Testosterone increases neurotoxicity of glutamate in vitro and ischemia-reperfusion injury in an animal model

• DOI: 10.1152/jappl.2002.92.1.195
• Publication Date: 2017-12-22T23:25:08Z
• Authors: Shao-Hua Yang; Evelyn Perez; Jason Cutright; Ran Liu; Zhen He; Arthur L. Day; James W. Simpkins
• Keywords: Neurotoxicity

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