Here's an article that says T increases glutamate neurotoxicity and ischemia-reperfusion injury.
http://www.ncbi.nlm.nih.gov/pubmed/11744660
Glutamate: The most abundant neurotransmitter in the human nervous system. When there is excessive Glutamate in the body, it can lead to Glutamate excitotoxicity.
Ischemia-reperfusion injury: The tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen.
[h=4]Testosterone increases neurotoxicity of glutamate in vitro and ischemia-reperfusion injury in an animal model.[/b]
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 microM concentration, whereas 17beta-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 mm(3) in control to 122.5 +/- 28.6 mm(3) 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.
I am confused.
Glutamate neurotoxicity is implicated in a wide variety of diseases: MS, ALS, CFS, FMS, Parkinson's, Alzheimer's, etc. Study after study has shown that a majority of brain and CNS diseases are adversely affected by Glutamate neurotoxicity.
1. T combats all the above diseases.
2. T aggravates Glutamate neurotoxicity (as per the above study).
The 2 statements don't align. Does anyone understand why this is so? Can the experts throw some light on this?
http://www.ncbi.nlm.nih.gov/pubmed/11744660
Glutamate: The most abundant neurotransmitter in the human nervous system. When there is excessive Glutamate in the body, it can lead to Glutamate excitotoxicity.
Ischemia-reperfusion injury: The tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen.
[h=4]Testosterone increases neurotoxicity of glutamate in vitro and ischemia-reperfusion injury in an animal model.[/b]
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 microM concentration, whereas 17beta-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 mm(3) in control to 122.5 +/- 28.6 mm(3) 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.
I am confused.
Glutamate neurotoxicity is implicated in a wide variety of diseases: MS, ALS, CFS, FMS, Parkinson's, Alzheimer's, etc. Study after study has shown that a majority of brain and CNS diseases are adversely affected by Glutamate neurotoxicity.
1. T combats all the above diseases.
2. T aggravates Glutamate neurotoxicity (as per the above study).
The 2 statements don't align. Does anyone understand why this is so? Can the experts throw some light on this?
