Estradiol and neurodegenerative oxidative stress Export

@article{citeulike:4682348, abstract = {Estradiol is a potent preventative against neurodegenerative disease, in part, by activating antioxidant defense systems scavenging reactive oxygen species, limiting mitochondrial protein damage, improving electron transport chain activity and reducing mitochondrial DNA damage. Estradiol also increases the activity of complex IV of the electron transport chain, improving mitochondrial respiration and ATP production under normal and stressful conditions. However, the high oxidative cellular environment present during neurodegeneration makes estradiol a poor agent for treatment of existing disease. Oxidative stress stimulates the production of the hydroperoxide-dependent hydroxylation of estradiol to the catecholestrogen metabolites, which can undergo reactive oxygen species producing redox cycling, setting up a self-generating toxic cascade offsetting any antioxidant/antiapoptotic effects generated by the parent estradiol. Additional disease-induced factors can further perpetuate this cycle. For example dysregulation of the catecholamine system could alter catechol- O -methyltransferase-catalyzed methylation, preventing removal of redox cycling catecholestrogens from the system enhancing pro-oxidant effects of estradiol.}, author = {NILSEN,, J}, citeulike-article-id = {4682348}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.yfrne.2007.12.005}, citeulike-linkout-1 = {http://linkinghub.elsevier.com/retrieve/pii/S009130220700074X}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/18275991}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=18275991}, doi = {10.1016/j.yfrne.2007.12.005}, issn = {00913022}, journal = {Frontiers in Neuroendocrinology}, keywords = {aging, anti-aging, endocrinology, neurobehaviour, neurology, oxidative-stress, reproduction}, month = {October}, number = {4}, pages = {463--475}, posted-at = {2009-06-30 09:53:00}, priority = {2}, title = {Estradiol and neurodegenerative oxidative stress}, url = {http://dx.doi.org/10.1016/j.yfrne.2007.12.005}, volume = {29}, year = {2008} }

TY - JOUR ID - citeulike:4682348 L3 - citeulike-article-id:4682348 N2 - Estradiol is a potent preventative against neurodegenerative disease, in part, by activating antioxidant defense systems scavenging reactive oxygen species, limiting mitochondrial protein damage, improving electron transport chain activity and reducing mitochondrial DNA damage. Estradiol also increases the activity of complex IV of the electron transport chain, improving mitochondrial respiration and ATP production under normal and stressful conditions. However, the high oxidative cellular environment present during neurodegeneration makes estradiol a poor agent for treatment of existing disease. Oxidative stress stimulates the production of the hydroperoxide-dependent hydroxylation of estradiol to the catecholestrogen metabolites, which can undergo reactive oxygen species producing redox cycling, setting up a self-generating toxic cascade offsetting any antioxidant/antiapoptotic effects generated by the parent estradiol. Additional disease-induced factors can further perpetuate this cycle. For example dysregulation of the catecholamine system could alter catechol- O -methyltransferase-catalyzed methylation, preventing removal of redox cycling catecholestrogens from the system enhancing pro-oxidant effects of estradiol. IS - 4 JF - Frontiers in Neuroendocrinology SN - 00913022 EP - 475 TI - Estradiol and neurodegenerative oxidative stress VL - 29 SP - 463 KW - aging KW - anti-aging KW - endocrinology KW - neurobehaviour KW - neurology KW - oxidative-stress KW - reproduction AU - NILSEN,, J PY - 2008/10// UR - http://dx.doi.org/10.1016/j.yfrne.2007.12.005 ER -