RADIATION-INDUCED SKIN ULCER, CEREBRAL MENINGIOMA, AND SKIN CANCER FOLLOWING RADIATION AND RADIUM TREATMENT FOR ACTINOMYCOSIS

The aim: To follow-up nitric oxide content values in rat serum at the development of Staphylococcus aureus infected radiation skin injuries and their photodynamic therapy. Materials and methods: Eighty WAG male rats were studied in an experiment. Four groups were identified for evaluation. Group 1 included unaffected intact rats (n=20). Group 2 involved rats (n=20) with a modeled radiation-induced ulcer of the skin. The rats (n=20) with a modeled radiation-induced skin ulcer followed by infecting with Staphylococcus aureus were referred to group 3. Group 4 included rats (n=20) with Staphylococcus aureus infected radiation skin ulcer exposed to photodynamic therapy. Rats of groups 1-4 were sampled for biochemical blood examination on days 7, 14, 21, 30 and 45. Total nitric oxide metabolites (nitrites and nitrates) were measured according to V.A. Metelskaya et al. method. Results: Infectious agent (Staphylococcus aureus) present in skin ulcer impairs nitric oxide metabolism in rat blood serum that manifested in decreased total nitric oxide metabolites content on day 7, followed by its increase within days 14 to 45. While photodynamic therapy exposed on the Staphylococcus aureus infected radiation skin ulcer, total nitric oxide metabolites in blood serum had increased by day 7, but days 14 to 45 level was compliant with physiological norm. Conclusions: Infecting radiation skin ulcers with Staphylococcus aureus causes impaired nitric oxide metabolism, while photodynamic therapy helps to normalize the metabolism of the above-mentioned chemical compound that can improve healing of radiation skin ulcers.

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Sensitivity to Sunburn Is Associated with Susceptibility to Ultraviolet Radiation–Induced Suppression of Cutaneous Cell–Mediated Immunity

Journal of Experimental Medicine ◽

10.1084/jem.191.3.561 ◽

2000 ◽

Vol 191 (3) ◽

pp. 561-566 ◽

Cited By ~ 126

Author(s):

Deirdre A. Kelly ◽

Antony R. Young ◽

Jane M. McGregor ◽

Paul T. Seed ◽

Christopher S. Potten ◽

...

Keyword(s):

Skin Cancer ◽

Ultraviolet Radiation ◽

Contact Hypersensitivity ◽

Risk Assessments ◽

Cell Mediated Immunity ◽

Solar Exposure ◽

Radiation Induced ◽

N 93 ◽

Ambient Levels

Skin cancer incidence is highest in white-skinned people. Within this group, skin types I/II (sun sensitive/tan poorly) are at greater risk than skin types III/IV (sun tolerant/tan well). Studies in mice demonstrate that ultraviolet radiation (UVR)-induced suppression of cell-mediated immune function plays an important role in the development of skin cancer and induces a susceptibility to infectious disease. A similar role is suspected in humans, but we lack quantitative human data to make risk assessments of ambient solar exposure on human health. This study demonstrates that ambient levels of solar UVR, typically experienced within 1 h of exposure to noonday summer sunlight, can suppress contact hypersensitivity (CHS) responses in healthy white-skinned humans in vivo (n = 93). There was a linear relationship between increase in erythema and suppression of CHS (P < 0.001), and a moderate sunburn (two minimal erythema doses [2 MED]) was sufficient to suppress CHS in all volunteers by 93%. However, a single suberythemal exposure of either 0.25 or 0.5 MED suppressed CHS responses by 50 and 80%, respectively, in skin types I/II, whereas 1 MED only suppressed CHS by 40% in skin types III/IV. The two- to threefold greater sensitivity of skin types I/II for a given level of sunburn may play a role in their greater sensitivity to skin cancer.

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