Oxidative stress and apoptotic effects of copper and cadmium in the zebrafish liver cell line ZFL

Kwok, Man Long; Chan, King Ming

doi:10.1016/j.toxrep.2020.06.012

Cited by 7 publications

(3 citation statements)

References 69 publications

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“…However, in SH-SY5Y cells, copper applied alone did not induce an increase in caspase-3 activity, and this effect was not modified in the presence of myricetin. Similar findings, i.e., a copper-induced increase in ROS production accompanied with the suppression of apoptosis, were observed in zebrafish cells exposed to copper [44] and in malignant cells [45]. In P19 neuronal cells, we also failed to detect caspase activation during mild copper-induced neuronal damage [8,19].…”

Section: Discussionsupporting

confidence: 85%

Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper

et al. 2021

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Oxidative stress (OS) induced by the disturbed homeostasis of metal ions is one of the pivotal factors contributing to neurodegeneration. The aim of the present study was to investigate the effects of flavonoid myricetin on copper-induced toxicity in neuroblastoma SH-SY5Y cells. As determined by the MTT method, trypan blue exclusion assay and measurement of ATP production, myricetin heightened the toxic effects of copper and exacerbated cell death. It also increased copper-induced generation of reactive oxygen species, indicating the prooxidative nature of its action. Furthermore, myricetin provoked chromatin condensation and loss of membrane integrity without caspase-3 activation, suggesting the activation of both caspase-independent programmed cell death and necrosis. At the protein level, myricetin-induced upregulation of PARP-1 and decreased expression of Bcl-2, whereas copper-induced changes in the expression of p53, p73, Bax and NME1 were not further affected by myricetin. Inhibitors of ERK1/2 and JNK kinases, protein kinase A and L-type calcium channels exacerbated the toxic effects of myricetin, indicating the involvement of intracellular signaling pathways in cell death. We also employed atomic force microscopy (AFM) to evaluate the morphological and mechanical properties of SH-SY5Y cells at the nanoscale. Consistent with the cellular and molecular methods, this biophysical approach also revealed a myricetin-induced increase in cell surface roughness and reduced elasticity. Taken together, we demonstrated the adverse effects of myricetin, pointing out that caution is required when considering powerful antioxidants for adjuvant therapy in copper-related neurodegeneration.

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Section: Discussionsupporting

confidence: 85%

Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper

et al. 2021

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“…In a recent study on ZFL cells, co-exposure of increasing concentrations of Cu 2+ with a constant concentration of Cd 2+ could increase toxicity, whereas lower concentrations of Cu 2+ did not alter intracellular Cd 2+ levels. These results indicate that Cu 2+ might reduce Cd 2+ uptake [ 43 ]. Combining these observations with our findings in the present study, Cd 2+ antagonizes Cu 2+ accumulation via CTR1 in ZFL cells, but the effect is very limited.…”

Section: Discussionmentioning

confidence: 99%

Promotion of cadmium uptake and cadmium-induced toxicity by the copper transporter CTR1 in HepG2 and ZFL cells

Kwok

Law

et al. 2020

Toxicology Reports

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“…However, the upregulation of antioxidant genes can also have negative consequences. Kwok and Chan (2020) found that chronic exposure to copper induced the expression of antioxidant genes, including gstt1a and gsr, in the liver of zebra sh. The authors suggested that prolonged upregulation of antioxidant genes can lead to oxidative stress due to the accumulation of reactive oxygen species.…”

Section: Molecular Studiesmentioning

confidence: 95%

Assessment of Oxidative Stress in Zebrafish (Danio rerio) Exposed to Fenvalerate: Analysis of Antioxidant Enzyme Gene Expression and Enzyme Activity

Güneş,

Bayır,

Bayır

2023

Preprint

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This study aimed to investigate the effects of fenvalerate treatment on the expression of sod1, cat, gstt1a, gpx1a, gsr, and g6pd genes, as well as the activities of SOD, CAT, GST, GPX, GR, and G6PD enzymes in zebrafish. The assessment of oxidative stress was conducted by analyzing liver and gill tissue samples. Both the concentration of fenvalerate (3.125 and 6.25 µg/L) and the duration of exposure influenced the changes observed in antioxidant enzyme activities and gene expression in zebrafish. The RT-PCR results indicated that the expression of these genes in fenvalerate-exposed zebrafish might function as an immediate response mechanism to chemical-induced stress. Furthermore, the activities of CAT, GST, and G6PD enzymes in both tissues exhibited an increase exposure to fenvalerate doses of 3.125 and 6.25 µg/L. The activities of CAT, GST, and G6PD enzymes in both liver and gill tissues demonstrated a decrease. However, prolonged exposure (over 72 hours) resulted in significantly higher MDA concentrations in the liver and gill tissues compared to the control sample. These findings contribute to our understanding of the role of antioxidant enzymes in oxidative stress and have practical implications for designing aquaculture selection programs to enhance stress tolerance in fish.

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Oxidative stress and apoptotic effects of copper and cadmium in the zebrafish liver cell line ZFL

Abstract: Graphical abstract

Cited by 7 publications

References 69 publications

Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper

Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper

Promotion of cadmium uptake and cadmium-induced toxicity by the copper transporter CTR1 in HepG2 and ZFL cells

Assessment of Oxidative Stress in Zebrafish (Danio rerio) Exposed to Fenvalerate: Analysis of Antioxidant Enzyme Gene Expression and Enzyme Activity

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