Neuroprotective and neurotoxic outcomes of androgens and estrogens in an oxidative stress environment.
Phong DuongMavis A A TenkorangJenny TrieuClayton McCuistonNataliya RybalchenkoRebecca L CunninghamPublished in: Biology of sex differences (2020)
Sex hormone action on cell viability is dependent on the cellular environment. In healthy neuronal cells, sex hormones are protective against oxidative stress insults via the estrogen receptor, regardless of sex chromosome complement (XX, XY). However, in unhealthy (e.g., high oxidative stress) cells, sex hormones exacerbated oxidative stress-induced cell loss, regardless of cell type or sex chromosome complement. The non-genomic AR45 receptor, which is present in humans, mediated androgen's damaging effects, but it is unknown which receptor mediated estrogen's damaging effects. These differential effects of sex hormones that are dependent on the cellular environment, receptor profile, and cell type may mediate the observed sex differences in oxidative stress-associated CNS disorders.
Keyphrases
- oxidative stress
- induced apoptosis
- estrogen receptor
- dna damage
- endoplasmic reticulum stress
- diabetic rats
- ischemia reperfusion injury
- cell cycle arrest
- stem cells
- copy number
- cell death
- gene expression
- mesenchymal stem cells
- single cell
- dna methylation
- metabolic syndrome
- heat shock
- blood brain barrier
- subarachnoid hemorrhage
- brain injury
- cerebral ischemia
- pi k akt