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In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice
Published on: November 22, 2017
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Bioimaging tools reveal copper processing in fish cells by mitophagy
1School of Energy and Environment and State Key Laboratory of Marine Pollution, City University of Hong Kong, Kowloon, Hong Kong, China; Research Centre for the Oceans and Human Health, City University of Hong Kong Shenzhen Research Institute, Shenzhen 518057, China.
Aquatic Toxicology (Amsterdam, Netherlands)
|July 14, 2023
Summary
Copper (Cu) accumulation in fish cells is primarily targeted to mitochondria. Damaged mitochondria are cleared via mitophagy, preventing prolonged copper toxicity.
Area of Science:
- Cell Biology
- Environmental Toxicology
- Trace Metal Metabolism
Background:
- Copper (Cu) is an essential trace metal, but its cellular regulation, distribution, and detoxification mechanisms are not fully understood.
- Understanding how cells handle excess copper is crucial for assessing environmental toxicity.
Purpose of the Study:
- To visualize copper localization within cellular organelles in fish fin cells.
- To investigate the cellular response and detoxification mechanisms following copper exposure.
Main Methods:
- Utilized bioimaging techniques to track copper in fish fin cells (Siganus fuscescens).
- Assessed cell viability at various copper concentrations and exposure times.
- Performed organelle purification to quantify copper levels in mitochondria and lysosomes.
- Observed mitophagy as a cellular response to copper-induced mitochondrial damage.
Main Results:
- Copper exposure damaged cells and reduced viability, particularly at 100 µM.
- Mitochondria were the primary target for copper accumulation, showing immediate changes in number, size, and network.
- Despite initial damage, copper toxicity did not increase over extended exposure, suggesting a detoxification process.
- Lysosomes interacted with and digested damaged mitochondria, indicating mitophagy, with increased lysosomal numbers and decreased size/pH.
- Quantification confirmed high copper levels in mitochondria and lysosomes, supporting the mitophagy pathway.
Conclusions:
- Mitochondria are the initial cellular targets for excess copper.
- Fish cells employ mitophagy, involving lysosomes, to remove copper-damaged mitochondria and mitigate toxicity.
- This study elucidates a key detoxification pathway for copper in aquatic organisms.
