Avian eggshell thinning caused by transovarian exposure to <i>o,p</i>′-DDT: changes in histology and calcium-binding protein production in the oviduct uterus

Abstract

Reproductive disorders in birds are the most characteristic effects of DDT contamination of wildlife. Experimental exposure of avian eggs to the estrogenic substance o,p′-DDT causes abnormal development of the reproductive tract (shortening of the left oviduct and aberrant development of the right oviduct) and eggshell thinning in mature birds, but it is still not known how eggshell thinning occurs in the abnormal oviduct. To fill this information gap, we examined the histology of the uterine part of the oviduct in Japanese quail treated in ovo with o,p′-DDT or a synthetic estrogen, diethylstilbestrol (DES), and we performed immunohistochemical staining for the calcium-binding proteins CALB1, SPP1, and TRPV6. Both o,p′-DDT-treated and DES-treated quail had few, and scattered, gland cells in the left uterus, unlike vehicle controls, in which gland cells tightly occupied the lamina propria. The aberrantly developed right uterus retained all the components of the normal left uterus, but in immature form. Immunostaining for CALB1, SPP1, and TRPV6 was greatly reduced by both o,p′-DDT and DES; SPP1 and TRPV6 immunostaining patterns, in particular, differed distinctly from those in the controls. These findings suggest that CALB1, SPP1, and TRPV6 are molecular factors, decreased production of which is responsible for eggshell thinning. Our findings also could contribute to understanding of the eggshell formation mechanism in birds.

In ovo o,p′‐DDT exposure induces malformation of reproductive organs and alters the expression of genes controlling sexual differentiation in Japanese quail embryo

“…In birds, estrogens that are synthesized by ovary in female embryos play an important role in the development and sexual differentiation of the reproductive organs (Barske & Capel, 2010;Elbrecht & Smith, 1992;Guioli et al, 2020;Vaillant, Magre, et al, 2001). As expected, in ovo exposure to o,p 0 -DDT induces abnormal morphology of the reproductive organs, impairs sexual behaviors, and decreases reproductive abilities in adult Japanese quail (Bryan et al, 1989;Halldin et al, 2003;Kamata et al, 2020). An endocrine-disrupting action of o,p 0 -DDT in the embryonic period may be responsible for the impaired reproduction of adult Japanese quail.…”

No effects of the antiandrogens cyproterone acetate (CPA), flutamide and p,p’-DDE on early sexual differentiation but CPA-induced retardation of embryonic development in the domestic fowl (Gallus gallus domesticus)

“…P,p’- DDE is the primary metabolite of the insecticide DDT, which was used widely from the 1940s until its ban in most industrial countries in the 1970s ( Quinn, Summitt & Ottinger, 2008 ). DDT and its metabolites are known to induce eggshell thinning and developmental disorders in fish-eating and raptorial seabirds ( Bouwman et al, 2019 ; Buck et al, 2020 ; Fry & Toone, 1981 ; Hickey & Anderson, 1968 ; Holm et al, 2006 ; Peakall & Lincer, 1996 ; Ratcliffe, 1970 ) and affect sexual development in quail and chicken ( Blomqvist et al, 2006 ; Halldin et al, 2003 ; Kamata, Shiraishi & Nakamura, 2020 ; Quinn, Summitt & Ottinger, 2008 ). Furthermore, DDT and its main metabolite p,p’- DDE can act as endocrine disruptors in humans and wildlife.…”