Protective Actions of 17β-Estradiol and Progesterone on Oxidative Neuronal Injury Induced by Organometallic Compounds

Figure 3

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.