Researchers may be a step closer to understanding what causes cataracts and what may help prevent them.
In a study published in the American Journal of Ophthalmology, School of Medicine researchers report the culprit may be oxygen.
They measured oxygen concentrations in the eyes of patients undergoing retinal surgery. When a person has retinal surgery, standard practice calls for removal of the vitreous gel, a clear, jelly-like structure in the center of the eye.
This removal, called a vitrectomy, makes it easier for surgeons to repair the damaged retina.
After vitrectomy surgery, the surgeon replaces the vitreous gel with fluid. But not long after that, the eye begins to develop the clouding of the lens known as a nuclear cataract.
“It’s fairly well-accepted in the field that anyone over 50 who has vitrectomy surgery will develop a cataract within two years,” said Nancy M. Holekamp, M.D., the study’s lead author. “But if we could understand this process and prevent it, patients would be better off.”
Just before surgery, Holekamp, an associate professor of clinical ophthalmology and visual sciences, measured oxygen levels adjacent to the lens and near the center of the eye in the vitreous gel of 69 eyes.
Before retinal surgery, oxygen concentrations were very low in both places. After surgery, oxygen levels in both locations were about eight times higher than normal.
Although the retina has many blood vessels and high oxygen concentrations, the lens, separated from the retina by the vitreous gel, normally gets very little oxygen.
After surgery, however, oxygen from the retina can migrate toward the lens because the replacement fluid used to replace the vitreous gel doesn’t prevent that movement the way the natural gel does.
“It seems one of the important functions of the vitreous gel is to keep oxygen away from the lens,” Holekamp said. “When we remove the gel, we remove that protective mechanism.”
Even after the vitreous gel has been removed, Holekamp said it may be possible to lower the amount of oxygen near the lens by lowering the oxygen level in the fluid that is pumped into the eye.
“We’re proposing that we deoxygenate the fluid used to replace the vitreous gel,” she said. “There’s no good reason to infuse such a highly oxygenated fluid into the eye. If we want to perform surgery under more natural conditions, we should remove the oxygen from that fluid.”
A co-investigator, David C. Beebe, Ph.D., the Janet and Bernard Becker Professor of Ophthalmology and Visual Sciences and professor of cell biology and physiology, believes the same kind of mechanism may contribute to cataracts that form as people age.
The difference is that in age-related cataracts, the gel breaks down over several years. In vitrectomy patients, the gel disappears all at once.
Beebe and his colleague Ying-Bo Shui, M.D., Ph.D., a staff scientist in ophthalmology, have demonstrated a statistical relationship between breakdown of the vitreous gel and the risk for cataracts.
They believe that when the gel separates from the retina or begins to break down and liquefy, it allows fluid to flow over the surface of the oxygen-rich retina and carry that oxygen to the lens.
That’s true whether a person’s vitreous has begun to liquefy with age — a process known as vitreous liquefaction — or the vitreous gel has been removed in retinal surgery patients.
Beebe plans to conduct animal studies to see if he can prevent oxygen from reaching the lens.
“If we can remove or reduce the amount of molecular oxygen that reaches the lens, and that turns out to protect against nuclear cataracts in either human patients or in animals, I think it will make a very strong case for oxygen being the culprit,” he said.
Beebe, Holekamp and Ying-Bo Shui are launching a Clinical Cataract Research Center in the School of Medicine. They plan to study both the cataracts that form rapidly in vitrectomy patients and, in future studies, to look at drugs that may slow the onset or progression of cataracts.