Vitellogenesis in flatfish liver with toxipathic lesions

Dab (Limanda limanda) displaying various stages of gonadal maturation were collected from two different sites (one was contaminated). Liver histopathology was complemented by detecting DNA strand breaks (TUNEL assay) and lysosomal latency. The yolk precursor protein vitellogenin and the multixenobiotic transporter (P-gp) were detected in liver by immunocytochemistry; NADPH-dependent EROD activity was measured biochemically. At the contaminated site liver pathologies were linked to significantly reduced lysosomal latency and there was a 40-fold increased DNA strand breaks in dab at all stages of maturity. EROD activity and P-gp expression, which were elevated 5–7-fold in immature dab at the contaminated site, decreased with the onset of gonadal development. Liver vitellogenin increased with different dynamics after the onset of gonadal development at both sites. At the contaminated site vitellogenin production in liver was reduced by 50% before spawning which might result in minimized serum levels and yolk internalization by oocytes with subsequent reduced internal food supply for embryos.