Hydrogen Solution Prevents Blindness from Chemical Eye Burns
- Authors
- Miyuki Kubota, Shigeto Shimmura, Shunsuke Kubota, Hideyuki Miyashita, Naoko Kato, Kousuke Noda, Yoko Ozawa, Tomohiko Usui, Susumu Ishida, Kazuo Umezawa, Toshihide Kurihara, Kazuo Tsubota
- Journal
- Investigative Opthalmology & Visual Science
- Year
- 2011
- DOI
- 10.1167/iovs.10-6167
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Chemical Eye Burns
- Body System
- Ocular
TL;DR
Antioxidants can significantly reduce unwanted blood vessel growth in the eye after a chemical burn by blocking stress-related processes.
Key Finding
Hydrogen-enriched water irrigation significantly reduced abnormal blood vessel growth in chemically burned mouse corneas by suppressing harmful molecules and a cellular pathway involved in the injury response.
Summary
Researchers used mice to study how a chemical burn to the eye causes abnormal blood vessel growth that can lead to blindness. They found that harmful molecules called reactive oxygen species (ROS) trigger this blood vessel growth through a specific cellular pathway. When they treated the burned corneas with hydrogen-enriched water, it reduced these harmful molecules and prevented excessive blood vessel growth, working similarly to other antioxidant treatments.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen water may help prevent vision loss from severe eye chemical burns, but it has not been tested in humans. The findings are promising for potential eye injury treatment, but much more research would be needed before any clinical application.
Abstract
To investigate the role of reactive oxygen species (ROS) as the prime initiators of the angiogenic response after alkali injury of the cornea and observe the effects of antioxidants in preventing angiogenesis. The corneal epithelia of SOD-1-deficient mice or wild-type (WT) mice were removed after application of 0.15 N NaOH to establish the animal model of alkali burn. ROS production was semiquantitatively measured by dihydroethidium (DHE) fluorescence. Angiogenesis was visualized by CD31 immunohistochemistry. The effects of the specific NF-κB inhibitor DHMEQ, the antioxidant N-acetyl-L-cysteine (NAC), and hydrogen (H2) solution were observed. ROS production in the cornea was enhanced immediately after alkali injury, as shown by increased DHE fluorescence (P<0.01). NF-κB activation and the upregulation of vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein-1 (MCP-1) were significantly enhanced (P<0.01), leading to a significantly larger area of angiogenesis. Angiogenesis in SOD-1-/- mice corneas were significantly higher in WT mice (P<0.01), confirming the role of ROS. Pretreatment with the specific NF-κB inhibitor DHMEQ or the antioxidant NAC significantly reduced corneal angiogenesis by downregulating the NF-κB pathway (P<0.01) in both WT and SOD-1-/- mice. Furthermore, we showed that irrigation of the cornea with hydrogen (H2) solution significantly reduced angiogenesis after alkali-burn injury (P<0.01). Immediate antioxidant therapy with H2-enriched irrigation solution is a new potent treatment of angiogenesis in cornea to prevent blindness caused by alkali burn.