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Irradiated skin

Since p-nitrosobenzoic acid has been shown to have a half-life of some 4 min in rat blood, this intermediate, once formed in the capillaries of the irradiated skin, may meet the requirement of sufficient stability to reach sensitive targets as the bone marrow while travelling through the blood141. The reactivity of p-nitrosobenzoic acid with thiols appears not to have been tested hitherto. From the known Hammett constant (ap = +0.4555) one may deduce that the compound will show a reactivity in between the reactivities of nitrosobenzene and p-nitrosoacetophenone. [Pg.1026]

Ghoreishi M. Dutz JP Tolerance induction by transcutaneous immunization through ultraviolet-irradiated skin is transferable through CD44-CD254- T regulatory cells and is dependent on host-derived IL-10. J Immunol 2006 176 2635-2644. [Pg.100]

Kirihara T, Matsumoto-Miyai K, Nakamura Y, Sadayama T, Yoshida S, Shiosaka S. Prolonged recovery of ultraviolet B-irradiated skin in neuropsin (KLK8)-deficient mice. Br J Dermatol 2003 149 700-706. [Pg.76]

Anaesthetized mice (female, SKH-1, from Simonsen, injected intraperitoneally with sodium pentobarbital, 50 mg/kg body weight) were irradiated on one flank with light from the solar simulator. Mice were killed by cervical dislocation immediately after irradiation, and irradiated skin as well as control, non-irradiated skin from the contralateral flank were removed. Adhering fat and subcutis were gently scraped free and the samples were frozen in liquid nitrogen. [Pg.246]

The immediate appearance of lipid hydroperoxides after irradiation in this study contrasts with several other studies, which have either reported no increase in lipid-peroxidation products in skin after UV irradiation [21] or an increase only several hours after irradiation [27-29], In these studies the background level of lipid-peroxidation products has been high, even in control, non-irradiated skin. In contrast, in our experiments lipid hydroperoxides were undetectable before irradiation, but appeared at very high concentrations in skin immediately after irradiation. The discrepancies between various studies may be due to differences in technique. The HPLC-chemiluminescence assay used in the present study is specific for lipid hydroperoxides, and has less potential for artifact than the TBARS assay, which is known to suffer from many possibilities for artifact [30] -... [Pg.250]

Fig. 12. Lipid hydroperoxide concentration in irradiated skin from control and a-tocopherol supplemented mice. Asterisk supplemented concentration of lipid hydroperoxides was lower, p < 0.05. Fig. 12. Lipid hydroperoxide concentration in irradiated skin from control and a-tocopherol supplemented mice. Asterisk supplemented concentration of lipid hydroperoxides was lower, p < 0.05.
Fig. 13. Relationships between lipophilic antioxidants and lipid hydroperoxides in irradiated skin. (A) There was no relationship between decrease in a-tocopherol and appearance of lipid hydroperoxides. (B) There was a significant (p < 0.05) relationship between decrease in total Q (quinols + quinones) and appearance of lipid hydroperoxides. Fig. 13. Relationships between lipophilic antioxidants and lipid hydroperoxides in irradiated skin. (A) There was no relationship between decrease in a-tocopherol and appearance of lipid hydroperoxides. (B) There was a significant (p < 0.05) relationship between decrease in total Q (quinols + quinones) and appearance of lipid hydroperoxides.
In tests on irradiated skin of guinea pigs, anti-inflammatory compounds reduced the permeability of the dermal vasculature to plasma proteins by up to 30% (Song et al. 1968). However, since drug treatment was administered both before and after irradiation, this study is not definitive proof of the efficacy of these compounds. [Pg.208]

NIICRs to benzoic acid and methyl nicotinate can be inhibited by exposure to ultraviolet (UV) B and A light. The inhibition lasts for at least 2 weeks (Larmi et al. 1988). The reactions on non-irradiated skin sites also decrease, suggesting the possibility that UV irradiation may have systemic effects (Larmi 1989). While the mechanism of UV inhibition is unknown, it does not seem to be due to thickening of the stratum corneum as speculated earlier (Gollhausen and Kligman 1985). [Pg.222]

SMn Among 48 kidney transplant patients immxmosuppressed either by AZA (n = 32) or mycopheno-late (n = 16), AZA was subsequently replaced by mycophenolate in 23 patients. Three months after replacing AZA by MMF minimal erythema dose to ultraviolet (UV) A increased from 15 to 25J/cm (p< 0.001) and DNA 6-TG content was reduced. P53 protein expression in irradiated skin indicated reduced susceptibility to UVA-induced DNA damage. 6-TG DNA in peripheral blood mononuclear cells remained measurable for over 2 years [78 ]. [Pg.598]

A. Nagler, M. Ghana, M. Leiba, L. Levdansky and R. Gorodetsky, Effect of halofuginone, a collagen alphal(l) inhibitor, on wound healing in normal and irradiated skin implication for hematopoietic stem cell transplantation, Acta Haematol., 2007, 118, 77-83. [Pg.157]


See other pages where Irradiated skin is mentioned: [Pg.1429]    [Pg.264]    [Pg.267]    [Pg.267]    [Pg.49]    [Pg.47]    [Pg.782]    [Pg.874]    [Pg.239]    [Pg.240]    [Pg.242]    [Pg.248]    [Pg.252]    [Pg.434]    [Pg.44]    [Pg.126]    [Pg.271]    [Pg.92]    [Pg.472]    [Pg.177]    [Pg.122]   
See also in sourсe #XX -- [ Pg.239 ]




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