Normal protein and glycoprotein profiles of reflex tears and trace element composition of basal tears from heavy and slight deposits on soft contact lenses

Baguet, J.; Claudon-Eyl, V.; Sommer, F.; Chevallier, P.

Clao Journal Official Publication of the Contact Lens Association of Ophthalmologists Inc 21(2): 114-121

1995


ISSN/ISBN: 0733-8902
PMID: 7796521
Document Number: 448290
We investigated the hypothesis that lacrimal component accumulation on soft contact lenses (SCL) may be induced by an abnormal protein, glycoprotein, or trace element composition of the tear fluid. Individual tear samples were collected from healthy non-SCL wearers (normal patients) and SCL wearers grouped as either "slight-depositor" or "heavy depositor" following SCL spoilage rate and frequency. The reflex tear proteins were analyzed by three electrophoretic procedures: sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) on minigels, isoelectric focusing (IEF) on immobilized pH gradients (IPG 47), and two-dimensional separation combining IEF in the first dimension to orthogonal SDS-PAGE. After separation, the proteins were detected by silver staining and identified by immunologic probes. The reflex tear glycoproteins were analyzed by lectin affinity associated electrotransfer of SDS-PAGE with a panel of five biotinylated lectin probes: Canavalia ensiformis (Con A), Artocarpus integrifolia (Jacalin), Glycine max (SBA), Ulex europaeus (UEA 1), and Triticum vulgaris (WGA) agglutinins. The basal tear trace elements were analyzed by Synchrotron Radiation X-ray Fluorescence. Despite the highly sensitive techniques used in the study, the profiles of reflex tear proteins, glycoproteins, and trace elements appeared to vary slightly among individuals. No evident qualitative difference in reflex tear fluid related to SCL wear or deposit formation susceptibility was found. The presence or absence of a particular protein, glycoprotein, or trace element could not be correlated with a different reactivity to SCL. However, potassium and carbohydrate residues having affinity with Jacalin and WGA presented little but not significant variations. These results Indicated that the mechanism responsible for abnormal protein deposition on SCL should not be due to an evident abnormal protein, glycoprotein, or trace element profile of reflex tear fluid and could provide valuable insights into the other suspected mechanisms.

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