摘要:
原油毒性主要源于多环芳烃(PAHs),而烷基化多环芳烃是PAHs的主要组分,氧化衍生物是PAHs降解和代谢过程所产生的重要产物。为评估比较烷基PAHs和氧化PAHs与其母体化合物对海洋生物的毒性,本研究以菲、3-甲基菲和菲醌为研究对象,对海洋经济鱼种——红鳍东方鲀(Takifugu rubripes)幼鱼进行了肝损伤评价。结果显示,线粒体、内质网是对上述3种化合物最为敏感的细胞器;3种化合物对肝损伤的表现形式不同:1.菲导致线粒体数量增加形态改变、内质网减少纹理模糊、出现脂滴、细胞空泡化、出血,2.3-甲基菲导致内质网减少、出现脂滴、细胞空泡化、出血,3.菲醌导致线粒体和内质网水肿、出现脂滴及细胞空泡化;随化合物浓度升高,肝损伤程度加重;同一浓度下,不同化合物损伤程度也有差异,总体趋势为菲醌>3-甲基菲>菲。上述结果表明,PAHs衍生物的毒性可能强于其母体化合物;除浓度外,化合物的结构可能对其毒性有重要影响。
关键词:
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多环芳烃
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肝毒性
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超微结构
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河鲀
Abstract:
The aquatic toxicity of crude oil is believed to be mainly caused by polycyclic aromatic hydrocarbons (PAHs), in which group alkyl-PAHs are the major components and oxygenated-PAHs are their importantly degradative and metabolic intermediates. In this study, the hepatic toxicities of alkyl PAHs, oxygenated PAHs and their parent compound to marine economic fish species, Takifugu rubripes were investigated. Phenanthrene, 3-methyl phenanthrene and phenanthraquinone were selected as model compounds and their impacts on the liver tissue injury of pufferfish were histologically assessed and compared through ultrastructure observation under microscope. The results showed that mitochondria and endoplasmic reticulum were the most sensitive organelles after exposure to the three compounds, and the injury patterns were different among the three compounds. Exposure to phenanthrene resulted in the quantity increase and morphological change of mitochondria, quantity decrease and fuzzy morphology of endoplasmic reticulum, appearance of lipid droplets and cell vacuoles as well as hemorrhage. The liver injury of 3-methyl phenanthrene manifested as the quantity decrease of endoplasmic reticulum, appearance of lipid droplets and cell vacuoles and hemorrhage. In comparison, phenanthraquinone induced the edema of mitochondria and endoplasmic reticulum and appearance of lipid droplets and cell vacuoles. In general, the liver lesions aggravated with the increasing of exposure concentrations in all three exposure groups. However, the liver injury extents were different among the three compounds under the same exposure concentration with a general trend of phenanthraquinone > 3-methyl phenanthrene > phenanthrene. Our results demonstrated that the hepatic toxicities of PAHs derivatives were possibly higher than their parent compound and the toxic mode of action should not ignore the importance of compound structure.
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