Genotoxicant induced DNA damage and repair in early and late developmental stages of the grass shrimp Paleomonetes pugio embryo as measured by the comet assay

• Published in: Aquatic toxicology 2004-01, Vol.66 (1), p.1-14
• Main Authors: Hook, Sharon E, Lee, Richard F
• Format: Article
• Language: English
• Subjects: Animal, plant and microbial ecology; Animals; Applied ecology; benzo(a)pyrene; Biological and medical sciences; Brackish; Chemical mutagenesis; Comet Assay; Crustacea; Danio rerio; Developmental toxicity; DNA damage; DNA Damage - drug effects; DNA repair; DNA Repair - genetics; Ecotoxicology, biological effects of pollution; Effects of pollution and side effects of pesticides on protozoa and invertebrates; Embryo, Nonmammalian; Fundamental and applied biological sciences. Psychology; Genotoxicity; hexavalent chromium; hydrogen peroxide; Medical sciences; Mutagens - toxicity; Palaemonetes pugio; Palaemonidae - embryology; Palaemonidae - genetics; Paleomonetes pugio; Reproduction - genetics; Toxicology
• ISSN: 0166-445X; 1879-1514
• DOI: 10.1016/j.aquatox.2003.06.002

In this study, data are presented which link frequency of DNA strand breaks and repair capability to developmental stage. Stages 4 and 7 embryos of the grass shrimp ( Palaemonetes pugio) were exposed to various concentrations of benzo[α]pyrene (BαP), Cr(VI) and hydrogen peroxide. Following exposure, responses were measured as changes in hatching rates and DNA strand breaks (using the comet assay). The comet assay was modified by treatment of isolated nuclei with endonucleases which cleave DNA at oxidative lesions in DNA prior to electrophoresis. DNA repair was followed by transfer of toxicant exposed embryos to clean water and periodic determination of strand breaks. DNA strand breaks were higher in stage 7 embryos than in stage 4 embryos after exposure to the same concentration of different genotoxicants. However, when samples were treated with endonucleases to measure oxidative lesions, the total amount of DNA damage between stages 4 and 7 were similar. After toxicant exposure and transfer to clean water, DNA strand breaks in stage 7 embryos returned to background levels more rapidly than in stage 4 embryos. Similarly, samples treated with endonucleases during DNA repair studies showed that oxidative lesions were repaired more rapidly in stage 7 than in stage 4. These findings suggest that because of rapid DNA repair in late embryo stages that early embryo stages are more likely to have developmental effects after genotoxicant exposure.