Related Experiment Videos
Inhibition of apoptosis by zinc: a reappraisal
D Barbieri1, L Troiano, E Grassilli
1Istituto di Patologia Generale, University of Modena, Italy.
Abstract:
Apoptosis--or programmed cell death--is an active type of cell death, occurring in several pathophysiological conditions. One of the most important characteristics of apoptosis is that cell death is preceded by DNA fragmentation, consequent to the activation of nuclear calcium- and magnesium-dependent endonuclease(s). DNA fragmentation can be inhibited by zinc ions. By using several techniques, such as DNA agarose gel electrophoresis, cytofluorimetric analysis of DNA content and of cell cycle, 3H-thymidine incorporation and trypan blue dye exclusion test, we show that zinc, despite completely inhibiting DNA fragmentation and the consequent loss of nuclear DNA content, does not protect rat thymocytes from spontaneous or dexamethasone-induced death. Our data also suggest that DNA fragmentation, although characteristic, is not a critical event for thymocyte death of apoptotic type.
Insights
Zinc ions inhibit DNA fragmentation during apoptosis (programmed cell death) but do not prevent cell death in rat thymocytes. DNA fragmentation is not essential for this type of cell death.
Area of Science:
- Cell Biology
- Biochemistry
Background:
- Apoptosis, or programmed cell death, is a critical physiological process.
- DNA fragmentation is a hallmark of apoptosis, often mediated by calcium- and magnesium-dependent endonucleases.
- Zinc ions are known inhibitors of DNA fragmentation.
Purpose of the Study:
- To investigate the role of DNA fragmentation in thymocyte apoptosis.
- To determine if inhibiting DNA fragmentation with zinc ions affects cell death.
Main Methods:
- DNA agarose gel electrophoresis
- Cytofluorimetric analysis of DNA content and cell cycle
- 3H-thymidine incorporation
- Trypan blue dye exclusion test
Main Results:
- Zinc ions completely inhibited DNA fragmentation and nuclear DNA content loss in rat thymocytes.
- Zinc ions did not prevent spontaneous or dexamethasone-induced thymocyte death.
- Data suggest DNA fragmentation is not a critical event for apoptotic thymocyte death.
Conclusions:
- DNA fragmentation, while characteristic, is not essential for thymocyte apoptosis.
- Inhibition of DNA fragmentation does not equate to prevention of programmed cell death.