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Effect of Artificial Tear Formulations on the Metabolic Activity of Human Corneal Epithelial Cells after Exposure to Desiccation
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Tear metabolite changes in keratoconus.

D Karamichos1, J D Zieske2, H Sejersen3

  • 1Ophthalmology, University of Oklahoma - Dean McGee Eye Institute, Oklahoma City, OK, USA.

Experimental Eye Research
|January 13, 2015
PubMed
Summary
This summary is machine-generated.

Keratoconus (KC) tears show altered metabolites, particularly in the urea cycle, citric acid cycle (TCA), and oxidative stress pathways. These findings offer new insights into keratoconus pathogenesis.

Keywords:
KeratoconusMetabolomicsOxidative stressPentacamRigid Gas Permeable lenses

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Area of Science:

  • Biochemistry
  • Ophthalmology
  • Metabolomics

Background:

  • The exact cause of keratoconus (KC), a progressive eye condition, remains unknown.
  • Understanding tear metabolite alterations may reveal KC's underlying mechanisms.

Purpose of the Study:

  • To identify and compare endogenous tear metabolites in keratoconus patients versus healthy controls.
  • To investigate metabolic pathway dysregulation in KC.

Main Methods:

  • Tear samples collected from three groups: healthy controls, KC patients with rigid gas permeable lenses, and KC patients without correction.
  • Metabolomics analysis performed using liquid chromatography-tandem mass spectrometry (LC-MS/MS).

Main Results:

  • Over 40 out of 296 identified metabolites were significantly altered between groups.
  • Significant changes observed in glycolysis, gluconeogenesis, and the citric acid cycle (TCA).
  • Elevated oxidative stress markers, including decreased GSH-to-GSSG ratio and increased lactate-to-pyruvate ratio, were found in KC patients.

Conclusions:

  • Tear metabolite profiles in KC patients are significantly altered.
  • Dysregulation of urea cycle, TCA cycle, and oxidative stress pathways are implicated in keratoconus.
  • These findings contribute to understanding KC pathophysiology and may guide future therapeutic strategies.