Reproductive potential of mosquitofish is reduced by the masculinizing effect of a synthetic progesterone, gestodene: Evidence from morphology, courtship behaviour, ovary histology, sex hormones and gene expressions

The ever-increasing use of synthetic hormones, especially progestins, for medical applications has drawn growing concerns due to their potential endocrine disrupting effects that may diminish the reproductive outputs of aquatic organisms. Using mosquitofish (Gambusia affinis) as a model species, we tested whether gestodene (GES), a commonly used progestin, can alter the expressions of genes associated with sex hormone synthesis and cause ensuing changes in morphological features, courtship behaviour and oocyte development. After exposing to GES at environmentally relevant concentrations (2.96, 32.9 and 354 ng L-1) for 40 days, we found that GES, especially at 354 ng L-1, induced masculinization of female fish, indicated by the reduced body weight to length ratio and development of gonopodia (i.e. anal fins of male fish). Thus, the males showed less intimacy and mating interest towards the GES-exposed females, indicated by the reduced time spent on attending, following and mating behaviours. While oocyte development was seemingly unaffected by GES, spermatogonia were developed in the ovary. All the aforementioned masculinizing effects of GES were associated with the increased testosterone level and decreased estradiol level, driven by upregulating androgen receptor genes (Ar alpha and Ar beta). Overall, our findings suggest that progestins could undermine the reproductive potential of aquatic organisms and hence their persistence in the progestin-contaminated environment. (C) 2021 Elsevier B.V. All rights reserved.

Automated summary

Exposure to the progestin gestodene can lead to masculinization in female mosquitofish, affecting their body weight, morphology, and courtship behavior. While oocyte development seems unaffected, the presence of spermatogonia in the ovary suggests a potential disruption in reproductive processes. Increased testosterone levels and decreased estradiol levels were associated with these masculinizing effects, driven by upregulation of androgen receptor genes.