Participación de las especies reactivas de oxígeno en la formación de la catarata / Involvement of reactive oxygen species in cataract formation

La catarata comprende la opacidad del cristalino, la cual puede afectar la corteza y el núcleo subcapsular anterior y posterior de manera progresiva, secundario a la acumulación de proteínas dañadas a este nivel, con pérdida del equilibrio entre la producción y la eliminación de las especies reactivas libres de oxígeno. La importancia de retrasar o identificar marcadores específicos, además de promover un nuevo blanco terapéutico, también es motivo de análisis y de estudio en diferentes líneas de investigación. Se realizó una revisión de la literatura del 01 de enero al 20 de julio del año 2020. Se utilizaron metabuscadores en inglés y español de PUBMED, INFOMED, CLINICALKEY, LILACS, EBSCO, SCIELO, PRISMA y UPTODATE, con el objetivo de identificar la nueva evidencia científica relacionada con el estrés oxidativo y su participación en la formación de la catarata. La barrera del cristalino funciona como un medio de intercambio entre diferentes moléculas, lo que impide el paso de antioxidantes al núcleo y provoca su opacificación. Las mitocondrias a nivel de la corteza del cristalino permiten la remoción de oxígeno. Posteriormente la fosforilación oxidativa forma radicales libres de superóxido que, de manera natural, con el paso del tiempo se acumulan a este nivel. Con la edad, la homeostasis adaptativa pierde la capacidad de responder ante los cambios de estrés oxidativo, por lo que el uso de antioxidantes -de manera profiláctica e intencionada- puede cambiar el destino último para esta patología. La falta de equilibrio en los procesos de óxido-reducción es responsable de la formación de la catarata(AU)

Cataract comprises opacification of the crystalline lens, which may progressively affect the cortex and the anterior subcapsular nucleus, secondary to accumulation of damaged proteins on this level, with loss of balance between production and elimination of free reactive oxygen species. The importance of delaying or identifying specific markers, as well as promoting a new therapeutic target, is the object of study and analysis of a variety of research lines. A review was conducted of the literature published from 1 January to 20 July 2020. Use was made of PubMed, Infomed, Clinical Key, Lilacs, EBSCO, SciELO, Prisma and UpToDate metasearch engines in English and Spanish to identify new scientific evidence about oxidative stress and its involvement in cataract formation. The crystalline lens barrier serves as a medium for exchange between various molecules, preventing entrance of antioxidants into the nucleus, which results in opacification. Mitochondria on the crystalline lens cortex allow oxygen removal. Oxidative phosphorylation then forms free superoxide radicals which naturally accumulate on this level with the passing of time. With aging, adaptive homeostasis loses its ability to respond to oxidative stress changes, but the prophylactic, targeted use of antioxidants may change the ultimate fate of this condition. Lack of balance in oxidation-reduction processes is the cause of cataract formation(AU)

Mini-rhexis for white intumescent cataracts

PURPOSE: To compare the intraoperative safety of two techniques of capsulorhexis for intumescent white cataracts: traditional one-stage continuous curvilinear capsulorhexis and two-stage continuous curvilinear capsulorhexis. METHODS: This prospective comparative randomized study included two groups: the 1-CCC group (11 patients) received traditional one-stage continuous curvilinear capsulorhexis with 5-6 mm diameter, and the 2-CCC (13 patients) group received a deliberately small continuous curvilinear capsulorhexis that was secondarily enlarged, or a two-stage continuous curvilinear capsulorhexis. Patients were stratified according to cataract subset, which was characterized echographically. Six patients were considered as type 1, fifteen as type 2 and three as type 3. Type 1 included intumescent white cataracts with cortex liquefaction and extensive internal acoustic reflections, type 2 included white cataracts with voluminous nuclei, a small amount of whitish solid cortex, and minimal internal acoustic reflections, and type 3 included white cataracts with fibrous anterior capsules and few internal echo spikes. RESULTS: With the one-stage technique, 46.15 percent of patients had leakage of the liquefied cortex; in addition, the surgeon perceived high intracapsular pressure in 61.53 percent of cases. Anterior capsule tears occurred in 23.07 percent of cases, discontinuity of capsulorhexis in 30.79 percent of cases and no posterior capsular rupture occurred. With the two-stage technique, leakage of the liquefied cortex occurred in 45.45 percent of cases; additionally, the surgeon perceived high intracapsular pressure in 36.36 percent of cases. No anterior capsule tears, discontinuity of capsulorhexis or posterior capsular rupture occurred. Considering each cataract subset, there was a higher incidence of leakage for type 2 as compared to types 1 and 3. CONCLUSIONS: Two-stage continuous curvilinear capsulorhexis helps prevent unexpected ...

Human lens epithelial layer in cortical cataract.

Normal and cataractous human eye lenses were studied by morphology and protein analysis. A marked decrease in protein sulfhydryl (PSH) and nonprotein sulfhydryl (NSPH) was observed in nuclear and cortical cataractous epithelia. Moreover, decrease in PSH contents and an increase in insoluble proteins were found to be correlated only in cortical cataractous epithelium which is also accompanied by various morphological abnormalities. In nuclear cataractous epithelium, however, there was very little insolubilisation of proteins. The epithelial morphology in nuclear cataracts was almost similar to normal lens epithelium. Hence, it is assumed that the protein insolubilisation and various morphological abnormalities are characteristics of cortical cataractous epithelium. This leads us to believe that opacification in cortical cataract might initiate in the epithelial layer.