Effects of early life stage exposure of largemouth bass to atrazine or a model estrogen (17α-ethinylestradiol).

Endocrine disrupting contaminants are of continuing concern for potentially contributing to reproductive dysfunction in largemouth and smallmouth bass in the Chesapeake Bay watershed (CBW) and elsewhere. Exposures to atrazine (ATR) have been hypothesized to have estrogenic effects on vertebrate endocrine systems. The incidence of intersex in male smallmouth bass from some regions of CBW has been correlated with ATR concentrations in water. Fish early life stages may be particularly vulnerable to ATR exposure in agricultural areas, as a spring influx of pesticides coincides with spawning and early development. Our objectives were to investigate the effects of early life stage exposure to ATR or the model estrogen 17α-ethinylestradiol (EE2) on sexual differentiation and gene expression in gonad tissue. We exposed newly hatched largemouth bass (LMB, Micropterus salmoides) from 7 to 80 days post-spawn to nominal concentrations of 1, 10, or 100 µg ATR/L or 1 or 10 ng EE2/L and monitored histological development and transcriptomic changes in gonad tissue. We observed a nearly 100% female sex ratio in LMB exposed to EE2 at 10 ng/L, presumably due to sex reversal of males. Many gonad genes were differentially expressed between sexes. Multidimensional scaling revealed clustering by gene expression of the 1 ng EE2/L and 100 µg ATR/L-treated male fish. Some pathways responsive to EE2 exposure were not sex-specific. We observed differential expression in male gonad in LMB exposed to EE2 at 1 ng/L of several genes involved in reproductive development and function, including star, cyp11a2, ddx4 (previously vasa), wnt5b, cyp1a and samhd1. Expression of star, cyp11a2 and cyp1a in males was also responsive to ATR exposure. Overall, our results confirm that early development is a sensitive window for estrogenic endocrine disruption in LMB and are consistent with the hypothesis that ATR exposure induces some estrogenic responses in the developing gonad. However, ATR-specific and EE2-specific responses were also observed.

Atrazine induced transgenerational reproductive effects in medaka (Oryzias latipes).

Atrazine is presently one of the most abundantly used herbicides in the United States, and a common contaminant of natural water bodies and drinking waters in high-use areas. Dysregulation of reproductive processes has been demonstrated in atrazine exposed fish, including alteration of key endocrine pathways on hypothalamic-pituitary-gonadal (HPG) axis. However, the potential for atrazine-induced transgenerational inheritance of reproductive effects in fish has not been investigated. The present study examined the effects of early developmental atrazine exposure on transgenerational reproductive dysregulation in Japanese medaka (Oryzias latipes). F0 medaka were exposed to atrazine (ATZ, 5 or 50 µg/L), 17α-ethinylestradiol (EE2, 0.002 or 0.05 µg/L), or solvent control during the first twelve days of development with no subsequent exposure over three generations. This exposure overlapped with the critical developmental window for embryonic germ cell development, gonadogenesis, and sex determination. Exposed males and females of the F0 generation were bred to produce an F1 generation, and this was continued until the F2 generation. Sperm count and motility were not affected in F0 males; however, both parameters were significantly reduced in the males from F2 Low EE2 (0.002 µg/L), Low ATZ (5 µg/L), and High ATZ (50 µg/L) lineages. Fecundity was unaffected by atrazine or EE2 in F0 through F2 generations; however, fertilization rate was decreased in low atrazine and EE2 exposure lineages in the F2 generation. There were significant transgenerational differences in expression of the genes involved in steroidogenesis and DNA methylation. These results suggest that although early life exposure to atrazine did not cause significant phenotypes in the directly exposed F0 generation, subsequent generations of fish were at greater risk of reproductive dysfunction.

Sensitivity of lake sturgeon (Acipenser fulvescens) early life stages to 2,3,7,8-tetrachlorodibenzo-P-dioxin and 3,3',4,4',5-pentachlorobiphenyl.

The aquatic food web of the Great Lakes has been contaminated with polychlorinated biphenyls (PCBs) since the mid-20th century. Threats of PCB exposures to long-lived species of fish, such as lake sturgeon (Acipenser fulvescens), have been uncertain because of a lack of information on the relative sensitivity of the species. The objective of the present study was to evaluate the sensitivity of early-life stage lake sturgeon to 3,3',4,4',5-pentachlorobiphenyl (PCB-126) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure. Mortality, growth, morphological and tissue pathologies, swimming performance, and activity levels were used as assessment endpoints. Pericardial and yolk sac edema, tubular heart, yolk sac hemorrhaging, and small size were the most commonly observed pathologies in both TCDD and PCB-126 exposures, beginning as early as 4 d postfertilization, with many of these pathologies occurring in a dose-dependent manner. Median lethal doses for PCB-126 and TCDD in lake sturgeon were 5.4 ng/g egg (95% confidence interval, 3.9-7.4 ng/g egg) and 0.61 ng/g egg (0.47-0.82 ng/g egg), respectively. The resulting relative potency factor for PCB-126 (0.11) was greater than the World Health Organization estimate for fish (toxic equivalency factor = 0.005), suggesting that current risk assessments may underestimate PCB toxicity toward lake sturgeon. Swimming activity and endurance were reduced in lake sturgeon survivors from the median lethal doses at 60 d postfertilization. Threshold and median toxicity values indicate that lake sturgeon, like other Acipenser species, are more sensitive to PCB and TCDD than the other genus of sturgeon, Scaphirhynchus, found in North America. Indeed, lake sturgeon populations in the Great Lakes and elsewhere are susceptible to PCB/TCDD-induced developmental toxicity in embryos and reductions in swimming performance. Environ Toxicol Chem 2017;36:988-998. Published 2016 Wiley Periodicals Inc. on behalf of SETAC. This article is a US government work and, as such, is in the public domain in the United States of America.