PubMed · 2970948
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K D Gayer, J W Burnett. 1988. Toxicodendron dermatitis.. https://pubmed.ncbi.nlm.nih.gov/2970948/
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Tyrosinase (EC 1.14.18.1) exhibits unusual kinetic properties in the oxidation of monohydric phenol substrates consisting of a lag period that increases with increasing substrate concentration. The cause of this is an autocatalytic process dependent on the generation of a dihydric phenol substrate, which acts as an activator of the enzyme. Experiments with N-substituted dihydric phenol substrates (N-methyldopamine, N-acetyldopamine) demonstrate that oxygen consumption is retarded in the N-acetyl substituted material due to a diminished rate of cyclization. The oxygen uptake exhibited a similar pattern when N-acetyltyramine was oxidized, and this was reflected by a prolongation of the lag period. N,N-Dipropyldopamine was oxidized with normal kinetics but with an oxygen stoichiometry of 0.5 mol of oxygen/mol of substrate. We show that this is the result of the formation of a stable indoliumolate product with oxidation-reduction properties that prevent the formation of dopaminochrome, thus blocking further stages in the tyrosinase-catalyzed oxidation. Evidence that the indoliumolate product is formed by cyclization of the ortho-quinone is presented by pulse radiolysis studies, which demonstrate the formation of the ortho-quinone (by disproportionation of the corresponding semiquinones), which cyclizes to give the indoliumolate. The rate constant for cyclization was shown to be 48 s-1 (at pH 6.0). Tyrosinase-catalyzed oxidation of the monohydric phenol analogue, N, N-dimethyltyramine, was shown to require the addition of a dihydric phenol. Oxygen utilization then exhibited a stoichiometry of 1.0, indicating that the reactions proceed only as far as the cyclization. The analogous stable cyclic indoliumolate product was shown to be formed, with UV absorption and NMR spectra closely similar to the indoliumolate derived from N,N-dipropyldopamine. This material was methylated by catechol O-methyltransferase but was unreactive to redox reagents. The formation of the cyclic product accounts for the indefinite lag when N,N-dimethyltyramine is used as the substrate for tyrosinase in the absence of a dihydric phenol cofactor.
Reactive oxygen and nitrogen species play an important role in many human diseases including cancer. We have found that incubation of pBR322 plasmid DNA with a nitric oxide (NO)-releasing compound such as diethylamine NONOate and a polyhydroxyaromatic compound such as catechol, 1,4-hydroquinone, or pyrogallol caused synergistic induction of single-strand breakage, whereas either compound alone induced much less breakage. Phenol, resorcinol, or guaiacol (O-methylcatechol) did not exhibit this synergistic effect of DNA damage with NO. The strand breakage induced by NO with pyrogallol was prevented by excess superoxide dismutase, carboxy-PTIO (an NO-trapping agent), or anti-oxidants (urate, ascorbate). Possible mechanisms for the induction of this synergistic effect of NO and polyhydroxyaromatic compounds on the strand breakage are proposed, including involvement of peroxynitrite formed from NO and O2.- derived from autooxidation of polyhydroxyaromatics. This pathway for generation of reactive species from NO and catechol-type compounds (e.g., L-dopa, catechol-estrogen) may be important in many pathological conditions, because both compounds are concurrently formed or present in vivo. On the other hand, NO dose-dependently inhibited the strand breakage mediated by 1,4-hydroquinone plus Cu2+ or Fenton reaction (H2O2, iron or copper). This inhibition could be due to formation of a complex between NO and a metal ion, inhibiting generation of reactive species from H2O2. Our results can account for contrasting activities of NO reported in relation to tissue injury. NO can play both detrimental and beneficial roles in DNA damage, depending on the type and amounts of reactive oxygen species and metal ions concurrently present.
Native cashew (Semecarpus australiensis) is a well-known food source for aboriginal people of northeastern Queensland and the Northern Territory. It is also well known that contact with the seeds at a certain stage of growth can cause sever dermatitis in susceptible individuals. To prepare the fruits for eating, they are commonly treated by leaching for 2-7 days with water followed by heating in bark, and this treatment apparently produces an edible cashew nut. Recently, attempts have been made to use this valuable source of food by a commercial company. It was necessary to identify the active principle(s) in the seeds to determine the most effective way of rendering the seed suitable for human consumption without altering the flavour. By using solvent extraction and silica-gel chromatography, a fraction containing one major urushiol was obtained. Its structure was confirmed by comparison of its NMR and mass spectral (MS) data with that previously reported. This compound, which is found in high yield, is also found in poison ivy (Toxiodenron radicans) and is responsible for dermatitis in susceptible individuals. A method of removing the active principle from the seed has been suggested.