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

@article{Yang2002TestosteroneIN,
  title={Testosterone increases neurotoxicity of glutamate in vitro and ischemia-reperfusion injury in an animal model.},
  author={Shao-Hua Yang and E. Perez and J. Cutright and Ran Liu and Zhenli He and A. Day and J. Simpkins},
  journal={Journal of applied physiology},
  year={2002},
  volume={92 1},
  pages={
          195-201
        }
}
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… Expand
Neuroendocrine mechanism for tolerance to cerebral ischemia-reperfusion injury in male rats.
TLDR
Stress-induced testosterone reduction contributes to ischemia tolerance in cerebral ischemIA-reperfusion injury in males, which could be related to the loss of inhibition by testosterone of Hsp70 and -90 expression. Expand
Deleterious Effects of Dihydrotestosterone on Cerebral Ischemic Injury
  • Jian Cheng, N. Alkayed, P. Hurn
  • Biology, Medicine
  • Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2007
TLDR
The data suggest that androgens are important mediators of ischemic damage in male brain and that transcriptional mechanisms should be considered as the authors seek to understand innate male sensitivity to cerebral ischemia. Expand
Effects of progesterone and testosterone on ICH-induced brain injury in rats.
TLDR
Progesterone can reduce brain edema and improve functional outcome, whereas testosterone may have a deleterious effect after ICH in male rats. Expand
Flutamide Enhances Neuroprotective Effects of Testosterone during Experimental Cerebral Ischemia in Male Rats
TLDR
It seems that the beneficial effects of flutamide are the prevention of the deleterious effects and enhancement of neuroprotective effects of testosterone during cerebral ischemia. Expand
17β-Estradiol attenuates blood–brain barrier disruption induced by cerebral ischemia–reperfusion injury in female rats
TLDR
Estrogens could attenuate BBB disruption induced by transient cerebral ischemia, by inhibition of MMP2 and MMP9 activation, which would suggest an important role of estrogens as multiple targeting protectants against ischemic stroke on cellular as well as vascular components of central nervous system. Expand
17β-Estradiol extends ischemic thresholds and exerts neuroprotective effects in cerebral subcortex against transient focal cerebral ischemia in rats
TLDR
It is indicated that estrogens could be used as a neuroprotectant to prolong the therapeutic window of thrombolysis and prolong the time of cerebral circulation intervention for neurosurgical procedure. Expand
Testosterone exacerbates neuronal damage following cardiac arrest and cardiopulmonary resuscitation in mouse
TLDR
It is indicated that testosterone may have a role in determining sex-linked differences in cerebrovascular disease as well as having important health implications in clinical conditions of elevated testosterone. Expand
Effect of endogenous androgens on 17beta-estradiol-mediated protection after spinal cord injury in male rats.
TLDR
Delayed post-SCI administration of a clinically relevant dose of 17beta-estradiol is protective in male rats, and endogenous androgens do not alter estrogen-mediated protection, which could be readily translated to clinical trials. Expand
Dose-Dependent Effects of Androgens on Outcome after Focal Cerebral Ischemia in Adult Male Mice
TLDR
It is concluded that testosterone exhibits dose-dependent and time-sensitive effects after ischemia and that testosterone is likely to be an important factor in sex-linked differences in cerebrovascular disease. Expand
Sex Differences in Mechanisms and Outcome of Neonatal Hypoxia-Ischemia in Rodent Models: Implications for Sex-Specific Neuroprotection in Clinical Neonatal Practice
TLDR
Results support the idea that sex-specific gonadal hormones may modulate developmental response to injury and dovetail with overwhelming evidence of developmental androgen effects on typical brain morphology and behavior and suggest that infants might benefit from sex- specific neuroprotection following HI injury. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 46 REFERENCES
Estradiol Protects against Ischemic Injury
  • D. Dubal, M. Kashon, +4 authors P. Wise
  • Medicine, Chemistry
  • Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 1998
TLDR
The finding that estradiol pretreatment reduces injury demonstrates that physiologic levels of Estradiol can protect against neurodegeneration. Expand
Androgen treatment of neonatal rats decreases susceptibility of cerebellar granule neurons to oxidative stress in vitro
TLDR
Results suggest that in’vivo treatment with androgens render CGC less vulnerable to oxidative stress‐induced apoptosis by potentiating antioxidant defences. Expand
Testosterone protects cerebellar granule cells from oxidative stress-induced cell death through a receptor mediated mechanism
TLDR
It is demonstrated that cerebellar granule cells treated in vitro with testosterone are protected from oxidative stress via a mechanism mediated by the androgen receptor, similar to what was observed after in vivo administration of testosterone. Expand
Estrogen-mediated neuroprotection after experimental stroke in male rats.
TLDR
Both acute and chronic 17beta-estradiol treatments protect male brain in experimental stroke and testosterone availability does not alter estradiol-mediated tissue salvage after MCAO. Expand
Estrogens may reduce mortality and ischemic damage caused by middle cerebral artery occlusion in the female rat.
TLDR
The present study provides the first evidence that estrogens exert neuroprotective effects in an animal model of ischemia and suggests that estrogen may be a useful therapy to protect neurons against the neurodegenerative effects of stroke. Expand
Testosterone increases and estradiol decreases middle cerebral artery occlusion lesion size in male rats
TLDR
Evidence is provided that testosterone exacerbates and estrogens ameliorate ischemic brain damage in an animal model of cerebral ischemia, and a strong positive correlation between plasma testosterone concentrations and isChemic lesion size was observed. Expand
Effects of gender and estradiol treatment on focal brain ischemia
TLDR
The results strongly suggest that the level of circulating estrogens play an important role in protecting brain tissues against ischemia induced by MCA occlusion. Expand
Estrogens Decrease Reperfusion-Associated Cortical Ischemic Damage: An MRI Analysis in a Transient Focal Ischemia Model
TLDR
This study strongly suggests that estrogens selectively protect cortical tissue from ischemic damage during MCAO and that this protection is exerted during both the occlusion and reperfusion phases of ischemia and does not involve an estrogen-related change in CBF. Expand
The nonfeminizing enantiomer of 17beta-estradiol exerts protective effects in neuronal cultures and a rat model of cerebral ischemia.
TLDR
The enantiomer of 17 beta-estradiol (ENT-E(2), which has identical chemical properties but interacts only weakly with known ERs, was assessed for neuroprotective efficacy and was both as potent and efficacious as 17beta-ESTradiol in attenuating oxidative stress-induced death in HT-22 cells, a murine hippocampal cell line. Expand
Estrogen protects against while testosterone exacerbates vulnerability of the lateral striatal artery to chemical hypoxia by 3-nitropropionic acid
TLDR
Data suggest that 1STR artery and astrocytes are highly vulnerable to 3-NPA intoxication in males and the greater vulnerability of the ISTR artery may contribute to the pathogenesis of neurodegenerative diseases, striatal bleeding, etc. Expand
...
1
2
3
4
5
...