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Title: [Mechanisms of nongenomic effect of 17beta-estradiol on human spermatozoa]. Author: Gu XB, Zhang JH, Yue LM, Wang Q, Mao YQ, He YP. Journal: Sichuan Da Xue Xue Bao Yi Xue Ban; 2009 Sep; 40(5):861-4. PubMed ID: 19950600. Abstract: OBJECTIVE: To study the mechanisms of nongenomic effect of 17beta-estradiol on human spermatozoa. METHODS: The intracellular calcium ([Ca2+]i) in the spermatozoa was measured by flow cytometry after the spermatozoa was treated with the inhibitors of trans-membrane signaling transduction pathways and impermeable 17beta-estradiol (E2-BSA). Western blot was used to detect the activation of the signal proteins after the spermatozoa was treated with 1 x 10(-6) mol/L E2-BSA and tamoxifen, an estrogen receptor inhibitor. RESULTS: Adenylyl cyclase (AC) inhibitor SQ22536, phospholipase C (PLC) inhibitor U73122 and protein tyrosine kinase (TPK) inhibitor Genistein all deterred the increase of [Ca2+]i caused by E2-BSA. E2-BSA also increased the PLC protein and PKC protein significantly. Tamoxifen, an antagonist of estrogen receptor, did not inhibit the activation of PLC caused by E2-BSA. CONCLUSION: The E2-BSA has an effect on human spermatozoa in a nongenomic pathway, possibly through the transmembrane signal transduction in relation to AC, PLC and TPK.[Abstract] [Full Text] [Related] [New Search]