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. 2015 Mar 1;2015:343706. doi: 10.1155/2015/343706

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Copyright © 2015 Yasuhiro Ishihara et al.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Putative antioxidative mechanisms of 17β-estradiol and progesterone in TBT-induced oxidative neuronal injury. 17β-Estradiol (E2) suppresses TBT-induced neuronal injury via an ER-dependent nongenomic pathway. The attenuation of oxidative stress downstream of Akt activation is considered to be involved in the neuroprotection mediated by 17β-estradiol. Progesterone is readily converted to allopregnanolone, and the neuroprotective activity of allopregnanolone is attributed to modulation of GABA_A receptor activity. TBT-induced oxidative stress could be suppressed by multiple pathways stimulated by neuroactive steroids. Allo, allopregnanolone; E2, 17β-estradiol; ER, estrogen receptor; 3α-HSD, 3α-hydroxysteroid dehydrogenase; Prog, progesterone; PR, progesterone receptor; 5α-red, 5α-reductase; ROS, reactive oxygen species.