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The role of free oxygen radicals in the aetiopathogenesis of rosacea
M. O. Öztas, M. Balk*, E. Ögüs, M. Bozkurt, I. H. Ögüs and N. Özer
Experimental Dermatology Original article
Summary
A possible link between superoxide dismutase activity and malondialdehyde level with the clinical manifestations of rosacea was investigated. We found differences in superoxide dismutase activities between mild rosacea (stages I and II) and severe involvement (stage III) groups, as well as between disease and control groups that were statistically significant (P < 0.05). In the mild involvement group (stages I and II), the superoxide dismutase activity was higher than in the control group (P < 0.05), while the malondialdehyde levels did not differ from the control.
In the severe involvement group (stage III), the superoxide dismutase activity was lower than in the control group (P < 0.05), and this was coupled to a raised level of malondialdehyde (P < 0.05). These findings clearly show that in the mild involvement phase of rosacea patients, superoxide dismutase activity was stimulated to protect the skin against reactive oxygen species so that the malondialdehyde levels were maintained. In contrast, in more severe disease, due to a decrease in the capacity of the antioxidant defence system, the malondialdehyde levels were increased. These findings support the 'antioxidant system defect hypothesis' in rosacea patients.Clinical & Experimental Dermatology, Volume 28 Issue 2 Page 188 - March 2003
What does all this mean? Marjorie Lazoff, MD, offers this explanation:
Regardless of its pathogenesis, any physical insult, if severe enough, induces the release of proinflammatory mediators, including ROIs. This is not unique to rosacea, it is a common pathway for injury. In fact, some people hypothesize it as THE common pathway explaining all tissue injury and death, holding the key to perfect health and theoretical immortality.For those not familiar, reactive oxygen species (ROS), including tissue-toxic reactive oxygen intermediates (ROI), are normal byproducts whenever oxygen is metabolized into water -- a process which occurs in every cell of the body. ROIs are potentially damaging to tissues but they are extremely short lived and local enzymes and metabolic processes usually keep ROIs in check.However, increased ROIs are generated in times of high metabolic demands -- illness or other physical stressors, local or systemic inflammation (as in the presence of neutrophils and other immune mediators) -- and also specific environmental forces such as sunlight (to the skin) and smoking and pollution (to the lungs). In these conditions -- and considering genetic, age, and general health status -- protective controls may not be adequate. Local damage from these ROIs occurs, and the damage may even become widespread and deadly. The pathophysiology involving ROIs is called oxidative stress.The damage in oxidative stress includes the lipid-rich cell membranes where, in the presence of ROIs, lipids are abnormally metabolized.
Cell membranes are very important because they filter chemicals going in and out of the cell, and because they house receptors that activate or inhibit cell activities.This study uses common lab measurements to evaluate oxidative stress in the skin of rosaceans. Superoxide dismutase (SOD) is one of many enzymes that destroy ROS, in this case the particular ROS called superoxide. One of the lipid peroxidation metabolites in plasma and cell membrane dysfunction is malondialdehyde (MD). SOD and MD are commonly used to measure oxidative stress in any organ system, or systemically.
I've noticed through the years that some countries, esp in Eastern Europe and Japan, are researching free oxygen radicals and oxidative stress in all diseases, one by one. So taken in context, this is a banal study documenting what was already known -- in ANY inflammatory situation, ROIs are formed. The same group has measured SOD and MD in many other condition -- rosacea is just an example of literally hundreds of diseases where free radical formation can be shown to occur. It gets a little silly -- I recall one Japanese study measured fewer ROSs in children who swam more laps in a pool than other group of children! <g>But most research in this area that I'm familiar with over the past ten years or so is much more serious, and revolves around critical care -- systemic infections, multiple organ failure, heart attacks and brain injuries and other situations when low blood flow, and so decreased oxygen, is occurring. It's truly fascinating stuff but, at present, has unfortunately not yielded many clinical therapies.The article reposted by Matija on rosacea-support about the anti-oxidant properties of topical metronidazole (Metros, Noritate) provides clinical perspective supporting the same view this article does: that rosacea is primarily an inflammatory condition with secondary vascular effects. I don't necessarily agree or disagree but I see it as increasing important theory in understanding rosacea, esp recently over the past five years.
For the full context, see Millikan's Proposed Inflammatory
Pathophysiology of Rosacea article:
http://groups.yahoo.com/group/rosacea-knowledge/message/1447
source > http://groups.yahoo.com/group/rosacea-knowledge/message/1466 |
