Adverse effects of methylmercury (MeHg) on life parameters, antioxidant systems, and MAPK signaling pathways in the copepod Tigriopus japonicus

被引:31
作者
Lee, Young Hwan [1 ]
Kang, Hye-Min [1 ]
Kim, Duck-Hyun [1 ]
Wang, Minghua [2 ]
Jeong, Chang-Bum [1 ,3 ]
Lee, Jae-Seong [1 ]
机构
[1] Sungkyunkwan Univ Suwon, Dept Biol Sci, Coll Sci, Suwon, South Korea
[2] Xiamen Univ, Coll Environm Ecol, Ctr Marine Environm Chem & Toxicol, Xiamen 361102, Peoples R China
[3] Hanyang Univ, Dept Chem, Coll Nat Sci, Seoul 04763, South Korea
关键词
MeHg; Methyl mercury; Reactive oxygen species; Copepod; Tigriopus japonicus; Antioxidant system; MAPK signaling pathway; ACTIVATED PROTEIN-KINASES; GLUTATHIONE-S-TRANSFERASE; OXIDATIVE STRESS; INTERTIDAL COPEPOD; PARACYCLOPINA-NANA; CAENORHABDITIS-ELEGANS; HEAVY-METALS; MALIGNANT-TRANSFORMATION; MITOCHONDRIAL-FUNCTION; DIETARY METHYLMERCURY;
D O I
10.1016/j.aquatox.2017.01.010
中图分类号
Q17 [水生生物学];
学科分类号
071004 ;
摘要
Methylmercury (MeHg) is a concerning environmental pollutant that bioaccumulates and biomagnifies in the aquatic food web. However, the effects of MeHg on marine zooplankton are poorly understood even though zooplankton are considered key mediators of the bioaccumulation and biomagnification of MeHg in high-trophic marine organisms. Here, the toxicity of MeHg in the benthic copepod Tigriopus japonicus was assessed, and its adverse effects on growth rate and reproduction were demonstrated. Antioxidant enzymatic activities were increased in the presence of MeHg, indicating that these enzymes play an important role in the defense response to MeHg, which is regulated by a complex mechanism. Subsequent activation of different patterns of mitogen-activated protein kinase (MAPK) pathways was demonstrated, providing a mechanistic approach to understand the signaling pathways involved in the effects of MeHg. Our results provide valuable information for understanding the toxicity of MeHg and the underlying defense mechanism in response to MeHg exposure in marine zooplankton. (C) 2017 Elsevier B.V. All rights reserved.
引用
收藏
页码:133 / 141
页数:9
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