ISSN:
1432-069X
Keywords:
Allergic contact dermatitis
;
Monohydric alkylbenzenes
;
Dihydric alkylbenzenes
;
Quinols
;
Resorcinols
;
Catechols
;
Urushiols
;
Prohapten activation
;
NADH
;
Cysteine
;
Glutathione
;
Diphenylpicrylhydrazyl
;
2-Oxo-4-thiazolidine carboxylate
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary The induction of allergic contact dermatitis to urushiols from poison ivy and related plants is generally believed to involve an initial oxidation event by which a protein-reactive quinone is formed. However, this does not readily account for the contact allergenicity of closely related mono- and dihydric alkylbenzenes such as the alkylphenols and alkylresorcinols which are not so easily oxidised to quinones in vitro. When the redox processes known to occur in living tissues are taken into consideration, a more plausible unifying mechanism involving the formation of protein-reactive radical species becomes apparent. Experiments described here examine the autoxidation of p-benzoquinone and various mono- and dihydric benzenes and alkylbenzenes, and their reactions with the diphenylpicrylhydrazyl radical, cysteine, glutathione, and NADH. We have also demonstrated that administration to mice of 2-oxo-4-thiazolidine carboxylate, a compound known to elevate intracellular glutathione levels, inhibits the irritancy and sensitising activity of 3-pentadecylphenol. This work suggests that redox cycling in the skin following penetration of allergenic mono- and dihydric alkylbenzenes initially depletes local levels of endogenous reducing equivalents such as glutathione and NADH; once depleted, further cycling results in the uncontrolled generation of radical species which may reasonably be expected to exhibit protein reactivity.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00505646
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