Oxidative stress, cell cycle arrest, DNA damage and apoptosis in the mud crab (Scylla paramamosain) induced by cadmium exposure

被引:86
作者
Cheng, Chang-Hong [1 ]
Ma, Hong-Ling [1 ]
Deng, Yi-Qin [1 ]
Feng, Juan [1 ]
Jie, Yu-Kun [1 ]
Guo, Zhi-Xun [1 ]
机构
[1] Chinese Acad Fishery Sci, South China Sea Fisheries Res Inst, Key Lab South China Sea Fishery Resources Exploit, Minist Agr, Guangzhou 510300, Guangdong, Peoples R China
关键词
Oxidative stress; DNA damage Response; Physiological response; Caspase-3; pathway; FRESH-WATER CRAB; ULTRASTRUCTURAL-CHANGES; HEPATOPANCREAS; PATHWAYS;
D O I
10.1016/j.chemosphere.2020.128277
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Cadmium is one of the most common heavy metal pollutants in the aquatic environment. Mud crab (Scylla paramamosain) is considered a model organism to monitor the impact of heavy metals. However, knowledge about toxicological mechanism of cadmium in crustaceans still remains limited. In this study, mud crabs were exposed to different concentrations of cadmium (0, 1.25, 2.5, 5 and 10 mg/L) for 72 h. Cadmium exposure significantly decreased superoxide dismutase (SOD) activity, catalase (CAT) activity and total antioxidative capacity (T-AOC), and significantly increased malondialdehyde (MDA) and H2O2 levels. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) activity significantly increased after cadmium exposure. Moreover, integrated biological responses version 2 (IBRv2) analysis suggested that cadmium exposure exerted stronger toxicity on mud crab. Furthermore, oxidative stress induced by cadmium exposure could decrease total hemocyte count (THC), interrupt Ca2+ homeostasis, and lead to cytological damage. Cadmium exposure induced DNA damage, which activated DNA damage response signaling ATR-CHK1-p53 pathway. Our results also showed that cadmium exposure significantly increased the apoptosis and caspase-3 mRNA levels, which implied that cadmium induced apoptosis through a caspase-3 pathway. (C) 2020 Elsevier Ltd. All rights reserved.
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页数:11
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