Hydrogen Therapy Protects Eyes from Age-Related Damage in Mice
- Authors
- Ruichan Li, Yanli Liu, Jing Xie, Xudong Huang, Li Zhang, Hua Liu, Lihua Li
- Journal
- Free Radical Biology and Medicine
- Year
- 2019
- DOI
- 10.1016/j.freeradbiomed.2019.02.005
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Retinal Senescence
- Body System
- Visual System
TL;DR
Hydrogen treatment may slow down aging in the retina by reducing oxidative stress and preserving retinal function in mice.
Key Finding
In mice with chemically-induced retinal damage, hydrogen water reduced oxidative stress markers, prevented retinal thinning, and preserved light-detection ability by activating a protective protein called Sirt3.
Summary
This study tested whether hydrogen water could protect mouse eyes from damage caused by oxidative stress (harmful molecules that accumulate in cells). Researchers gave some mice a chemical that damages the retina (the light-sensitive part of the eye) and treated them with hydrogen water. Hydrogen water reduced harmful molecules in the retina, prevented the retina from thinning, and preserved the eye's ability to detect light—suggesting hydrogen may protect against age-related vision loss.
Practical Takeaway
This is early evidence from mouse studies only, so it cannot yet be applied to human health. The study suggests hydrogen water may have protective effects against oxidative stress in the eye, but human trials would be needed to determine if these benefits translate to people or if hydrogen water could help prevent age-related vision problems.
Abstract
Hydrogen possesses antioxidative effects and cures numerous types of ophthalmopathy, but the mechanism of hydrogen on ROS-induced retinal senescence remains elusive. In this study, retinal morphology revealed that hydrogen reduced the number and size of vitreous black deposits in Bruch's membrane in NaIO3 mice. Hydrogen also reduced ROS levels in the retina as assessed by DHE staining. Moreover, this result was consistent with the downregulation of expression of the oxidative stress hallmark OGG1. These findings suggested that hydrogen can reduce retinal oxidative stress induced by NaIO3, and this result was further verified using the antioxidant ALCAR. Mechanistic analysis revealed that hydrogen significantly inhibited the downregulation of Sirt3 expression, and this notion was confirmed using AICAR, which restores Sirt3 expression and activity. Moreover, hydrogen reduced the expression of p53, p21 and p16 and the number of blue-green precipitations in the retinas of NaIO3 mice as assessed by SA-β-gal staining. We also found that hydrogen decreased the expression of the DNA damage-related protein ATM, cyclinD1 and NF-κB but increased the expression of the DNA repair-related protein HMGB1, suggesting that hydrogen inhibits senescence in retinas of NaIO3 mice. Additionally, OCT examination revealed that hydrogen suppressed retinal high reflex formation significantly and prevented the retina from thinning. This result was supported by ERG assays that demonstrated that hydrogen prevented the reduction in a- and b-wave amplitude induced by NaIO3 in mice. Thus, our data suggest that hydrogen may inhibit retinal senescence by suppressing the downregulation of Sirt3 expression through reduced oxidative stress reactions.