260 JOURNAL OF COSMETIC SCIENCE already existing enzymes that would cause permanent cell damage. Thus, using Deofix TM in the incubating media with human foreskin fibroblasts prevented cell rep- lication. However, the replication of cells resumed normally when the Deofix•M media was replaced with media free of Deofix•. Experiments with Deofix TM and microorganisms demonstrated relatively low minimum inhibitory concentrations but considerably higher minimum lethal concentrations. This further supports the mode of action: limiting the availability of essential first transition series elements while not disrupting the function of existing enzyme systems containing these elements. The extended duration of the deodorant effects observed with Deofix TM (high efficacy even 48 hours after last treatment) may also be explained by its proposed mode of action. A conventional antimicrobial deodorant would be expected to function only as long as the skin surface concentration of the antimicrobial agent in the axilla remains at a level required to inhibit microbial growth. With time, however, deodorant ingredients ap- plied to the axilla are inactivated by skin and sweat components, rubbed off, diluted by sweat, or otherwise transferred to articles of clothing, thereby reducing their antimi- crobial effects in the axilla. The principle is simple: if you remove or otherwise inactivate the antimicrobial agent, you also lose deodorant efficacy. With deodorants that function like DeofixV• (by complexing elements essential for microbial proliferation), the situation is very different. On application to the axilla, DeofixVM forms very strong complexes with any first transition series metal ions that are present. Removal of these complexes from the axilla surface by any of the mechanisms proposed above does not decrease the deodorant efficacy. Resumed rapid bacterial mul- tiplication (and odor generation) can only occur when the trace elements that were removed by the DeofixV• are replaced. The replacement may come from skin cells, sweat, or external sources. The extended deodorant efficacy observed with Deofix TM suggests that this replacement occurs slowly. Finally, it should be mentioned that DeofixV• may be exhibiting some of its deodorant efficacy based on its antioxidant properties. The oxidation of sebum components has been proposed as one route in the production of underarm malodor. The use of anti- oxidants with antimicrobial agents has been reported for deodorant use (22-24). Simi- larly, it has been proposed that lipoxidases are capable of catalyzing the hyperoxidation of polyunsaturated fatty acids in sebum, which can further decompose into odiferous aldehydes, ketones, and acids. Inhibition by antioxidants of the hyperoxidation might also lead to reduction of malodor. Oxidation in biological systems usually involves the formation of reactive oxygen species (ROS). ROS have been invoked as a major cause of skin damage and aging. One of the most damaging ROS species is the hydroxyl radical. Formation of hydroxyl radicals is catalyzed by trace quantities of iron or copper via Haber-Weiss pathways. In these reactions the reduced form of ionic iron, Fe(II), or ionic copper, Cu(I), initiates the hydroxyl radical-generating reaction. Because of the central role of iron in catalyzing the formation of free radicals, as well as other toxic oxygen species, the use of iron chelators to reduce the tissue concentration of catalytically active iron has been examined. However, unless the chelator can reduce the iron concentration to below the catalytic levels required for free radical generation, and the chelated iron is not catalytically active in Haber-Weiss pathways, they cannot

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