Acute waterborne cadmium exposure induces liver ferroptosis in Channa argus
Year: 2024
Type: article
Abstract: , ROS, MDA and significantly decreasing the level of Ferritin, GSH, GSH-Px, GPX4, GST and SOD (p < 0.05 in all cases). In addition, the mRNA expression of ferroptosis related genes, gpx4 and slc7a11, were significantly downregulated by Cd. Moreover, Cd exposure significantly inhibited the Nrf2/Keap1 signaling pathway, one of the pathways involved in ferroptosis, by upregulating the mRNA levels of keap1a and keap1b, and downregulating the mRNA levels of nrf2 and its target genes (ho-1, nqo1 and cat). Cd exposure also caused extensive accumulation of vacuoles and lipid droplets in liver, as well as an increase in triglyceride content. Cd significantly affected lipid metabolism related enzyme activity and gene expression, which were also regulated by Nrf2/Keap1 signaling pathway. In summary, these results indicate that ferroptosis is a mechanism in waterborne Cd exposed fish liver injury via the Nrf2/Keap1 signaling pathway and the Cd induced hepatic steatosis is also modulated by Nrf2/Keap1 pathway at the whole-body level in fish. These findings provide new insights into the fish liver injury and molecular basis of Cd toxicity.
Authors: Xingyu Chen, Wenqian Sun, Yanting Song, Shangong Wu, Shouqi Xie, Wen Xiong, Chengdong Peng, Yu Peng, Zhengxiang Wang, Sovan Lek, Christer Hogstrand, Mette Sørensen, Lei Pan, Dong Liu
Institutions: Hubei University, Chinese Academy of Sciences, Institute of Hydrobiology, State Key Laboratory of Freshwater Ecology and Biotechnology, Hubei Normal University, Tongji Hospital, Huazhong University of Science and Technology, Université Toulouse III - Paul Sabatier, Evolution et Diversité Biologique, King's College London, Nord University
Language: English
Subfield: Health, Toxicology and Mutagenesis
Field: Environmental Science
Domain: Physical Sciences
Open Access status: gold
Estimated APC paid: $2,990
Awards: G266464369, G7611541313
OpenAlex ID: W4402027798