Objective Using rat cortical brain slices as study models to investigate the effects of
estradiol on the neurotoxicity of deltamethrin.Methods Using HPLC to detect the
excitatory amino acids (EAAs)
release and employing colorimeter method to measure the
activities of ATPase of different 17-β estradiol dose level (10 -5 ,10 -8 ,10 -11 mol/L)on the cortical brain slices treated with deltamethrin. The estrogen receptor(ER) antagonist tamoxifen was used to investigate the possible mechanisms of estradiol.Results The ASP and GLU release was increased significantly by 2×10 -5 mol/L deltamethrin at the depolarizing state,and 10 -5 ,10 -8 ,10 -11 mol/L 17-β-estradiol could partly block the release of GLU,10 -11 mol/L 17-β-estradiol could partly block the release of ASP.The
effect of 10 -8 mol/L 17-β-estradiol on the GLU release can be antagonisted by 10 -6 mol/L tamoxifen.The activities of ATPase were inhibited by 2×10 -4 mol/L deltamethrin,and 10 -5 ,10 -8 mol/L estradiol could block this effects in some aspects,whereas tamoxifen had not any effects on the function of estradiol on the activities of ATPase. Conclusion Estradiol has showed a neuroprotective effect on the release of EAAs or inhibition of ATPase by deltamethrin,and this effect on GLU release may be partly attributed to the genomic mechanism of estradiol.