In vitro glucose-induced cataract in copper–zinc superoxide dismutase null mice
- Resource Type
- Authors
- Anders Behndig; Kurt Karlsson; Eva Olofsson; Stefan L. Marklund; Thomas Brännström
- Source
- Experimental Eye Research. 81:639-646
- Subject
- Male
Null mice
medicine.medical_specialty
genetic structures
SOD1
chemistry.chemical_element
Zinc
Cataract
Superoxide dismutase
Mice
Cellular and Molecular Neuroscience
Organ Culture Techniques
Internal medicine
Diabetes mellitus
Lens, Crystalline
Image Processing, Computer-Assisted
medicine
Animals
Mice, Knockout
biology
Superoxide Dismutase
medicine.disease
Copper
eye diseases
Sensory Systems
In vitro
Ophthalmology
Cytosol
Glucose
Endocrinology
chemistry
Biochemistry
biology.protein
Female
sense organs
- Language
- ISSN
- 0014-4835
The purpose of this study was to evaluate the involvement of the superoxide radical in glucose-induced cataract using lenses from mice lacking the cytosolic copper-zinc superoxide dismutase (SOD1). Lenses from wild-type mice and SOD1 null mice were kept in organ culture with either 5.6 or 55.6 mM glucose for 6 days. The cataract formation was followed with digital image analysis and ocular staging. The lens damage was further quantified by analysis of the leakage of lactate dehydrogenase into the medium by the uptake of 86Rb and by determining the water content of the lenses. The formation of superoxide radicals in the lenses was assessed with lucigenin-derived chemiluminescence. Immunohistochemical staining for SOD1 was also performed on murine lenses. The SOD1 null lenses exposed to high glucose developed more cataract showed an increased leakage of lactate dehydrogenase and developed more oedema compared to the control lenses. At 5.6 mM glucose there was no difference between the SOD1 null and wild-type lenses. Staining for SOD1 was seen primarily in the cortex of the wild-type lens. This in vitro model suggests an involvement of the superoxide radical and a protective effect of SOD1 in glucose-induced cataract formation.