Investigating the relationship between embryotoxic and genotoxic effects of benzo[a]pyrene, 17α-ethinylestradiol and endosulfan on Crassostrea gigas embryos

Abstract

Genotoxicity biomarkers are widely measured in ecotoxicology as molecular toxic endpoints of major environmental pollutants. However, the long-term consequences of such damage still have to be elucidated. Some authors have suggested that the accumulation of unrepaired DNA lesions could explain the embryotoxicity of certain chemical pollutants. As embryotoxicity exerts a direct impact on the recruitment rate, genotoxicity could be closely related to disturbances of ecological concern and produce a possible impact upon population dynamics. The aim of the present work was to study the genotoxicity and the embryotoxicity of three relevant pollutants for oyster embryos: the polycyclic aromatic hydrocarbon, benzo[a]pyrene (BaP), the synthetic estrogenic hormone, 17alpha-ethinylestradiol (EE2), and the organochlorine pesticide, endosulfan (ES). For each substance, gamete fertilization was performed and embryo development followed in contaminated reference seawater. Following exposure, embryotoxicity was evaluated by calculating the percentage of abnormal D-larvae obtained at 20 h development. Genotoxicity was measured in parallel by conducting a comet assay on enzymatically dissociated cells of pre-shelled larvae (16 h development). The oxidized DNA base, 8-oxodGuo, was also measured by HPLC coupled to electrochemical detection. For each contaminant, the relationship between genotoxicity and embryotoxicity was then studied to check for the possible significance of genotoxicity in the population dynamics of marine bivalves from polluted areas. For BaP, embryotoxicity and DNA strand breakage were both observed from the lowest tested concentration of 0.2 nM. Induction of 8-oxodGuo was significant from 20 nM. Endosulfan exposure resulted in similar effects for oyster embryos but from higher concentrations and followed a concentration-dependent manner. Embryotoxicity and genotoxicity in terms of DNA strand breaks were observed for endosulfan from 300 and 150 nM, respectively. No change in 8-oxodGuo level was observed following endosulfan exposure. EE2 displayed no toxic effect for oyster embryos within the range of tested concentrations (from 0.02 to 1.7 nM). Taking into account all the data collected during this study, a positive and significant correlation was demonstrated in oyster embryos between genotoxicity as measured by the comet assay and embryotoxicity.

Reproductive toxicity of the water accommodated fraction (WAF) of crude oil in the polychaetes Arenicola marina (L.) and Nereis virens (Sars)

“…Other studies using individual PAHs have described teratogenic effects on early development stages, including disruption of axial development in sea urchins (Pillai et al, 2003) and abnormal development in oyster larvae (Wessel et al, 2007).…”

Toxicity of lead, cadmium and mercury on embryogenesis, survival, growth and metamorphosis of Meretrix meretrix larvae

“…Heavy metal concentrations causing lethal toxicity in embryos and larvae are much lower than those which are lethal to adults (Connor 1972;Beiras and His 1994). It has been shown that early developmental stages are highly sensitive to toxicants such as heavy metals (His et al 1999), pesticides (Wessel et al 2007) and antifouling paints (Bellas 2006). The toxicity of heavy metals such as copper to bivalves is well known since they have been used as antifouling agents for centuries (Laughlin et al 1988;Lapota et al 1993).…”

Effects of the pyrethroid insecticide deltamethrin on the hemocytes of Galleria mellonella

“…Therefore, hemocytes (via changes in cell number and development of structural abnormalities) are frequently used to demonstrate the cytogenetic damage caused by toxic chemicals (Yeh et al, 2005). Genotoxicity biomarkers are widely measured in ecotoxicology as molecular toxic effects of major environmental pollutants (Wessel et al, 2007). The micronucleus is a biomarker widely used in biomonitoring studies performed to evaluate the effects of pesticide exposure (Siu et al, 2004;Bolognesi et al, 2011).…”