Disease relevance of resorcinol

• Histological examination after sacrifice at wk 52 revealed that the incidences of tongue papillomas and esophageal squamous cell carcinomas in the groups given MNAN followed by catechol (57.1% and 64.3%) or resorcinol (50% and 58.8%) were significantly higher than those in the carcinogen only controls (9.1, and 0%, respectively) [1].
• The lower toxicity of monophenols and resorcinol as compared with that of di- and tri-phenols is due, in our opinion, to the fact that they are less oxidized under the conditions existing in the culture medium, and therefore do not produce sufficient levels of oxygen radicals [2].
• Suppression of cyclooxygenase-2 promoter-dependent transcriptional activity in colon cancer cells by chemopreventive agents with a resorcin-type structure [3].
• Metabolism of resorcinylic compounds by bacteria: alternative pathways for resorcinol catabolism in Pseudomonas putida [4].
• Azoarcus anaerobius sp. nov., a resorcinol-degrading, strictly anaerobic, denitrifying bacterium [5].

Psychiatry related information on resorcinol

• Of the phenols studied, resorcinol gave the best response time of 6 min for 4-AP determination [6].

High impact information on resorcinol

• Structurally dissimilar catechols (1,2-diphenols) and hydroquinones (1,4-diphenols) induce quinone reductase in these systems, but resorcinol (1,3-diphenol) and its substituted analogues are inactive [7].
• Tunicamycin blocks incorporation of glucosamine label into practically all ganglioside species except for a resorcinol-positive, sialidase-sensitive band tentatively identified as GQ1b tetrasialoganglioside (Svennerholm ganglioside nomenclature) [8].
• Selectivity for the beta 2-adrenoceptor was improved with tertiary branching at the gamma-carbon and further increased by aromatic substitution with resorcinol or saligenin [9].
• Thin-layer chromatography of the isolated ganglioside fraction from T-cell lymphoblasts revealed two major resorcinol-positive bands [10].
• Furthermore, using EPO-deficient mice and an EPO inhibitor resorcinol we demonstrate that eosinophil-derived peroxidase is critical in the development of GI dysfunction in experimental UC [11].

Chemical compound and disease context of resorcinol

• Resorcinol is converted to pyrogallol by resorcinol-grown cells of Azotobacter vinelandii [12].
• E. coli cells containing Ncgl1111 and Ncgl1113 sequentially converted resorcinol into maleylacetate [13].
• Two strains of Pseudomonas putida isolated by enrichment cultures with orcinol as the sole source of carbon were both found to grow with resorcinol [4].
• Symptomatic caliceal diverticula treated with extraperitoneal laparoscopic marsupialization fulguration and gelatin resorcinol formaldehyde glue obliteration [14].
• Cloning and expression of NCgl1111 in E. coli revealed that NCgl1111 encoded a resorcinol hydroxylase that needs NADPH as a cofactor [13].

Biological context of resorcinol

• Steps in the hydroxylation pathway of the flavoprotein phenol hydroxylase with resorcinol as substrate have been studied by a combination of fluorescence and absorbance stopped flow techniques [15].
• Structure activity relationships on methoxy-resveratrol analogs showed that the m-hydroquinone moiety was essential for irreversible inactivation of COX-1 [16].
• This study investigated the mechanism by which resorcinol inhibits glycolysis [17].
• The interactions of the phosphorylated derivatives of hydroquinone (HQN-P2), resorcinol (RSN-P2), 4-hydroxybenzaldehyde (HBA-P) and 2, 4-dihydroxybenzaldehyde (DHBA-P; phosphate group at position 4) with fructose bisphosphate aldolase were analysed by enzyme kinetics, UV/visible difference spectroscopy and site-directed mutagenesis [18].
• After enzymatic hydrolysis, we reacted the free compound with resorcinol in the presence of manganese ions to form an indophenol dye, which is measured at 550 nm [19].

Anatomical context of resorcinol

• It is then exported out of the plastids and converted to 5-pentadecatriene resorcinol by a polyketide synthase [20].
• The widespread occurrence of resorcinol derivatives in the environment suggests that exposure to these compounds may cause thyroid dysfunction in humans [21].
• Proglycosyn and resorcinol stimulate glycogen synthesis and inhibit glycolysis in hepatocytes [17].
• We studied the effects of resorcinol, phenol, 3,5-xylenol, chloroxylenol, and 4-hexyl-resorcinol on normal human epidermal keratinocytes and dermal fibroblasts for cytotoxicity and cytokine release, determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide methodology and enzyme-linked immunosorbent assay, respectively [22].
• Immune and resorcinol staining detected the presence of gangliosides GM3, GM2, GD3, GD2 and GD1a but not GM1a, GD1b or GT1b in the extracts of normal prostatic epithelial cells (PrEC) and neoplastic androgen-insensitive (PC-3, DU145) and -sensitive (LNCaP-FGC and LNCaP-FGC-10) CaP cells [23].

Associations of resorcinol with other chemical compounds

• The inhibitory effects of leptin on phosphorylase a were counteracted by short-term incubation with glucagon but were additive with the inhibitory effects of insulin and also with the inhibition caused by resorcinol (25 pmol/l), which inhibits phosphorylase kinase by a mechanism analogous to the antidiabetic drug proglycosyn [24].
• Both the catalytic and the inhibiting effects were dependent on pH and on the concentration of phenolic compounds; catalysis by resorcinol and catechin was increased at optimal ratios of [nitrite]: [phenolic compound] [25].
• The rate constants for all the reaction steps as well as the hydroxylation efficiency (coupling between NADPH oxidation and resorcinol consumption) are comparable to those of the wild-type enzyme [26].
• Catalysis of nitrosation in vitro and in vivo in rats by catechin and resorcinol and inhibition by chlorogenic acid [25].
• The effects of 8 weeks of oral administration of five different phenolic antioxidants, e.g. catechol (CC), resorcinol, hydroquinone (HQ), 2-tert-butyl-4-methylphenol (TBMP) and propylparabene (PP), on forestomach and glandular stomach epithelium of male F344 rats were evaluated using a combined immunohistochemical and histopathological approach [27].

Gene context of resorcinol

• The enzymatic oxidation of resorcinol by lactoperoxidase was linked to inactivation since the same products were observed spectrally, albeit at a much lower level, as were observed with horseradish peroxidase [21].
• The results are consistent with thyroid peroxidase- and lactoperoxidase-catalyzed oxidation of resorcinol derivatives to reactive radical species that covalently bind to amino acid residues unique to these two enzymes [21].
• Concentrations of total serum N-acetyl-neuraminic acid (NANA) by high-performance liquid chromatography (HPLC) and lipid-bound sialic acid (LSA) by resorcinol procedure were evaluated and compared to carcinoembryonic antigen (CEA) as markers for colorectal carcinoma [28].
• Fourteen novel CB2 receptor selective cannabinoids were synthesized via initial Lewis acid catalyzed rearrangement of resorcinol precursors to obtain the cannabinoid moiety [29].
• The evidence for this mechanism includes irreversible, hydrogen peroxide-dependent loss of enzymatic activity by kinetics consistent with a suicide mechanism, concomitant with changes in the visible spectrum of the prosthetic heme group and covalent binding of resorcinol (ca. 10 mol/mol of lactoperoxidase inactivated) [21].

Analytical, diagnostic and therapeutic context of resorcinol

• Resorcinol-induced hypothydroidism in a patient on chronic hemodialysis [30].
• The locations of isolated gangliosides on thin-layer chromatograms were determined by visualization with resorcinol, and each spot was quantified by digital image densitometry [31].
• The intracellular concentrations of the glucuronide derivatives of proglycosyn and resorcinol have been measured by HPLC in hepatocytes incubated for 5 min or 30 min with different concentrations of these agents [32].
• Extracts of the cultures of yeasts growing on resorcinol plus chlororesorcinol were analyzed for residual resorcinol and chlororesorcinol with high pressure liquid chromatography [33].
• Contact dermatitis due to resorcinol in a radiotherapy dye [34].

References