Oxidative Stress and Antioxidant Defense Mechanisms in Sepia esculenta Larvae Induced by Co-Exposure to Environmental Cadmium and Copper
- 1College of Life Sciences, Yantai University, Yantai 264005, China
- 2School of Fisheries, Ludong University, Yantai 264025, China
- 3College of Marine Life Science, Ocean University of China, Qingdao 266003, China
Abstract
Cu and Cd, as common heavy metals occurring in the oceans, can induce oxidative stress and toxic responses in marine organisms. Important economic cephalopods inhabit the eastern coastal areas of China, and exposure to Cu and Cd poses a threat to their normal physiological activities, resulting in serious inhibition of their growth. However, the underlying toxicological mechanisms affecting these cephalopods’ larval stages remain to be elucidated. Here, indicators of oxidative stress and transcriptomics were employed to analyze the toxicological mechanisms of S. esculenta larvae exposed to Cd and Cu. GO and KEGG analysis results indicated that material transport, cellular processes, DNA replication, and other processes were inhibited. A comprehensive analysis of a protein–protein interaction network and KEGG pathways was used to explore the mechanism underlying the toxicity of co-exposure to Cu and Cd toward S. esculenta larvae. We found that Cu and Cd induce significant damage and oxidative stress. The results showed that among 20 identified key genes, ITGA4, LAMA1, and LAMC1, which are involved in the adhesion and connection between cells and the extracellular matrix; COL6A1, COL6A3, COL6A4, and COL6A6, which maintain the integrity of the extracellular matrix; and ABCA1, ABCC5, and ABCC7, which regulate the transmembrane transport of Cu and Cd were involved in the mechanism of toxicity. We suggest that co-exposure to the metals primarily inhibits the connection and adhesion between the cells of the larvae and disrupts the structure and function of the extracellular matrix. The results provide a foundation for understanding the toxicological mechanism of S. esculenta and should be of benefit to artificial breeding programs.
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BibTeX
@article{zhu2026oxidative,
title = {{Oxidative Stress and Antioxidant Defense Mechanisms in Sepia esculenta Larvae Induced by Co-Exposure to Environmental Cadmium and Copper}},
author = {Xueyu Zhu and Xiaokai Bao and Mingzhi Guo and Weijun Wang and Xiumei Liu and Jianmin Yang and Zan Li},
journal = {Antioxidants},
year = {2026},
month = may,
doi = {10.3390/antiox15060695},
url = {https://doi.org/10.3390/antiox15060695},
note = {CC BY},
}
RIS
TY - JOUR
TI - Oxidative Stress and Antioxidant Defense Mechanisms in Sepia esculenta Larvae Induced by Co-Exposure to Environmental Cadmium and Copper
AU - Xueyu Zhu
AU - Xiaokai Bao
AU - Mingzhi Guo
AU - Weijun Wang
AU - Xiumei Liu
AU - Jianmin Yang
AU - Zan Li
PY - 2026
DA - 2026/05/30
JO - Antioxidants
DO - 10.3390/antiox15060695
UR - https://doi.org/10.3390/antiox15060695
AB - Cu and Cd, as common heavy metals occurring in the oceans, can induce oxidative stress and toxic responses in marine organisms. Important economic cephalopods inhabit the eastern coastal areas of China, and exposure to Cu and Cd poses a threat to their normal physiological activities, resulting in serious inhibition of their growth. However, the underlying toxicological mechanisms affecting these cephalopods’ larval stages remain to be elucidated. Here, indicators of oxidative stress and transcriptomics were employed to analyze the toxicological mechanisms of S. esculenta larvae exposed to Cd and Cu. GO and KEGG analysis results indicated that material transport, cellular processes, DNA replication, and other processes were inhibited. A comprehensive analysis of a protein–protein interaction network and KEGG pathways was used to explore the mechanism underlying the toxicity of co-exposure to Cu and Cd toward S. esculenta larvae. We found that Cu and Cd induce significant damage and oxidative stress. The results showed that among 20 identified key genes, ITGA4, LAMA1, and LAMC1, which are involved in the adhesion and connection between cells and the extracellular matrix; COL6A1, COL6A3, COL6A4, and COL6A6, which maintain the integrity of the extracellular matrix; and ABCA1, ABCC5, and ABCC7, which regulate the transmembrane transport of Cu and Cd were involved in the mechanism of toxicity. We suggest that co-exposure to the metals primarily inhibits the connection and adhesion between the cells of the larvae and disrupts the structure and function of the extracellular matrix. The results provide a foundation for understanding the toxicological mechanism of S. esculenta and should be of benefit to artificial breeding programs.
SN - 2076-3921
ER -