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Updated: Jul 11, 2026
08:26
Saturated Fatty Acids Induce Ceramide-associated Macrophage Cell Death
Published on: October 31, 2017
Ceramide-induced cell death in lens epithelial cells
1Department of Biochemistry, A.T. Still University of Medical Sciences, Kirksville College of Osteopathic Medicine, Kirksville, MO 63501, USA. asamadi@atsu.edu
Molecular Vision
|September 26, 2007
Summary
Ceramide treatment reduces lens epithelial cell viability and increases apoptosis, suggesting a role in age-related cataracts. This study investigated ceramide
Area of Science:
- Cell biology
- Ophthalmology
- Biochemistry
Background:
- Lens epithelial cells (LECs) are crucial for maintaining lens transparency.
- Dysfunction of LECs is implicated in the pathogenesis of age-related cataracts.
- Ceramides are bioactive lipids with diverse cellular functions.
Purpose of the Study:
- To investigate the impact of ceramide treatment on LEC viability and apoptosis.
- To determine if ceramide induces caspase activation and reactive oxygen species (ROS) generation in LECs.
Main Methods:
- Cell viability assessed using the MTT assay.
- Apoptosis evaluated via DAPI staining and DNA fragmentation analysis.
- Caspase-3/7 activation measured using the Apo-ONE Assay.
- ROS generation detected by carboxy-H2DCFDA staining and lipid peroxidation assay.
Main Results:
- C2-ceramide and C6-ceramide significantly reduced LEC viability in a dose- and time-dependent manner.
- Ceramide induced apoptosis, evidenced by nuclear changes and DNA fragmentation.
- Ceramide treatment activated caspase-3/7 and led to increased ROS generation.
Conclusions:
- Ceramides decrease LEC viability and promote apoptosis, indicating cellular stress.
- Ceramide-induced oxidative stress in LECs suggests a potential link to age-related cataracts.
- Modulation of ceramide levels may offer a therapeutic strategy for cataracts.
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