Sexual hormones: Effects on cardiac and mitochondrial activity after ischemia–reperfusion in adult rats. Gender difference

  title={Sexual hormones: Effects on cardiac and mitochondrial activity after ischemia–reperfusion in adult rats. Gender difference},
  author={Natalia Pav{\'o}n and Eduardo Mart{\'i}nez-Abundis and Luz Hern{\'a}ndez and Juan Carlos Gallardo-P{\'e}rez and Carolina {\'A}lvarez‐Delgado and Marco Cerb{\'o}n and Israel P{\'e}rez-Torres and Alberto Aranda and Edmundo Ch{\'a}vez},
  journal={The Journal of Steroid Biochemistry and Molecular Biology},
Cross-sex hormonal replacement: is this really effective? an experimental clue
Estradiol replacement protected female rats from variations in all of the parameters evaluated, whereas testosterone did not show a protective effect.
Developmental and sex differences in cardiac tolerance to ischemia-reperfusion injury: the role of mitochondria 1.
The data suggest that age- and sex-dependent specificity of the MPTP is not the result of different amounts of ATP synthase and cyclophilin D: neonatal and adult hearts, similarly as the male and female hearts, contain comparable amounts of MPTP and its regulatory protein cyclophILin D.
Age and ischemia differentially impact mitochondrial ultrastructure and function in a novel model of age-associated estrogen deficiency in the female rat heart
Reductions in both SSM and IFM function may play an additive role in enhanced susceptibility to regional I/R injury in aged estrogen-deficient female hearts.
Sex effect on insulin secretion and mitochondrial function in pancreatic beta cells of elderly Wistar rats
A sex dimorphism in the age-associated impairment of pancreatic beta cell function in elderly rats is demonstrated, while the potential mechanism may be related to the sexual differences in mitochondrial biogenesis and function.
Sex‐based differences in cardiac ischaemic injury and protection: therapeutic implications
There is an urgent need for intensive experimental and clinical research to develop female‐specific therapeutic strategies to offer patients better evidence‐based treatment, a better quality of life and lower mortality.
In female rat heart mitochondria, oophorectomy results in loss of oxidative phosphorylation.
Data strongly suggest that in the female rat heart, estrogen depletion leads to progressive, severe mitochondrial dysfunction, as well as compromised Ca2+ buffering ability.


Gender differences in post-infarction hypertrophy in end-stage failing hearts.
In hyperthyroid rats octylguanidine protects the heart from reperfusion damage
It is concluded that octylguanidine inhibits the hypersensitivity of the hyperthyroid myocardium to undergo reperfusion damage due to its inhibitory action on the permeability transition pore.
Role of protein phosphatases and mitochondria in the neuroprotective effects of estrogens
Sex differences on the electrocardiographic pattern of cardiac repolarization: possible role of testosterone.
It is concluded that testosterone plays an important role in modulating cardiac repolarization and the changes observed in castrated men may be reverted by testosterone.
Estrogen Receptor β as a Mitochondrial Vulnerability Factor*
We recently demonstrated mitochondrial localization of estrogen receptor β (ERβ). We herein confirm the mitochondrial localization of ERβ by the loss of mitochondrial ERβ immunoreactivity in ERβ
Functional estrogen receptors in the mitochondria of breast cancer cells.
It is reported that in MCF-7, estrogen inhibits UV radiation-induced cytochrome C release, the decrease of the mitochondrial membrane potential, and apoptotic cell death, and E2 (estradiol) inhibited all these events, directly acting in mitochondria to inhibit mROS by rapidly up-regulating manganese superoxide dismutase activity.
The mitochondrial origin of postischemic arrhythmias.
These findings directly link instability of DeltaPsi(m) to the heterogeneous electrophysiological substrate of the postischemic heart and highlight the mitochondrial membrane as a new therapeutic target for arrhythmia prevention in ischemic heart disease.