Phenols and hydroquinone

Rapid oxidation by acidic hexachloriridate of phenol and 2,6-dimethylphenol takes place to give the corresponding phenoxyl radical . At low Ir(iri) concen- 

Trisacetylacetonecobalt(III) oxidises phenols to phenoxyl radicals at 71-120 °C in chlorobenzene with simple second-order kinetics, E = 33 kcal.mole and AS = 13.6 eu) . When 2,4,6-tcrt-butylphenol was employed, the characteristic ESR spectrum of the phenoxyl radical was obtained with an intensity corresponding to almost quantitative conversion, viz. 

Oxidation of hydroquinone by Mn(III) in acid perchlorate media is simple second-order. The acidity dependence indicates both Mn and MnOH to be effective oxidants with second-order rate coefficients at 25 °C of (0.48 + 0.12) x 10  

A second investigation included an observation of an increase in absorption at 470 nm on mixing the reactants suggesting fast complex formation this absorption then decayed with first-order kinetics and with a rate linearly dependent upon hydroquinone concentration. k2 decreases with increasing acidity in a manner indicating the complex between MnOH and hydroquinone to be the exclusive reactant. E2 = 14.0+0.7 kcal.mole and AS = 7.5+ 2.1 eu. 

---

Recendy, the myelotoxicity has been proposed to occur through initial conversion of benzene to phenol and hydroquinone in the fiver, selective accumulation of hydroquinone in the bone marrow, followed by conversion of hydroquinone to benzoquinone via bone marrow myeloperoxidase. Benzoquinone is then proposed to react with macromolecules dismpting cellular processes (108). 

Phenol is a tumor promoter in laboratory animals. In mice, dermal exposure to phenol in benzene (Boutwell and Bosch 1959) or in acetone (Salaman and Glendenning 1957 Wynder and Hoffmann 1961) increased the incidence of tumors resulting from dermal exposure to the tumor initiator, DMBA. When injected with mixtures of phenol and hydroquinone, a hydrolyzed metabolite of phenol, mice exhibited significantly depressed bone marrow erythropoiesis compared to injection with phenol alone (Chen and Eastmond 1995a). The involvement of peripheral acetylcholine in phenol-induced tremors was implicated by studies in which mice were injected with phenol and pentobarbital, an inhibitor of acetylcholine release (Itoh 1995). 

Barale R, Marrazzini A, Betti C, et al. 1990. Genotoxicity of two metabolites of benzene Phenol and hydroquinone show strong synergistic effects in vivo. Mutat Res 244 15-20. 

Chen H, Eastmond DA. 1995a. Synergistic increase in chromosomal breakage within the euchromatin induced by an interaction of the benzene metabolites phenol and hydroquinone in mice. Carcinogenesis 16 1963-1969. 

Legathe A, Hoener B-A, Tozer TN. 1994. Pharmacokinetic interaction between benzene metabolites, phenol and hydroquinone, in B6C3F1 mice. Toxicol Appl Pharmacol 124 131-138. 

Wajon JE, Rosenblatt DH, Burrows EP. 1982. Oxidation of phenol and hydroquinone by chlorine dioxide. Environ Sci Technol 16 396-402. 

Krypton is an inert gas element. Its closed-shell, stable octet electron configuration allows zero reactivity with practically any substance. Only a few types of compounds, complexes, and clathrates have been synthesized, mostly with fluorine, the most electronegative element. The most notable is krypton difluoride, KrF2 [13773-81-4], which also forms complex salts such as Kr2F3+AsFe [52721-23-0] and KrF+PtFF [52707-25-2]. These compounds are unstable at ambient conditions. Krypton also forms clathrates with phenol and hydroquinone. Such interstitial substances are thermodynamicahy unstable and have irregular stoichiometric compositions (See Argon clathrates). 

A simple compartmental pharmacokinetic model was proposed by Seaton et al. (1995) to describe the phannacokinetics of hydroquinone in mice, rats and humans. The model did not include hydroquinone sulfation, which does occur in rats and possibly in mice, although glucuronidation is the major reaction. Phenol and hydroquinone may mutually inhibit their sulfation if both are present simultaneously in the rat (Legathe etal., 1994). 

Norland, D.E. Pierce, WM. (1990) Identification of V-acetyl-5 -(2,5-dihydroxyphenyl)-L-cysteine as a urinary metabolite of benzene, phenol and hydroquinone. DrugMetab. Disp., 18. 958-961... 

Schlosser, M.J., Shurina, R.D. Kalf, GF. (1989) Metabolism of phenol and hydroquinone to reactive products by macrophage peroxidase or purified prostaglandin H synthase. Environ. Health Perspect., 82, 229-237... 

Oxidation of phenols and hydroquinones.3 Both 1- and 2-naphthol are oxidized by benzeneseleninic anhydride to 1,2-naphthoquinone in comparable yield (62-63%). This orr/io-selectivity is general and is explained by a mechanism outlined in equation (I). As expected, the reagent oxidizes hydroquinones to the quinones in 84-92% yield. 

Bielicka-Daszkiewicz, K., A. Voelkel, M. Szejner, and J. Osypisk. 2006. Extraction properties of new polymeric sorbents in SPE/GC analysis of phenol and hydroquinone from water samples. Chemosphere 62 890-898. 

The antioxidants BHA and BHT are commonly used as food preservatives. Show how BHA and BHT can be made from phenol and hydroquinone. 

There are quantitative differences in the benzene metabolites produced by different species (Sabourin et al. 1988). Fischer 344 rats exposed to 50 ppm benzene had undetectable amounts of phenol, catechol, and hydroquinone in the liver, lungs, and blood. The major water-soluble metabolites were muconic acid, phenyl sulfate, prephenyl mercapturic acid, and an unknown The unknown was present in amounts equal to the amounts of phenyl sulfate in the liver phenyl sulfate and the unknown were the major metabolites in the liver. B6C3Fj mice exposed to 50 ppm benzene had detectable levels of phenol and hydroquinone in the liver, lungs, and blood catechol was detectable only in the liver and not in the lungs or blood. As in the rat, the unknown was present in amounts equal to the amounts of phenyl sulfate in the liver. Mice had... 

The benzene metabolites hydroquinone and muconic dialdehyde can produce hematotoxic effects (Eastmond et al. 1987 Gad-El Karim et al. 1985 Latriano et al. 1986). The co-administration of phenol (75 mg/kg/day) and hydroquinone (25-75 mg/kg/day) twice daily for 12 days to B6C3Fj mice produced myelotoxicity similar to that induced by benzene (Eastmond et al. 1987). The proposed mechanism suggested that selective accumulation of hydroquinone occurred in the bone marrow after the initial hepatic conversion of benzene to phenol and hydroquinone. Additionally, phenol is thought to stimulate the enzymatic activity of myeloperoxidase, which uses phenol as an electron donor, thus producing phenoxy radicals. These radicals further react with hydroquinone to form 1,4-benzoquinone, a toxic intermediate that inhibits critical cellular processes (Eastmond et al. 1987). 

The proposed mechanism suggested that selective accumulation of hydroquinone occurred in the bone marrow after the initial hepatic conversion of benzene to phenol and hydroquinone. Additionally, phenol is thought to stimulate the enzymatic activity of myeloperoxidase, which uses phenol as an electron donor, thus producing phenoxy radicals. These radicals further react with hydroquinone to form 1,4-benzoquinone, atoxic intermediate which inhibits critical cellular processes (Eastmond et al. 1987). 

Kenyon EM, Medinsky MA. 1995. Incorporation of heterogeneous enzyme distribution into a physiological model for benzene, phenol and hydroquinone. In Abstracts of the 34th annual meeting. Toxicologist 15(1) 49. 

It was thus proposed that the uptake of Hg(II) by activated carbons occurs by the parallel mechanisms of adsorption of molecular HgCE and reduction. Upon H 0 oxidation, the beneficial phenolic and hydroquinone groups were hypothesized to be lost and converted to carboxyl groups. In contrast to the earlier report by Sinha and Walker [219], significant uptake increase was observed upon sul-phurization (saturation with CS at 288 K and subsequent heating to 773 K) of the as-received (AS), and especially so, the oxidized carbon (AOS). This effect was attributed to the analogous reduction reaction ... 

Mercuric oxide, HgO (yellow modification or the less reactive red modification), resembles silver oxide in its oxidizing properties. This reagent transforms phenols and hydroquinones into quinones [383, 384] and is used especially for the conversion of hydrazones into diazo compounds [355, 386, 387, 388, 389, 390, 391, 392]. Dihydrazones of a-diketones furnish acetylenes [393, 394, 395, 396], A -Aminopiperidines are dehydrogenated to tetrazenes [397] or converted into hydrocarbons [395]. 

Benzene, phenol, and hydroquinone are metabolized in vivo to benzoquinone and excreted as the mer-capturate, N-acetyl-S-(2,5-dihydroxyphenyl)-L-cy-steine. Hydroquinone is a reducing cosubstrate for peroxidase enzymes, and the resultant semiquinone and p-benzoquinone may bind to DNA. 

---