4.7 Article

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

Journal

CHEMOSPHERE
Volume 263, Issue -, Pages -

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.chemosphere.2020.128277

Keywords

Oxidative stress; DNA damage Response; Physiological response; Caspase-3 pathway

Funding

  1. China Agricultural Research System [CARS-48]
  2. Science and Technology Program Project of Guangzhou [201904010327]
  3. scientific and technological innovation teamof China Academy of Fishery Sciences [2020TD42]
  4. Basic and applied basic research fund of Guangdong Province [2019A1515011548]
  5. Key Laboratory of Tropical Marine Bioresources and Ecology, South China Sea Institute of Oceanology [2019011007]

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This study found that mud crabs suffered various biological and molecular damages after cadmium exposure, including oxidative stress, decreased cell count, DNA damage, and increased apoptosis.
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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