top of page

Biological Effects of Singlet Oxygen

Singlet oxygen is involved in the induction of the body's natural defensive and healing mechanisms, which make the body's immune, nervous and other systems work at optimal capacity. Regular exposure to low levels of singlet oxygen lead to heightened neural functions, faster healing of damaged tissues, reduced susceptibility to disease and injury, and, ultimately, increased longevity. 

Beneficial Effects of Singlet Oxygen-Enriched Air

The singlet oxygen-enriched air produced by the ZMedicAir device enhances cellular energy production and, subsequently, metabolism. Making one feel more energized and refreshed, mind more alert and thought process faster and sharper. In addition, it has been shown that exposure to singlet oxygen-enriched air, reduces the level of ROS produced by monocytes as part of their defense mechanism against bacteria, cancer cells and other harmful elements. Monocytes are white blood cells that are involved in the inflammatory reaction in the body. The high levels of ROS produced during an inflammatory reaction have been shown to cause excessive tissue damage. Therefore, the reduction of the ROS levels will mitigate said damage. [Hulten et al. 1999]

Singlet Oxygen-Induced Damage Prevention and Healing

Energy in the body is produced in cellular breathing process where ATP is created. A side effect of the aerobic cellular breathing process is the production of reactive oxygen species (ROS) such as peroxides, hydroxyl radical, superoxide, singlet oxygen and so on. Most of these side products are free radical, which are highly reactive molecules. It has been shown that prolonged exposure to high ROS levels causes non-specific tissue damage by attacking membrane phospholipids, proteins, and DNA. Damage from ROS has been suspected to be cause cancer, cardiovascular and neurological diseases, psychiatric diseases, lung and kidney disorders, liver and pancreatic diseases, hypertension, infertility, aging, and so on [Brieger et al. 2012; Rahman et al. 2012].

However, it has become clearer that low to intermediate ROS levels, singlet oxygen in particular, play an essential role in the regulation of the body's functions through the induction of low level stress [D'Autréaux & Toledano, 2007]. This results in a form of stress-response hormesis [Gems & Partridge, 2008], which is a term referring to beneficial effects of a treatment that at high levels is actually harmful [Southam & Ehrlich, 1943]. This effect stems from low level activation of the intrinsic cellular ROS defense mechanism, which deals with oxidative stress, in addition to increasing the activity of phase II response enzymes that protect from damage beyond the ROS. As a result, low ROS levels lead to stress resistance, which manifests itself as reduced damage to tissues and slower aging, and ultimately, to an extended life span [Ristow & Zarse, 2010]. At the cellular level, ROS will induce mechanisms that regulate growth, programmed cell death, and other cellular signaling. At the systems level they contribute to complex functions such as blood pressure regulation, improved cognitive and immune function, and prevention of the development of degenerative and chronic diseases [Brieger et al. 2012; Rahman et al. 2012]. These competing effects make it clear that the level of ROS needs to be maintained within a certain range in the body, since not only ROS levels that are too high will interfere with the body's functions in such a way that potentially can lead to a disease and even death, but also ROS levels that are too low will have a similar detrimental effects.

Bibliography

D'Autréaux, B., & Toledano, M. B. (2007). ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis. Nature reviews Molecular cell biology, 8(10), 813-824.
Brieger, K., Schiavone, S., Miller Jr, F. J., & Krause, K. H. (2012). Reactive oxygen species: from health to disease. Swiss medical weekly, 142, w13659.
Gems, D., & Partridge, L. (2008). Stress-response hormesis and aging:“that which does not kill us makes us stronger”. Cell metabolism, 7(3), 200-203.
Hulten, L. M., Holmström, M., & Soussi, B. (1999). Harmful singlet oxygen can be helpful. Free Radical Biology and Medicine, 27(11), 1203-1207.
Krieger-Liszkay, A. (2005). Singlet oxygen production in photosynthesis. Journal of Experimental Botany, 56(411), 337-346.
Leisinger, U., Rüfenacht, K., Fischer, B., Pesaro, M., Spengler, A., Zehnder, A. J., & Eggen, R. I. (2001). The glutathione peroxidase homologous gene from Chlamydomonas reinhardtii is transcriptionally up-regulated by singlet oxygen. Plant molecular biology, 46(4), 395-408.
op den Camp, R. G., Przybyla, D., Ochsenbein, C., Laloi, C., Kim, C., Danon, A., ... & Apel, K. (2003). Rapid induction of distinct stress responses after the release of singlet oxygen in Arabidopsis. The Plant Cell, 15(10), 2320-2332.
Rahman, T., Hosen, I., Islam, M. T., & Shekhar, H. U. (2012). Oxidative stress and human health. Advances in Bioscience and Biotechnology, 3(07), 997.
Ristow, M., & Zarse, K. (2010). How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis). Experimental gerontology, 45(6), 410-418.
Southam, C. M., & Ehrlich, J. (1943). Decay resistance and physical characteristics of wood. Journal of Forestry, 41(9), 666-673.

bottom of page