We investigated the low-dose effects of CYP exposure during the perinatal stage and found impaired testicular development and steroidogenesis in the male offspring. The male-o-female ratio, BW, and TW were decreased at PD21.5. The structure of the seminiferous epithelium layer was also changed. The expression levels of steroidogenesis genes and hormone receptors were altered after CYP exposure both in vivo and in vitro. The mitosis and meiosis markers were also changed. The serum T levels were decreased, and E2 levels were increased. Androgen is a prerequisite for normal spermatogenesis and development, and the binding of androgen to the AR plays an important role in the induction of the male external genitalia during embryonic differentiation and spermatogenesis. In fetal and neonatal testes, AR expression is restricted to the interstitial compartment. Merlet et al. observed testicular dysgenesis during the embryonic period of gender differentiation in AR knockout mice. Thus, perinatal CYP exposure may affect the precursors of adult Leydig cells. Star and 3b-HSD were downregulated significantly in the CYP groups; in addition, in these groups, the T level was reduced, and the Cyp19a1 and E2 levels were increased. Moreover, the AR hormone receptor was downregulated, and ERa was upregulated. An imbalance of androgenic and estrogenic signals may lead to serious structural abnormalities. Previous results have demonstrated that mice overexpressing human aromatase possess a multitude of structural and functional alterations in the reproductive organs, and a decreased male-to-female ratio may arise from this overexpression. Taken together, the current results indicate that the inhibition of the androgenic signal during the prenatal and neonatal periods impairs the ability of Leydig cells to produce T in favor of E2 due to the overexpression of aromatase. The apoptosis of spermatogonia and spermatocytes occurs in the mitotic phase. Studies have also found that deltamethrin and diethylstilboestrol induce a greater degree of apoptosis in adult male testes. In this study, we found much greater apoptosis of germ cells in the CYP groups. Sufficient T plays a vital role in the inhibition of germ cell apoptosis. Reduced T levels lead to the separation of germ cells from the epithelium of the seminiferous tubules. In the present study, we found that the serum T levels were decreased significantly by maternal CYP exposure, which will weaken their ability to maintain spermatogenesis. Studies on bisphenol A and hexachlorocyclohexane have demonstrated that EDCs can affect mitosis and meiosis, and we also found that the expression of mitosis and meiosis marker genes was altered. The levels of Nanos3, which is important for maintaining undifferentiated spermatogonia, and the cell cycle regulator Cyclin D2 were evaluated. We found that the expression of these two genes was decreased in the CYP groups at PD21.5 and PD45.5.