Disease relevance of Polyvinylidene chloride

• Tissue-mediated mutagenicity of vinylidene chloride and 2-chlorobutadiene in Salmonella typhimurium [1].
• Oral toxicity of 1,1-dichloroethylene in the rat: effects of sex, age, and fasting [2].
• Vinylidene chloride (VDC) monomer dissolved in olive oil was given orally to female BD IV rats (150 mg/kg body weight) on the 17th day of gestation [3].
• Oxidation of trichloroethylene, 1,1-dichloroethylene, and chloroform by toluene/o-xylene monooxygenase from Pseudomonas stutzeri OX1 [4].
• Modification of 1,1-dichloroethylene hepatotoxicity by hypothyroidism [5].

High impact information on Polyvinylidene chloride

• Oxidation of the vinyl halide carcinogen and hepatotoxin vinylidene chloride (VDC) by microsomal cytochrome P-450 yields 2,2-dichloroacetaldehyde, 2-chloroacetyl chloride, 2-chloroacetic acid, and 1,1-dichloroethylene oxide [6].
• Canalicular and mitochondrial membranes were investigated as early foci of hepatocyte injury in fed and fasted male Sprague-Dawley rats given 50 mg of 1,1-dichloroethylene (DCE)/kg [7].
• Histochemical and immunocytochemical evidence of early, selective bile canaliculi injury after 1,1-dichloroethylene in rats [7].
• Non-ciliated Clara cells of the pulmonary bronchiolar epithelium are preferentially damaged by administration of 1,1-dichloroethylene (1,1-DCE) to mice [8].
• Conversion of the toxic vinyl halide 1,1-dichloroethylene (DCE) to S-(2-S-glutathionyl-acetyl)glutathione (GSCH2COSG) involves sequential acylation and alkylation of two glutathione (GSH) molecules by the microsomal DCE metabolite ClCH2COCl [9].

Chemical compound and disease context of Polyvinylidene chloride

• Compounds which were substrates for alkene monooxygenase exhibited various levels of toxicity, with 1,1-dichloroethylene and trichloroethylene being the most potent inactivators of propylene oxidation and 1,3- and 2,3-dichloropropylene being the most potent inactivators of propylene oxide-dependent O2 uptake [10].
• Vapours of vinylidene chloride and chloroprene induced a dose-related toxicity in the presence of liver supernatant from phenobarbitone-retreated rats, but these two compounds were not mutagenic in V79 Chinese hamster cells under the present assay conditions [11].
• Chromosomal aberration and sister-chromatid exchange (SCE) tests in vitro on 1,1-dichloroethylene (1,1-DCE), its two isomers, cis- and trans-1,2-DCE, and two possible metabolites of 1,1-DCE, chloroacetyl chloride and chloroacetic acid, were carried out using a Chinese hamster cell line, CHL [12].
• Effect of hypoxia on the metabolism and hepatotoxicity of carbon tetrachloride and vinylidene chloride in rats [13].
• Enhancement of 1,1-dichloroethylene toxicity by pretreatment of fasted male rats with 2,3-epoxypropan-1-ol [14].

Biological context of Polyvinylidene chloride

• Interim results of two-year toxicological studies in rats of vinylidene chloride incorporated in the drinking water or administered by repeated inhalation [15].
• In vitro biotransformation of 1,1-dichloroethylene by hepatic cytochrome P-450 2E1 in mice [16].
• Pharmacokinetics of vinylidene chloride [17].
• Evidence that 1,1-dichloroethylene induces apoptotic cell death in murine liver [18].
• Vinylidene chloride (VDC) was tested for its ability to induce both point mutation and mitotic gene conversion in a diploid strain (D7) of the yeast Saccharomyces cerevisiae in a suspension test with and without a mammalian microsomal activation system, and in the intrasanguineous host-mediated assay in mice [19].

Anatomical context of Polyvinylidene chloride

• Inhibition of liver-microsome calcium pump by in vivo administration of CCl4, CHCl3 and 1,1-dichloroethylene (vinylidene chloride) [20].
• 1,1-Dichloroethylene inhibition of liver endoplasmic reticulum calcium pump function [21].
• 1,1-Dichloroethylene (DCE) causes dysfunction of hepatic mitochondria [18].
• Histochemical evidence that plasma and mitochondrial membranes are primary foci of hepatocellular injury caused by 1,1-dichloroethylene [22].
• Functional integrity of liver cell organelles in rats given the model abrupt cytotoxin 1,1-dichloroethylene (1,1-DCE) was examined by enzymatic histochemistry [22].

Associations of Polyvinylidene chloride with other chemical compounds

• The observations are based upon carcinogenicity experimental bioassays of vinyl chloride and vinylidene chloride [23].
• Carbon tetrachloride (CCl4) and 1,1-dichloroethylene (DCE), both hepatotoxins, inhibit sequestration of Ca2+ by rat liver endoplasmic reticulum (ER) both in vivo and in vitro [24].
• The chlorinated ethylenes 1,1-dichloroethylene (vinylidene chloride), trans-1,2-dichloroethylene, trichloroethylene, and tetrachloroethylene (perchloroethylene) were assayed for their ability to induce mitotic gene conversion and point mutation as well as mitotic aneuploidy in diploid strains of the yeast Saccharomyces cerevisiae [25].
• Mutagenicity of vinyl chloride, vinylidene chloride and chloroprene in V79 Chinese hamster cells [11].
• Phospholipase A2 activation and cell injury in isolated rat hepatocytes exposed to bromotrichloromethane, chloroform, and 1,1-dichloroethylene as compared to effects of carbon tetrachloride [26].

Gene context of Polyvinylidene chloride

• Cytochrome P-450-dependent bioactivation of 1,1-dichloroethylene to a reactive epoxide in human lung and liver microsomes [27].
• These data suggest that cytochrome P450 2E1 or a P450 enzyme with very similar molecular weight, substrate specificities, and immunological properties is expressed only in male mouse kidney and bioactivates 1,1-dichloroethene [28].
• Bioactivation of 1,1-dichloroethylene to its epoxide by CYP2E1 and CYP2F enzymes [29].
• Selective induction of renal microsomal cytochrome P-450-linked monooxygenases by 1,1-dichloroethylene in mice [30].
• VOCs were detected in 11 wells, and two sites exceeded the MCL for 1,1-dichloroethylene (36.1 microg/L) and trichloroethylene (9.0 microg/L) [31].

Analytical, diagnostic and therapeutic context of Polyvinylidene chloride

• Bronchiolar Clara cell damage ensues after treatment of mice with 1,1-dichloroethylene (DCE) [32].
• Metabolism and pharmacokinetic profile of vinylidene chloride in rats following oral administration [33].
• Polyvinylidene chloride (PVDC; polymer of 1,1-dichloroethylene) was combusted with paper in a well-controlled, small-scale incinerator at an average grate temperature of 700 degrees C, and then dioxins (PCDDs, PCDFs, and coplanar-PCBs) formed in the exhaust gases were analyzed by gas chromatography/mass spectrometry [34].
• Factors were studied which modify the enzymatic capacity of mouse liver microsomal mixed-function oxidase to convert vinylidene chloride (1.1-dichloroethylene) (VDC) into mutagens in the Salmonella/microsome mutagenicity test [35].
• Autoradiography of mice injected i.p. with 14C-labelled 1,1-dichloroethylene (vinylidene chloride, VDC) in C57B1/6 mice revealed a selective covalent binding of radioactivity in the proximal tubules, in the midzonal parts of the liver lobules and in the mucosa of the upper and lower respiratory tract [36].

References