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We confirmed the binding ability of GPER1 with G1 and G15 in primary macrophages of C. carpio by testing the related gene expression levels after 6 h exposure, and similar to G1, bisphenol A (BPA), a typical environmental estrogen, could interact with GPER1 to increase the Ca2+ concentration in macrophages treated for 30 min. Furthermore, inhibition of GPER1 with GPER1 antagonist G36 rescued the cellular immunotoxicity caused by BPA, which further suggested that carp GPER1 could mediate the estrogen effect. Our findings contribute to be
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