Lipid peroxidation as a possible cause of cataract

• Published in: Mechanisms of ageing and development Vol. 44; no. 1; pp. 69 - 89
• Main Authors: Babizhayev, Mark A., Deyev, Anatoly I., Linberg, Leonid F.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 01.07.1988; Elsevier Science
• Subjects: Aggregates formation; Biological and medical sciences; Cataract; Cataract - etiology; Cataract - pathology; Cell Membrane - ultrastructure; Cell physiology; Fundamental and applied biological sciences. Psychology; Human lens; Humans; Lens, Crystalline - physiopathology; Lens, Crystalline - ultrastructure; Lipid layer damage; Lipid peroxidation; Lipid Peroxides - physiology; Microscopy, Electron; Molecular and cellular biology; Vision, photoreception; Lipid peroxidation; Cataract; Lipid layer damage; Human lens; Aggregates formation; Human; Fluorescence; Lipids; Arachidonic acid; Aggregation; Gas chromatography; Opacification; Transmission electron microscopy; Ultrastructure; Ultraviolet spectrum; Lens; Oxidation; Peroxidation
• ISSN: 0047-6374; 1872-6216
• DOI: 10.1016/0047-6374(88)90080-2

The role of free-radical-induced lipid oxidation in the development of human lens opacity was studied. Physico-chemical parameters of the lens fiber membranes at different stages of cataract have been investigated. The deterioration of lens fiber plasma membranes structure preceding formation of large aggregates in lenticular matter, leading to lens opacity, was observed by electron microscopy. Initial stages of cataract were characterized by the accumulation of primary (diene conjugates, cetodienes) lipid peroxidation (LPO) products, while in the later stages there was a prevalence of end LPO fluorescent products. Reliable increase in oxiproducts of fatty acyl content of lenticular lipids was shown by direct gas chromatography technique obtaining fatty acid fluorine-substituted derivatives. The lens opacity degree is found to correlate with the level of the end LPO fluorescent product accumulation in its tissue, accompanied by SH group oxidation of crystallins due to decrease of reduced glutathione concentration in the lens. The injection of LPO products into the vitreous has been shown to induce cataract. It was concluded that peroxide damage of the lens fiber membranes may be the initiatory cause of cataract development.