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very interesting article
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https://www.reviewofophthalmology.co...on-for-dry-eye
What exactly is oxidative stress? Oxidative stress occurs when the level of reactive oxygen species produced in cells and tissues exceeds normal levels. ROS are types of free radicals (an atom with one or more unpaired electrons) that play a beneficial role in cell signaling and overall cellular homeostasis. Antioxidants naturally present in tissues usually control ROS levels, but surplus ROS react with nearby proteins, lipids or other cellular components, leading to unpredictable, cumulative and often deleterious effects on normal cell function. Oxidative injury from ROS occurs in the tears and conjunctiva of Sjögren’s syndrome patients, and high levels of ROS and oxidative stress have been identified in the tear film of dry-eye patients2 and in animal models of dry eye.3
A primary source of cellular ROS is mitochondria, the intracellular organelles responsible for oxidation of glucose into H20, CO2 and the chemical energy of adenosine triphosphate; ROS are often a byproduct of this process. Antioxidants such as reduced glutathione or enzymes such as superoxide dismutase provide electrons to convert ROS into less-reactive forms, but the cellular supply of antioxidants can be overwhelmed by too much ROS. As electrons pass along the mitochondrial electron transport chain, a fraction is lost to ROS and subsequent local oxidation events. This theft of electrons by ROS can lead to a host of cellular dysfunctions including membrane disruption. ROS can also inflict damage on DNA, RNA or cell proteins, effects that can ultimately lead to cell apoptosis.
A primary source of cellular ROS is mitochondria, the intracellular organelles responsible for oxidation of glucose into H20, CO2 and the chemical energy of adenosine triphosphate; ROS are often a byproduct of this process. Antioxidants such as reduced glutathione or enzymes such as superoxide dismutase provide electrons to convert ROS into less-reactive forms, but the cellular supply of antioxidants can be overwhelmed by too much ROS. As electrons pass along the mitochondrial electron transport chain, a fraction is lost to ROS and subsequent local oxidation events. This theft of electrons by ROS can lead to a host of cellular dysfunctions including membrane disruption. ROS can also inflict damage on DNA, RNA or cell proteins, effects that can ultimately lead to cell apoptosis.
While high ROS levels within the mitochondria lead to oxidative stress and potential organelle damage, ROS outside the mitochondria may be involved in inflammation, a primary mechanism of dry-eye disease.1 This inflammation can be the result of ROS exiting the mitochondria, or the generation of ROS in other cellular structures. Macrophages and other phagocytes involved in fighting infection use ROS as a weapon against foreign invaders, but control of these ROS is not always adequate. In particular, pro-inflammatory cytokines, such as IL-1β, can stimulate ROS to levels that can lead to oxidative tissue injury.
In Russian clinical trials, SKQ1-induced reductions in dry-eye signs and symptoms were significantly greater than those seen with an artificial tear control.26 SKQ1 improved corneal cell function, increased tear-film stability and reduced dryness, burning, grittiness and blurred vision. In a subsequent U.S. clinical trial, SKQ1 reduced corneal and conjunctival staining, improved ocular discomfort scores and was generally superior to placebo control treatment.27 Of note, this study demonstrated SKQ1 improvements in both signs and symptoms of dry eye evoked through the use of the controlled adverse environment, a model that is designed to exacerbate dry-eye instigators, including oxidative stress effects. In both clinical trials, the compound exhibited a good safety profile and was well-tolerated by subjects.
https://www.reviewofophthalmology.co...on-for-dry-eye
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