Cataract pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The | The lens is composed of specialized proteins known as crystallins, having optical properties attributed to the fine arrangement of their three-dimensional structure and hydration. | ||
The membrane protein channels maintain osmotic and ionic balance across the lens, and the cytoskeleton provides for the specific shape of the lens cells, especially the fibre cells of the nucleus Protein-bound sulfhydryl (SH)-groups of the crystallins are protected against oxidation and cross-linking by high concentrations of reduced glutathione, thus maintaining its transparency. The molecular compositions, as well as tertiary and quaternary structures, provide a high spatial and timely stability principally of the larger crystallins, which are able to absorb shortwave visible light, ultraviolet and infrared radiation for longer durations while maintaining its transparency. This provides a substantial protective function for the activity of various enzymes of the carbohydrate metabolism.<br> | |||
As the person ages, the oxidative stress leads to an imbalance between the systemic manifestation of reactive oxygen species and the crystalline lens' ability to detoxify the reactive intermediates or to repair the resulting damage. The disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA. <br> | |||
The oxidative processes increase with age in the human lens, and concentration of proteins found is significant.This results in the breakdown and aggregation of protein and ends as damage to fiber cell membranes [8]. The ageing reduces the metabolic efficiency of the lens thus increasing its predisposition to noxious factors. The physiological changes with aging lead to an environment where ‘cataract noxae’ can act and interact to induce the formation of a cataract, many of which are associated with high protein-related light scattering and discolouration. The resulting from ageing, the glucose metabolic pathway functions rather an aerobically with low energetic efficiency making protein synthesis, transport and membrane synthesis problematic. In addition, the syncytial metabolicfunction of the denucleated fiber cells has to be maintained by the epithelium and the small group of fiber cells, which still have their metabolic armamentarium. This results in a steep inside-out metabolic gradient, which is complicated by the fact that the lens behaves like an overhaul system, shutting off damaged groups offiber cells -leading to wedge or sectorial cataract formation. All epithelial cells of the lens are subjected to light and radiation stress leading to alterations of the genetic code. Because defectivecells cannot be extruded, these are either degraded (by apoptosisor necrosis), or they are moved to the posterior capsular area,where they contribute to the formation of posterior sub capsular cataracts (PSC). | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WS}} | |||
{{WH}} | |||
[[Category:Ophthalmology]] | [[Category:Ophthalmology]] | ||
Latest revision as of 20:50, 29 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Pathophysiology
The lens is composed of specialized proteins known as crystallins, having optical properties attributed to the fine arrangement of their three-dimensional structure and hydration.
The membrane protein channels maintain osmotic and ionic balance across the lens, and the cytoskeleton provides for the specific shape of the lens cells, especially the fibre cells of the nucleus Protein-bound sulfhydryl (SH)-groups of the crystallins are protected against oxidation and cross-linking by high concentrations of reduced glutathione, thus maintaining its transparency. The molecular compositions, as well as tertiary and quaternary structures, provide a high spatial and timely stability principally of the larger crystallins, which are able to absorb shortwave visible light, ultraviolet and infrared radiation for longer durations while maintaining its transparency. This provides a substantial protective function for the activity of various enzymes of the carbohydrate metabolism.
As the person ages, the oxidative stress leads to an imbalance between the systemic manifestation of reactive oxygen species and the crystalline lens' ability to detoxify the reactive intermediates or to repair the resulting damage. The disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA.
The oxidative processes increase with age in the human lens, and concentration of proteins found is significant.This results in the breakdown and aggregation of protein and ends as damage to fiber cell membranes [8]. The ageing reduces the metabolic efficiency of the lens thus increasing its predisposition to noxious factors. The physiological changes with aging lead to an environment where ‘cataract noxae’ can act and interact to induce the formation of a cataract, many of which are associated with high protein-related light scattering and discolouration. The resulting from ageing, the glucose metabolic pathway functions rather an aerobically with low energetic efficiency making protein synthesis, transport and membrane synthesis problematic. In addition, the syncytial metabolicfunction of the denucleated fiber cells has to be maintained by the epithelium and the small group of fiber cells, which still have their metabolic armamentarium. This results in a steep inside-out metabolic gradient, which is complicated by the fact that the lens behaves like an overhaul system, shutting off damaged groups offiber cells -leading to wedge or sectorial cataract formation. All epithelial cells of the lens are subjected to light and radiation stress leading to alterations of the genetic code. Because defectivecells cannot be extruded, these are either degraded (by apoptosisor necrosis), or they are moved to the posterior capsular area,where they contribute to the formation of posterior sub capsular cataracts (PSC).