PUBLICATION
Oxidative stress and apoptotic effects of copper and cadmium in the zebrafish liver cell line ZFL
- Authors
- Kwok, M.L., Chan, K.M.
- ID
- ZDB-PUB-200717-9
- Date
- 2020
- Source
- Toxicology reports 7: 822-835 (Journal)
- Registered Authors
- Chan, King-Ming
- Keywords
- BCS, bathocuproinedisulfonic acid disodium salt, CAT, catalase protein, Casp3, caspase 3 protein, Casp8, caspase 8 protein, Casp9, caspase 9 protein, Cd, cadmium, Combined effects, Cu, copper, Cytotoxicity, GR, glutathione reductase protein, GST, glutathione-S-transferase protein, LC, lethal concentration, LC20, lethal concentration of 20 % population, LC50, median lethal concentration, Mitochondrial function, NAC, N-acetyl-l-cysteine, PBS, phosphate-buffered saline, SOD, superoxide dismutase proteins, VE, tocopherol (Vitamin E), cat, catalase gene, ccs, copper chaperone for superoxide dismutase gene, ef1a, elongation factor 1-alpha gene, gr, glutathione reductase gene, gst, glutathione-S-transferase gene, mtDNA, mitochondrial DNA, sod1, superoxide dismutase 1 gene, sod2, superoxide dismutase 2 gene, ybx1, Y box-binding protein 1 gene, z, zebrafish
- MeSH Terms
- none
- PubMed
- 32670800 Full text @ Toxicol Rep
Citation
Kwok, M.L., Chan, K.M. (2020) Oxidative stress and apoptotic effects of copper and cadmium in the zebrafish liver cell line ZFL. Toxicology reports. 7:822-835.
Abstract
Copper (Cu) and cadmium (Cd) are widely used in industrial activities, resulting in Cu and Cd contamination in aquatic systems worldwide. Although Cu plays an essential role in many biological functions, an excessive amount of the metal causes cytotoxicity. In contrast, Cd is a non-essential metal that usually co-exists with Cu. Together, they cause oxidative stress in cells, leading to cell damage. These metal ions are also believed to cause cell apoptosis. In this study, we used a zebrafish liver cell line, ZFL, to study combined Cu and Cd cytotoxicity. Although Cd is more toxic than Cu, both were found to regulate the expression of oxidative stress related genes, and neither significantly altered the activity of oxidative stress related enzymes. Co-exposure tests with the antioxidant N-acetyl-l-cysteine and the Cu chelator bathocuproinedisulfonic acid disodium salt demonstrated that Cd toxicity was due to the oxidative stress caused by Cu, and that Cu at a low concentration could in fact exert an antioxidant effect against the oxidative stress in ZFL. Excessive Cu concentration triggered the expression of initiator caspases (caspase 8 and caspase 9) but suppressed that of an executioner caspase (caspase 3), halting apoptosis. Cd could only trigger the expression of initiator caspases; it could not halt apoptosis. However, a low concentration of Cu reduced the mitochondrial superoxide level, suppressing the Cd-induced apoptotic effects in ZFL.
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Human Disease / Model
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