Reactive oxygen species treatment

Photodynamic therapy uses non-thermal red light to activate verteporfin, which produces reactive oxygen species that locally damage the neovascular endothelium.24 Verteporfin treatment reduces the risk of loss of visual acuity and legal blindness over 1 to 2 years. Long-term results are not yet available. Severe photosensitivity for 3 to 5 days after the procedure is common and some patients experience a severe loss of vision. Eventually, most patients have some visual recovery. This procedure requires multiple treatments over time.22... 

Different mechanisms to explain the disinfection ability of photocatalysts have been proposed [136]. One of the first studies of Escherichia coli inactivation by photocatalytic Ti02 action suggested the lipid peroxidation reaction as the mechanism of bacterial death [137]. A recent study indicated that both degradation of formaldehyde and inactivation of E. coli depended on the amount of reactive oxygen species formed under irradiation [138]. The action with which viruses and bacteria are inactivated by Ti02 photocatalysts seems to involve various species, namely free hydroxyl radicals in the bulk solution for the former and free and surface-bound hydroxyl radicals and other oxygen reactive species for the latter [139]. Different factors were taken into account in a study of E. coli inactivation in addition to the presence of the photocatalyst treatment with H202, which enhanced the inactivation... 

That the oxidative burst is directly involved in the chemical defense of these algae is clear. This reaction can be inhibited by diphenyleneiodonium, a suicide inhibitor of NADPH-oxidase which suppresses both the production of reactive oxygen species and the natural resistance to epiphytic bacteria. In addition a role in the defense against endophytes was indicated, since pre-treatment with oligomeric guluronates resulted in decreased infection of L. digitata with the pathogen Laminariocolax tomentosoides [141]. 

The above data suggest an important role of reactive oxygen species in the development of heart diseases. This suggestion has been supported by many studies, which also demonstrated a potential efficacy of antioxidants, free scavengers, and chelators in the treatment of these diseases. Mitochondrial oxygen radical overproduction can probably be one of the critical causes. 

Figure 9.2. Mechanisms of aminoglycoside toxicity. This schematic representation summarizes the principles of aminoglycoside toxicity discussed in the text. Treatment with the drugs leads to the formation of reactive oxygen species through a redox-active complex with iron and unsaturated fatty acid or by triggering superoxide production by way of NADPH oxidase. An excess of reactive oxygen species, not balanced by intracellular antioxidant systems, will cause an oxidative imbalance potentially severe enough to initiate cell death pathways. Augmenting cellular defenses by antioxidant therapy can reverse the imbalance and restore homeostasis to protect the cell.

Aminolevulinic acid (ALA HCl, Levulan Kerastick) is indicated for the treatment of nonhyperkeratotic actinic keratosis of the face and scalp. It has two components, an alcohol solution vehicle and ALA HCl as a dry solid. The two are mixed prior to application to the skin. When applied to human skin, ALA is metabolized to protoporphyrin, which accumulates and on exposure to visible light produces a photodynamic reaction that generates reactive oxygen species (ROS).The ROS produce cytotoxic effects that may explain therapeutic efficacy. Local burning and stinging of treated areas of skin due to photosensitization can occur. 

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