Disease relevance of Dihydro-p-chloranil

• Purification and characterization of a tetrachloro-p-hydroquinone reductive dehalogenase from a Flavobacterium sp [1].
• Pentachlorophenol (PCP) dehalogenase from Arthrobacter sp. strain ATCC 33790 converts PCP to tetrachlorohydroquinone [2].
• Cell extracts from an E. coli pcpB overexpression strain, as well as the whole cells, were proficient in the dechlorination of pentachlorophenol to tetrachlorohydroquinone [3].
• Characterization of tetrachlorohydroquinone reductive dehalogenase from Sphingomonas sp. UG30 [4].
• Oxidative stress and liver toxicity in rats and human hepatoma cell line induced by pentachlorophenol and its major metabolite tetrachlorohydroquinone [5].

High impact information on Dihydro-p-chloranil

• Protection by desferrioxamine and other hydroxamic acids against tetrachlorohydroquinone-induced cyto- and genotoxicity in human fibroblasts [6].
• New modes of action of desferrioxamine: scavenging of semiquinone radical and stimulation of hydrolysis of tetrachlorohydroquinone [7].
• Identification and localization of a stable sulfenic acid in peroxide-treated tetrachlorohydroquinone dehalogenase using electrospray mass spectrometry [8].
• Tetrachlorohydroquinone dehalogenase catalyzes the reductive dehalogenation of tetrachlorohydroquinone and trichlorohydroquinone during the biodegradation of the xenobiotic compound pentachlorophenol by Sphingobium chlorophenolicum [9].
• Bcl-2 overexpression inhibits tetrachlorohydroquinone-induced apoptosis in NIH3T3 cells: a possible mechanism for tumor promotion [10].

Chemical compound and disease context of Dihydro-p-chloranil

• Glutathione is the reducing agent for the reductive dehalogenation of tetrachloro-p-hydroquinone by extracts from a Flavobacterium sp [11].
• The pathway employed for pentachlorophenol (PCP) degradation by an aerobic, chlorophenol-utilizing Flavobacterium sp. was initiated by conversion of PCP to tetrachloro-p-hydroquinone (TCH) [12].

Biological context of Dihydro-p-chloranil

• Nevertheless, the para-hydroxylation reaction required the presence of molecular oxygen, whereas further metabolism of the reaction product, tetrachlorohydroquinone, proceeded also in anaerobiosis [13].
• Incubation of the cells in the presence of an external source of NADPH prevents the further degradation of tetrachlorohydroquinone, suggesting that the quinone derived from the two-electron oxidation of the hydroquinone is more likely the substrate for the second hydroxylation [14].
• The effect of pentachlorophenol and its metabolite tetrachlorohydroquinone on cell growth and the induction of DNA damage in Chinese hamster ovary cells [15].
• Free and conjugated PCP were found in the urine of dogs; no PCA or tetrachlorohydroquinone (TCH) were found [16].
• Different cell death mechanisms and gene expression in human cells induced by pentachlorophenol and its major metabolite, tetrachlorohydroquinone [17].

Anatomical context of Dihydro-p-chloranil

• When Jurkat human T cells were incubated with 20 microM of pentachlorophenol (PCP) or its metabolite, tetrachlorohydroquinone (TCHQ), for 10 hr, flow cytometric analyses revealed marked increase in the number of apoptotic cells [18].
• A sensitive capillary gas chromatographic method was developed for the simultaneous determination of pentachlorophenol and its major metabolite, tetrachlorohydroquinone, in plasma, urine and feces [19].
• The effect of pentachlorophenol and its metabolite tetrachlorohydroquinone on RNA, protein, and ribosome synthesis in Saccharomyces cells [20].
• To understand the initiating/promoting actions of pentachlorophenol (PCP), a non-mutagenic hepatocarcinogen, and its metabolite, tetrachlorohydroquinone (TCHQ), we investigated the effects of each chemical on gap junctional intercellular communication (GJIC) in rat liver epithelial cells (WB cells) by the scrape-loading and dye transfer method [21].

Associations of Dihydro-p-chloranil with other chemical compounds

• Purification and characterization of glutathione conjugate reductase: a component of the tetrachlorohydroquinone reductive dehalogenase system from Phanerochaete chrysosporium [22].
• The induction of micronuclei by tetrachlorohydroquinone was significantly inhibited by the hydroxyl radical scavenger dimethyl sulfoxide at 5% (v/v) [23].
• The role of hydroxyl radicals in tetrachlorohydroquinone induced DNA strand break formation in PM2 DNA and human fibroblasts [24].
• In these cell lines, stresses induced by exposure to inorganic [Sodium Arsenite (NaAsO2) and Cadmium Chloride (CdCl2)], and organic [Benzo(a)Pyrene (BaP), PentaChloroPhenol (PCP), TetraChloroHydroQuinone (TCHQ), 1-Chloro-2,4-DiNitro-Benzene (CDNB)] compounds, specifically induced hGH release in the culture medium [25].

Gene context of Dihydro-p-chloranil

• Effects of pentachlorophenol and tetrachlorohydroquinone on mitogen-activated protein kinase pathways in Jurkat T cells [18].
• The role of the GST in the degradation of biphenyls is less clear, but since it was found to contain, in the putative xenobiotic substrate-binding domain, a region which shares about 29% of identical amino acids with a bacterial tetrachlorohydroquinone dehalogenase, it may be involved in dehalogenation of PCB-degradative intermediates [26].
• However, B[a]P [J. Biol. Chem. 274 (1999) 35240] and a metabolite of PCP, tetrachlorohydroquinone (TCHQ) [Chem. Biol. Interact. 105 (1997) 1], induce p53 protein synthesis in vitro [27].

Analytical, diagnostic and therapeutic context of Dihydro-p-chloranil

• Simultaneous assay of pentachlorophenol and its metabolite, tetrachlorohydroquinone, by gas chromatography without derivatization [19].

References