A great deal of my research at the Duke Eye Center has been directed at trying to better understand keratoconus not simply as a disease but as a process, a susceptibility, and possibly even part of a more complex syndrome. In this endeavor, I freely and openly admit that I border on passionate obsession with understanding keratoconus better! While we have made enormous strides in Eye Banking and treatment options for keratoconus patients, it is embarrassing how little progress we have made in our understanding that connects the dots of observation with genuine understanding and practical knowledge that eventually leads to a nonsurgical cure for this condition. So keratoconus is not unlike other conditions like rosacea and glaucoma where progress has emphasized diagnosis and treatment without really getting to the bottom of what is going on (pathophysiology) at the subcellular and even the molecular levels. Researchers from Spain may be moving us a little closer in this regard as they examine the role of oxidative stress in the Keratoconus cornea:
Oxidative Stress in Keratoconus?
- Emma Arnal1,
- Cristina Peris-Martínez1,2,
- Jose Luis Menezo1,
- Siv Johnsen-Soriano1 and
- Francisco Javier Romero1,3
From the 1Fundación Oftalmológica del Mediterráneo (FOM), Valencia, Spain;
2Universidad CEU-Cardenal Herrera, Moncada, Spain; and
3Facultad de Medicina, Universidad Católica de Valencia ‘San Vicente Mártir’, Valencia, Spain.
- Corresponding author: Francisco Javier Romero, Facultad de Medicina, Universidad Católica de Valencia ‘San Vicente Mártir’, C/Quevedo, 2, 46001-Valencia, Spain;firstname.lastname@example.org.
Purpose. The purpose of this study was to establish the alterations of oxidative stress-related markers in keratoconus (KC) corneas.
Methods. A total of 6 healthy and 11 ectatic corneas (7 KC and 4 post-LASIK) were studied. Different oxidative stress-related markers were determined to assess their implication in the KC pathophysiology. Total antioxidant capacity and total nitrites present in the samples were assayed. Furthermore, lipid peroxidation products and the glutathione contents were determined, together with 4-hydroxynonenal (4-HNE) immunohistochemistry, to establish the relationship between KC and oxidative stress.
Results. The antioxidant capacity and glutathione content in KC corneas were decreased significantly when compared with healthy corneas. Moreover, the total nitrites and lipid peroxidation were significantly elevated in the corneas with KC when compared with the controls. There was a statistically significant difference in the amount of HNE-positive cells in KC corneas when compared with healthy corneas by immunohistochemistry. Post-LASIK ectatic corneas and KC corneas showed similar results.
Conclusions. The increased levels of oxidative stress markers and the decreased antioxidant capacity and antioxidant defenses in KC corneas, as well as in the post-LASIK ectatic corneas, indicate that oxidative stress might be involved in the development of this disease and may provide new insights for its prevention and treatment in the future.