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GSH Levels Serve As a Biological Redox Switch Regulating Sulforaphane-Induced Cell Fate in Human Lens Cells
Thao Phuong Ngoc Huynh1, Richard P Bowater1, Federico Bernuzzi1,2
1School of Biological Sciences, University of East Anglia, Norwich, United Kingdom.
Investigative Ophthalmology & Visual Science
|December 2, 2021
Summary
Sulforaphane (SFN) causes lens cell death by depleting glutathione (GSH) and inhibiting glutathione reductase (GR). This oxidative stress triggers mitochondrial dysfunction, endoplasmic reticulum stress, and DNA damage, highlighting SFN
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Sulforaphane (SFN) is a phytochemical with therapeutic potential.
- SFN-induced cytotoxicity shows promise for preventing posterior capsule opacification (PCO).
Purpose of the Study:
- To elucidate the mechanisms by which SFN induces lens cell death.
- To understand the link between SFN treatment and cellular damage in the context of PCO prevention.
Main Methods:
- Utilized human lens epithelial cell line (FHL124) and central anterior epithelium.
- Assessed cell death, mitochondrial function, endoplasmic reticulum stress (ERS), DNA damage, autophagy, and glutathione levels.
- Analyzed SFN metabolites and glutathione reductase (GR) activity.
Main Results:
- N-acetylcysteine (NAC) protected against SFN-induced cell death, mitochondrial dysfunction, ERS, DNA damage, and autophagy.
- SFN depleted glutathione (GSH), the primary ocular antioxidant, and inhibited GR activity.
- SFN-GSH conjugate was the most abundant metabolite; GSH addition protected lens cells.
Conclusions:
- SFN induces lens cell death by depleting GSH and inhibiting GR, leading to oxidative stress.
- Oxidative stress triggers mitochondrial dysfunction, ERS, autophagy, and DNA damage.
- This mechanistic understanding supports SFN's therapeutic use for PCO and other disorders.
