North Texas, Fort Worth, Texas 76107; and 2 Department of Pharmacodynamic, College of Pharmacy and 3 Department of Neurosurgery, College of Medicine, University of Florida, Gainesville, Florida 32610
Increasing evidence has demonstrated striking sex differences in
the outcome of neurological injury. Whereas estrogens contribute to
these differences by attenuating neurotoxicity and
ischemia-reperfusion injury, the effects of testosterone are
unclear. The present study was undertaken to determine the effects of
testosterone on neuronal injury in both a cell-culture model and a
rodent ischemia-reperfusion model. Glutamate-induced HT-22
cell-death model was used to evaluate the effects of testosterone on
cell survival. Testosterone was shown to significantly increase the
toxicity of glutamate at a 10 µM concentration, whereas
17
-estradiol significantly attenuated the toxicity at the same
concentration. In a rodent stroke model, ischemia-reperfusion
injury was induced by temporal middle cerebral artery occlusion (MCAO)
for 1 h and reperfusion for 24 h. To avoid the stress-related
testosterone reduction, male rats were castrated and testosterone was
replaced by testosterone pellet implantation. Testosterone pellets were
removed at 1, 2, 4, or 6 h before MCAO to determine the duration
of acute testosterone depletion effects on infarct volume.
Ischemic lesion volume was significantly decreased from
239.6 ± 25.9 mm3 in control to 122.5 ± 28.6 mm3 when testosterone pellets were removed at 6 h
before MCAO. Reduction of lesion volume was associated with
amelioration of the hyperemia during reperfusion. Our in vitro and in
vivo studies suggest that sex differences in response to brain injury
are partly due to the consequence of damaging effects of testosterone.
androgen; stroke; neuroprotection
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