Active and passive rubidium influx in normal human lenses and in senile cataracts

Maraini, G; Pasino, Mario

doi:10.1016/0014-4835(83)90048-9

Cited by 15 publications

(1 citation statement)

References 8 publications

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“…Human subcapsular cataracts but not cortical cataracts have also been found to be associated with activity loss in glutathione synthesis enzymes [6]. Ion analysis in early cortical cataracts showed the level of potassium to be twice as high as that of sodium [7, 8]. In 40 intracapsular extracted cortical and 40 subcapsular cataracts the differences in the quotients of K + and Na + values (mval/g lens fresh weight) were examined [9].…”

Section: Biochemical and Etiological Differencesmentioning

confidence: 99%

Cortical and Subcapsular Cataracts: Significance of Physical Forces

Pau¹

2005

Ophthalmologica

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Cortical cataracts usually begin with either sharp limited clear fluid clefts, resulting in opaque spokes, or clear lamellar separations, resulting in cuneiform opacities. They do not commence prior to 45 years of age. From this age on an increase in lens nuclei hardening can be detected. Therefore, during disaccommodation in older lenses, mechanical shear stresses must develop between the soft remaining cortices and the harder nuclei. These shear stresses are significant regarding the different cortical ruptures in predisposed lenses: in a privileged radial direction (according to zonular traction) of the sharp limited cortical spokes, or in parallel microridges at the commencement of lamellar separations, as observed when a rubber surface slides against a harder object. In pure cortical cataracts the ion pump (K⁺ > Na⁺) and investigated metabolic parameters remain largely intact. Therefore, it is not surprising that, in contrast to subcapsular cataracts, subcapsular opacities do not occur. Subcapsular cataracts are known to be caused by a variety of factors: aging, diabetes, corticosteroids, iridocyclitis, or X-ray, among many others. In contrast to cortical cataracts, subcapsular cataracts were found to be closely associated with ion pump damage (Na⁺ > K⁺) and a variety of metabolic activity alterations. In subcapsular cataracts passive fluids (from the vitreous and camera anterior) enter externally through the lens capsule. This initially forms numerous free clear, secondary grey, subcapsular fluid vacuoles. If the ion pump (metabolic barrier) is more severely damaged fluids may also enter the lens nucleus (secondary grey nuclear cataract), which rarely results in intumescent cataract. In cortical and subcapsular cataracts and lens perforations the main cause of grey opalescence appears to be the result of lens proteins (water-soluble crystalline) coming into direct contact with free fluids (water). In cortical cataracts this happens in the area of sharp limited mechanical cortical ruptures (fluid clefts), and in subcapsular cataracts during passive, external fluid entry, resulting in subcapsular fluid vacuoles and opacities, and also later grey-white nuclear opacities. The importance of water contact with water-soluble lens crystallines in behalf of light scattering and turbidness also has been investigated experimentally.

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Section: Biochemical and Etiological Differencesmentioning

confidence: 99%