Effects of 17α‐ethynylestradiol and nonylphenol on liver and gonadal apoptosis and histopathology in Chalcalburnus tarichi

Abstract

Chalcalburnus tarichi is an endemic cyprinid fish living in the Lake Van basin located in the Eastern Turkey. Fish (3+ ages) were exposed to 17α-ethynylestradiol (EE(2); 1, 10, 100 ng L(-1); nominal concentrations) and nonylphenol (NP; 10, 60, 200 μg L(-1) ; nominal concentrations) for 32 days under semistatic daily renewal conditions. The exposure period was followed by an evaluation of liver and gonadal apoptosis and gonad histopathology in males and females. Exposure to the highest concentrations of EE(2) (100 ng L(-1)) and NP (200 μg L(-1) ) caused significant increases in the extent of apoptosis in liver and gonads. Treatment with 100 ng L(-1) of EE(2) and 200 μg L(-1) NP increased the number of TUNEL positive hepatocytes significantly in both sexes compared to controls. The rates of apoptosis in testicular germ cells and ovarian follicular cells were significantly greater at the same concentrations. Exposure to EE(2) (100 ng L(-1)) and NP (60 and 200 μg L(-1)) caused thickening of interstitial connective tissue (fibrosis) in the seminiferous tubule wall and testis-ova formation in males. In females treated with 100 ng L(-1) EE(2) , increased percentage of atretic ooctytes and fibrotic areas in the ovarian somatic stromal tissue were found in the ovaries. Increase in atresia, without a statistical significance, and fibrotic stromal tissue were also noted in 60 and 200 μg L(-1) NP treatments. Results suggest that EE(2) - and NP-dependent hepatotoxicity and gonadotoxicity are causally related to the increase in apoptosis in C. tarichi.