ABSTRACT
ABSTRACT The hypothalamic-pituitary-gonadal (HPG) axis in anurans represents one of the most important endocrine systems triggering reproductive biology, maintenance of reproduction in adults, and sexual differentiation during larval development. Anurans are the classical endocrinological models concerning sexual differentiation, characterized by a high degree of plasticity during early developmental phases where sex reversal may occur, and therefore they provide a sentinel model for endocrine disrupting chemicals (EDCs) affecting reproductive biology. However, despite the well-established general knowledge about reproductive biology of anurans, the exact basic mechanisms underlying reproductive biology are yet not fully understood and in the focus of recent research. Recent findings about the endocrine regulation of reproductive biology in anurans demonstrate physiological implications for potential impacts of EDCs acting on the HPG axis. The HPG axis is regulated via gonadotropin releasing hormone triggering the gonadotropins, luteinizing hormone (LF) and follicle stimulating hormone (FSH), and gonadal sex steroid-synthesizing enzymes 5a-reductase type 1, type 2, and aromatase. Despite the general features for regulating the HPG axis seeming to be similar in anurans as in almost all vertebrates, based on recent findings concerning physiological regulation of the HPG axis, a more advanced hypothesis specific for sexual differentiation in anurans has been developed. In anurans, primary sex differentiation depends on the genotype, which belongs mainly to the XY but also to the ZW type represented by the mainly used model species Xenopus laevis. Secondary sex differentiation developing the gender-specific sex phenotype of gonads and of general morphological appearances during larval development is a phase where EDCs can adversely interfere with normal genotypic development, which seems to be a complex interplay by the sex steroidsynthesizing enzymes 5a-reductase type 1, type 2, and aromatase, resulting in a ratio for dihydrotestosterone (DHT) to 17b-estradiol (E2). Gender-specific ratios of DHT/E2 are high or low, leading to male or female phenotypes, respectively. Thus any change induced by (anti)estrogenic and (anti)androgenic EDCs results in impacts on gonadal differentiation. Estrogenic and antiandrogenic EDCs result in feminization, antiestrogenic EDCs cause neutralization, and androgenic EDCs reveal masculinization. In addition, most recent findings indicate that even in adult anurans, a continuous plasticity concerning gonadal development involved in gametogenesis exists, which can be termed “tertiary sexual differentiation.” Herewith, antiestrogens and androgens cause masculinization characterized by atresia of oocytes and occurrence of spermatogenic cysts in ovaries, whereas estrogens and antiandrogens reveal feminization indicated by disruption of lobules and appearance of previtellogenic oocytes in testes.
