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Terfenadine induces thymocyte apoptosis via mitochondrial pathway
Riyo Enomoto1, Tomoe Komai, Yukari Yoshida
1Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kobe Gakuin University, Japan.
European Journal of Pharmacology
|August 4, 2004
Summary
Terfenadine induces apoptosis in rat thymocytes by causing DNA fragmentation and activating caspases. This process involves the mitochondrial pathway, leading to cell death.
Area of Science:
- Immunology
- Cell Biology
- Toxicology
Background:
- Terfenadine is an antihistamine with known cardiotoxic effects.
- Apoptosis, or programmed cell death, is a critical cellular process.
- Thymocytes are T lymphocytes crucial for immune function.
Purpose of the Study:
- To investigate the effects of terfenadine on rat thymocytes.
- To determine the mechanism by which terfenadine induces cell death.
Main Methods:
- Treatment of rat thymocytes with varying concentrations of terfenadine.
- Assays for DNA fragmentation, phosphatidylserine translocation, and chromatin condensation.
- Measurement of caspase activities (caspase-8, -9, -3-like).
- Analysis of mitochondrial membrane potential and cytochrome c release.
Main Results:
- Terfenadine induced significant DNA fragmentation in a dose- and time-dependent manner.
- Morphological hallmarks of apoptosis, including phosphatidylserine externalization and chromatin condensation, were observed.
- Terfenadine activated caspase-3 and -9, but not caspase-8, in thymocytes.
- A decrease in mitochondrial membrane potential and cytochrome c release were detected.
Conclusions:
- Terfenadine induces apoptosis in rat thymocytes.
- The apoptosis is mediated through the mitochondrial pathway.
- Caspase-3 and -9 activation are key events in terfenadine-induced thymocyte apoptosis.