Lower antioxidant level might explain higher skin-cancer rate inmales – China Plain Chain Necklace

Men are three times more likely than women to develop a common formof skin cancer but medical science doesn’t know why. A new study may provide partof the answer. Researchers at The Ohio State University Comprehensive CancerCenter – Arthur G. James Cancer Hospital and Richard J.

SoloveResearch Institute (OSUCCC – James) have found that male mice hadlower levels of an important skin antioxidant than female mice andhigher levels of certain cancer-linked inflammatory cells. The antioxidant, a protein called catalase, inhibits skin cancer bymopping up hydrogen peroxide and other DNA-damaging reactive-oxygencompounds that form during exposure to ultraviolet B light (UVB), acommon source of sunburn and cancer-causing skin damage. Studies byothers have linked low catalase activity to skin cancerprogression. The research is published online in the Journal of Investigative Dermatology . The findings suggest that women may have more natural antioxidantprotection in the skin than men,” say study co-leaders GregoryLesinski and Tatiana Oberyszyn, both of the OSUCCC – James.

“As a result, men may be more susceptible to oxidative stress in the skin, which may raise the risk of skin cancer in mencompared to women,” says Lesinski, an assistant professor ofmolecular virology, immunology and medical genetics;. The study also found that UVB exposure caused a unique inflammatorywhite blood cell population called ‘myeloid-derived suppressorcells’ to migrate from the bone marrow into the exposed skin.Furthermore, higher numbers of these cells moved into the skin ofmale mice than female mice. “To our knowledge, we’ve shown for the first time that UVB exposurecauses a migration of systemic myeloid-derived suppressor cells,and it suggests that these cells might be a novel source ofUVB-induced immune suppression,” says first author NicholasSullivan, a research scientist in the Oberyszyn lab in theDepartment of Pathology. This, in turn, might mean that these UVB-induced inflammatory cellscontribute to the genesis of skin tumors and perhaps other tumorsrather than simply facilitating cancer progression, as generally thought, Sullivan notes. Normally, the body mobilizes the suppressor cells to limit immuneresponses to infection, sepsis or trauma so that healing can begin,Lesinski says. Engraved Silver Charm

“However, in the cancer setting, repeated UV light exposure orafter other chronic or repeated inflammatory stimuli, these cellspersist and become immunosuppressive,” he says. “They can renderhelpful immune cells such as T cells or natural killer cells unableto recognize and eliminate cancer cells in the skin.” Lesinski, Oberyszyn, Sullivan and their colleagues conducted thestudy using a strain of hairless mice that develops squamous cellcarcinoma of the skin – the second most common skin cancer inhumans – when exposed to UVB. The investigators also found that treating mice with topicalcatalase inhibited the migration of the suppressor cells intoUVB-exposed skin, suggesting that the influx of these cells inmales might be due to the relatively lower skin-catalase activity. In fact, male mice with UVB-induced skin tumors had 55 percent moreof the suppressor cells in the skin than did their femalecounterparts. “This is the first report to our knowledge of a sex discrepancy inthis group of inflammatory cells in tumor-bearing mice, and itsuggests that our findings might translate to other types ofcancer,” says Oberyszyn, associate professor of pathology. China Plain Chain Necklace

“Menface a higher risk of numerous types of cancers, and relativelyhigher levels of inflammatory myeloid cells might contribute tothis susceptibility.” Funding from the National Cancer Institute and The ValvanoFoundation for Cancer Research supported this research. Other Ohio State researchers involved in this study were KathleenL. Tober, Erin M. Burns, Jonathan S. Punk Rock Jewellery Manufacturer

Schick, Judith A. Riggenbach,Thomas A. Mace, Matthew A. Bill, and Gregory S.

Young. Additional References Citations.


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