Environmental pollutants with estrogenic activity have a potential to disrupt oestrogen-dependent developmental processes. Thus, the aim of this thesis was to investigated how embryonic exposure to the estrogenic pollutants EE2 (17 alpha- ethynyloestradiol) and o,p´-DDT (1-[2-chlorophenyl]-1-[4-chlorophenyl]-2,2,2-trichloro-ethane) affects the reproductive system in the domestic hen (Gallus domesticus). Hens exposed in ovo to 20 or 60 ng EE2/g egg or 37 or 75 micro g o,p´-DDT/g egg produced a normal number of eggs but with thinner shells as adults. These hens also showed a reduction of shell gland capillaries with carbonic anhydrase (CA) activity. CA is considered a key enzyme in shell formation and the developmentally induced disruption of this enzyme may explain the observed eggshell thinning. Left oviduct and infundibulum was shortened in exposed hens and severely malformed in hens exposed to 150 or 300 micro g o,p´-DDT/g egg, which likely explained the inhibited egg production in these birds. Semen output was significantly reduced in both o,p´-DDT and EE2 exposed roosters, whereas sperm quality was unaffected. The left testis was deformed with an atrophied epididymis. Altered plasma inhibin concentration and histological evaluation implied a disturbed Sertoli cell function resulting in reduced germ cell production. Structural malformations in the epididymis indicating disrupted fluid transfer and transport of spermatozoa are possible contributors to the reduced semen output. Exposure to o,p´-DDT resulted in a wider range of effects than EE2 such as feminisation of the cloaca at hatch, cloacal deformation in adult roosters and a reduced comb weight, while hens showed retained right oviducts. Right spur diameter was affected by both substances.Localisation of epididymal progesterone receptors and cytoplasmic and membrane associated oestrogen receptor alfa in late spermatids, spermatozoa and epididymal tissues were novel findings in rooster. Embryonic exposure of domestic fowl to o,p´-DDT or EE2 resulted in persistent malformations of the reproductive organs of both sexes, with eggshell thinning and reduced semen production as a consequence. The results provide a possible explanation for how eggshell thinning may be induced in wild birds and show that also male birds may suffer from reduced reproductive success due to oestrogen-like pollutants
