Disease relevance of p-Dichlorbenzol

• 1,4-Dichlorobenzene (DCB), a non-DNA-reactive compound, induced hepatocellular carcinomas at 600 mg/kg/day, but not 300 mg/kg/day in male and female B6C3F1 mice in a National Toxicology Program (NTP) bioassay [1].
• Degradation of 1,4-dichlorobenzene by Xanthobacter flavus 14p1 [2].
• Degradation of 1,4-dichlorobenzene by a Pseudomonas sp [3].
• Degradation of 1,4-dichlorobenzene by Alcaligenes sp. strain A175 [4].
• Reversible ataxia following chronic exposure to paradichlorobenzene [5].

High impact information on p-Dichlorbenzol

• Prolonged colchicine treatment induced the formation of numerous cytoplasmic para-crystals in tapetal cells of wheat anthers containing germ line cells at pre-meiotic mitosis or early pre-meiotic interphase [6].
• Copper-mediated DNA damage by metabolites of p-dichlorobenzene [7].
• Cell proliferation was increased in livers of both species of WY- and DCB-treated animals when compared to controls [8].
• Naphthalene in the higher triplet excited state Np(Tn) was generated from the two-step excitation method using two-colour two-laser flash photolysis technique and the lifetime of Np(Tn) was estimated to be 4.5 ps from the triplet energy quenching by quenchers such as p-dichlorobenzene, o-dicyanobenzene and carbon tetrachloride [9].
• Pseudomonas sp. strain P51 is able to use 1,2-dichlorobenzene, 1,4-dichlorobenzene, and 1,2,4-trichlorobenzene as sole carbon and energy sources [10].

Chemical compound and disease context of p-Dichlorbenzol

• The ability of the recombinant to utilize 3-chlorobenzoate, chlorobenzene, and 1,4-dichlorobenzene as well as its loss of utilization of xylenes and methylbenzoates appears to be associated with the transfer and integration of chromosomal DNA from P. alcaligenes into a Tol-like plasmid of P. putida R5-3 [11].
• Rhodococcus phenolicus sp. nov., a novel bioprocessor isolated actinomycete with the ability to degrade chlorobenzene, dichlorobenzene and phenol as sole carbon sources [12].
• Cell proliferation in the kidneys and livers of rats and mice exposed short-term to p-dichlorobenzene (p-DCB) was evaluated by immunohistochemical measurement of bromodeoxyuridine (BrdU) incorporation into nuclei of DNA-synthesizing cells. p-DCB was given by gavage at two doses up to 600 mg/kg body weight for 4 days [13].

Biological context of p-Dichlorbenzol

• Species and strain differences in the hepatic cytochrome P450-mediated biotransformation of 1,4-dichlorobenzene [14].
• Sister-chromatid exchanges (SCE) induced by p-dichlorobenzene in cultured human lymphocytes [15].
• LI was increased in all hepatocyte ploidy/nuclearity classes except the binucleated tetraploid cells (2 x 2N) and was elevated most in the mononucleated octoploid population (8N) (LI = 44 +/- 11, 49 +/- 14, and 1.3 +/- 0.4% of 8N hepatocytes for DCB, DEHP, and control, respectively) [16].
• All enzymes necessary to convert 1, 4-dichlorobenzene to 3-oxoadipate showed a low substrate specificity and also accepted the respective intermediates of chlorobenzene or 1, 3-dichlorobenzene degradation [17].
• Results from recent long-term inhalation, mutagenicity, embryotoxicity and metabolism studies on p-dichlorobenzene (p-DCB) are reviewed [18].

Anatomical context of p-Dichlorbenzol

• Cytochrome P450 catalyzed oxidation of monochlorobenzene, 1,2- and 1,4-dichlorobenzene in rat, mouse, and human liver microsomes [19].
• This is a case report of central nervous system toxicity associated with paradichlorobenzene (PDCB) ingestion [20].

Associations of p-Dichlorbenzol with other chemical compounds

• Single-solute sorption isotherms were measured for five pristine marine sediments using phenanthrene, naphthalene, 1,3,5-trichlorobenzene, and 1,4-dichlorobenzene as the sorbates [21].
• Extrapolation kinetics of low-exposure data showed more trichloroethylene (0.0016 micromol/h/kg), benzene (0.0014 micromol/h/kg), and p-dichlorobenzene (0.00052 micromol/h/kg) was absorbed by the rats than 1,1,1-trichloroethane (0.000019 micromol/h/kg) and tetrachloroethylene (0.000029 micromol/h/kg) [22].
• Use of a medium-term liver focus bioassay to assess the hepatocarcinogenicity of 1,2,4,5-tetrachlorobenzene and 1,4-dichlorobenzene [23].
• We have reported previously that 7-day dosing with DEHP induced a higher bromodeoxyuridine labeling index (LI) in binuclear octoploid (2x4N) rat hepatocytes than did DCB, suggesting that induction of DNA synthesis in 2x4N hepatocytes might represent a more substantial carcinogenic risk [24].
• The biotransformation and kinetics of 1,4-dichlorobenzene (1,4-DCB) were studied in male Wistar rats at three oral dose levels (10, 50 and 250 mg/kg) [25].

Gene context of p-Dichlorbenzol

• As regards sera cytokine levels, only TNF-alpha could be detected 6 h after administering 500 and 600 mg/kg doses of 1,2 dichlorobenzene [26].
• Involvement of reversible binding to alpha 2u-globulin in 1,4-dichlorobenzene-induced nephrotoxicity [27].
• p-Dichlorobenzene (pDCB) is a male rat kidney carcinogen believed to act through alpha2u-globulin nephropathy [28].
• 2. Rat and human liver slices were incubated with 1 mM of either dichlorobenzene to determine metabolism and toxicity, at 2 and 6 h of organ culture [29].
• The estrogenicity of o-, m-, and p-dichlorobenzene (DCB) was evaluated with a yeast estrogen screen (YES) and zebrafish (Danio rerio) vitellogenin (VTG) assays [30].

Analytical, diagnostic and therapeutic context of p-Dichlorbenzol

• Using flow cytometry, we investigated the effects of DEHP, CEA, and DCB on hepatocyte ploidy, nuclearity, and LI distribution among the ploidy/nuclearity classes in male Fischer 344 rats [16].
• Acid-induced phase separation of anionic surfactants for the extraction of 1,4-dichlorobenzene from honey prior to liquid chromatography [31].
• 1. The metabolism of 1,4-dichlorobenzene has been studied in the male and female Fisher 344 rat over 72 h after oral administration of 14C-1,4-dichlorobenzene (900 mg = 96.8 microCi/kg) [32].
• The ability of 1,4-dichlorobenzene (DCB) (300 mg/kg) (a noncarcinogenic rat liver mitogen), diethylhexyl phthalate (DEHP) (950 mg/kg), and chlorendic acid (120 mg/kg) (both nongenotoxic hepatocarcinogens) to induce c-fos, c-jun, and c-myc expression in rat liver was determined by Northern blot analysis and by in situ hybridization [33].

References