Abstract
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous contaminants produced from human activity, such as combustion of biofuels, often found in aquatic ecosystems. Embryonic fish have been shown to be significantly sensitive to PAH exposure. Further, PAH toxicity can be modulated by environmental factors such as hypoxia and temperature. This study investigated how sunlight exposure modifies the toxicity of carbazole, a hetereocyclic PAH. Zebrafish embryos were exposed at 6 hours post fertilization (hpf) until 96 hpf using photoactivated and parent carbazole. Photoactivation was induced using a sunlight simulator. Survival rates, deformities, CYP1A activity, and oxidative stress were examined. Additionally, chemical analysis of photoactivated carbazole is under development to identify photoproducts. Exposure to parent carbazole did not cause mortality, but did cause minor embryonic developmental effects. Contrarily, photoactivated carbazole caused significantly higher rates of mortality and deformities at 72 hpf at concentrations of 1000 µg/L and higher. Photoactivated carbazole induced higher CYP1A activity, indicating that photoproducts acted as aryl hydrocarbon receptor (AHR) agonists despite carbazole being a known AHR inhibitor. Such induction may be related to the increased toxicity, which remains to be tested. These results show that sunlight can play a role in modifying the toxicity of certain organic contaminants.
