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• W2509483356 abstract "Cataract is the leading cause of irreversible blindness worldwide. Increasing evidence indicates that oxidative stress is an important risk factor contributing to the development of cataract. Moreover, the enhancement of the antioxidant defense system may be beneficial to prevent or delay the cataractogenesis. The term oxidative stress has been defined as a disturbance in the equilibrium status of oxidant/antioxidant systems with progressive accumulation of reactive oxygen species (ROS) in intact cells. Superfluous ROS can damage proteins, lipids, polysaccharides, and nucleic acids within ocular tissues that are closely correlated with cataract formation. Therefore, prevention of oxidative stress damage by antioxidants might be considered as a viable means of medically offsetting the progression of this vision-impairing disease. Molecular hydrogen has recently been verified to have protective and therapeutic value as an antioxidant through its ability to selectively reduce cytotoxic ROS such as hydroxyl radical (OH). Hitherto, hydrogen has been used as a therapeutic element against multiple pathologies in both animal models and human patients. Unlike most well-known antioxidants, which are unable to successfully target organelles, hydrogen has advantageous distribution characteristics enabling it to penetrate biomembranes and diffuse into the cytosol, mitochondria, and nucleus. Consequently, we speculate that hydrogen might be an effective antioxidant to protect against lens damage, and it is important to further explore the biological mechanism underlying its potential therapeutic effects." @default.
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• W2509483356 date "2016-09-08" @default.
• W2509483356 modified "2023-10-06" @default.
• W2509483356 title "Hydrogen-Rich Saline as an Innovative Therapy for Cataract: A Hypothesis" @default.
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• W2509483356 doi "https://doi.org/10.12659/msm.899807" @default.
• W2509483356 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5019135" @default.
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• W2509483356 hasPublicationYear "2016" @default.
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