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Cadmium-induced ectopic apoptosis in zebrafish embryos
1Department of Biology and Chemistry, City University of Hong Kong, 83 Tat Chee Avenue, Kowloon, Hong Kong.
Archives of Toxicology
|February 19, 2003
Summary
Cadmium exposure causes developmental toxicity by inducing programmed cell death (apoptosis) in zebrafish embryos. This ectopic apoptosis, particularly in the neural tube, occurs at later developmental stages without disrupting cell cycle progression.
Area of Science:
- Developmental toxicology
- Cell biology
- Zebrafish models
Background:
- Cadmium is a toxic heavy metal with known adverse effects on development.
- The mechanisms underlying cadmium-induced developmental toxicity, specifically apoptosis, require further elucidation.
Purpose of the Study:
- To investigate if cadmium-induced developmental toxicity in zebrafish embryos is mediated by ectopic apoptosis.
- To determine the spatial and temporal distribution of apoptosis during embryonic development following cadmium exposure.
Main Methods:
- Confocal microscopy and 3D reconstruction of whole-mount stained zebrafish embryos.
- Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) assay on sectioned embryos.
- Flow cytometry to assess apoptosis dynamics and cell-cycle progression.
Main Results:
- Cadmium exposure led to significantly higher numbers of apoptotic cells in malformed zebrafish embryos.
- Apoptotic cells were localized in the degenerating neural tube of cadmium-treated embryos, but not in controls.
- Cadmium did not induce cell-cycle arrest, and apoptosis percentages were similar until 19 hours post-fertilization (hpf).
- A significant increase in apoptotic cells was observed at 28 hpf in cadmium-exposed embryos.
Conclusions:
- Cadmium induces ectopic apoptosis during zebrafish embryonic development, primarily affecting the neural tube.
- This apoptosis occurs at later developmental stages (28 hpf) and is not associated with cell-cycle arrest.
- The findings highlight apoptosis as a key mechanism in cadmium-induced developmental toxicity.