Cellular and molecular mechanisms mediating the effect of polychlorinated biphenyls on oocyte in vitro maturation
ABSTRACT Cellular and molecular mechanisms mediating the effect of polychlorinated biphenyls on oocyte in vitro maturation: Polychlorinated biphenyls (PCBs) are stable, lipophilic compounds that accumulate in the environment and in the food chain. Recent studies provide evidence that exposure to PCBs can cause reproductive problems. PCBs have been identified in the ovarian follicle of women and other mammals and many data in the literature clearly indicate that both follicles and oocytes are particularly susceptible to these pollutants. In the present review we describe the multifaceted effects of PCBs on mammalian oocyte maturation in detail. Published studies clearly indicate that PCB congeners, both singly or as complex mixtures, disrupt mammalian oocyte maturation and subsequent embryo development. Specifically, data point out to the ability of PCBs to interfere with the organization of the microtubules cytoplasmic network resulting in an altered compartmentalization of the ooplasm. Furthermore, a critical role of cumulus cells in mediating PCB ovotoxicity has been observed, most likely related to a disregulation in intracellular communication between the germinal and the somatic compartment. Finally, since coplanar PCBs, induce gene expression via a ligand-dependent transactivating factor, the aryl hydrocarbon receptor, this signalling pathway is also reviewed with respect to understanding the toxic mechanisms of these compounds.
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- "Prominent among these environmental estrogens are the PCBs (Ulbrich and Stahlmann, 2004). PCBs are a group of the halogenated aromatic hydrocarbons which are among the most persistent and widespread environmental estrogens (Safe, 1994; Pocar et al., 2006). Because of their chemical stability, lipophilic property and resistance to degradation, PCBs are making their way into all levels of food chain and preferentially bioaccumulate and biomagnify in wildlife as well as humans (McFarland and Clarke, 1989; Buckman et al., 2006). "
ABSTRACT: Cytosolic sulfotransferases (SULTs) constitute a family of Phase II detoxification enzymes that are involved in the protection against potentially harmful xenobiotics as well as the regulation and homeostasis of endogenous compounds. Compared with humans and rodents, the zebrafish serves as an excellent model for studying the role of SULTs in the detoxification of environmental pollutants including environmental estrogens. By searching the expressed sequence tag database, two zebrafish cDNAs encoding putative SULTs were identified. Sequence analysis indicated that these two putative zebrafish SULTs belong to the SULT1 gene family. The recombinant form of these two novel zebrafish SULTs, designated SULT1 ST7 and SULT1 ST8, were expressed using the pGEX-2TK glutathione S-transferase (GST) gene fusion system and purified from transformed BL21 (DE3) cells. Purified GST-fusion protein form of SULT1 ST7 and SULT1 ST8 exhibited strong sulfating activities toward environmental estrogens, particularly hydroxylated polychlorinated biphenyls (PCBs), among various endogenous and xenobiotic compounds tested as substrates. pH-dependence experiments showed that SULT1 ST7 and SULT1 ST8 displayed pH optima at 6.5 and 8.0, respectively. Kinetic parameters of the two enzymes in catalyzing the sulfation of catechin and chlorogenic acid as well as 3-chloro-4-biphenylol were determined. Developmental expression experiments revealed distinct patterns of expression of SULT1 ST7 and SULT1 ST8 during embryonic development and throughout the larval stage onto maturity.Aquatic Toxicology 08/2008; 89(2):94-102. DOI:10.1016/j.aquatox.2008.06.005 · 3.51 Impact Factor
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- "The type of toxicity exerted by PCBs depends on their ability to form coplanar structures. Coplanar PCBs, such as those having no chlorine atoms in the ortho positions are aryl hydrocarbon receptor (AhR) ligands and can induce CYP1A1 enzymes  . PCB77 (3,3′,4,4′-tetrachlorobiphenyl) is a coplanar PCB that is commonly found in the environment , because of its wide presence in commercial mixtures sold prior to 1979 (e.g., mixtures sold under the trademark Aroclor) . "
ABSTRACT: Palladium-based nanoparticles immobilized in polymeric matrices were applied to the reductive dechlorination of 3,3',4,4'-tetrachlorobiphenyl (PCB77) at room temperature. Two different dechlorination platforms were evaluated using (1) Pd nanoparticles within conductive polypyrrole films; or (2) immobilized Fe/Pd nanoparticles within polyvinylidene fluoride microfiltration membranes. For the first approach, the polypyrrole film was electrochemically formed in the presence of perchlorate ions that were incorporated into the film to counter-balance the positive charges of the polypyrrole chain. The film was then incubated in a solution containing tetrachloropalladate ions, which were exchanged with the perchlorate ions within the film. During this exchange, reduction of tetrachloropalladate by polypyrrole occurred, which led to the formation of palladium nanoparticles within the film. For the second approach, the membrane-supported Fe/Pd nanoparticles were prepared in three steps: polymerization of acrylic acid in polyvinylidene fluoride microfiltration membrane pores was followed by ion exchange of Fe(2+), and then chemical reduction of the ferrous ions bound to the carboxylate groups. The membrane-supported iron nanoparticles were then soaked in a solution of tetrachloropalladate resulting in the deposition of Pd on the Fe surface. The nanoparticles prepared by both approaches were employed in the dechlorination of PCB77. The presence of hydrogen was required when the monometallic Pd nanoparticles were employed. The results indicate the removal of chlorine atoms from PCB77, which led to the formation of lower chlorinated intermediates and ultimately biphenyl. Toxicity associated with vascular dysfunction by PCB77 and biphenyl was compared using cultured endothelial cells. The data strongly suggest that the dechlorination system used in this study markedly reduced the proinflammatory activity of PCB77, a persistent organic pollutant.Journal of Hazardous Materials 04/2008; 159(2-3):483-91. DOI:10.1016/j.jhazmat.2008.02.109 · 4.33 Impact Factor
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- "Due to their stability and lipophilic character, PCBs persist in the environment and accumulate in fatty tissues of animals and humans (Kimbrough, 1995; Hansen, 1999). PCBs are well known as potential neurotoxic (Seegal et al., 2005), teratogenic, and embriotoxic agents, effecting the embryonic development in fish (Arzuaga et al., 2004), birds (Hoffman et al., 1996; Summer et al., 1996), rodents (Goodwill et al., 2007; Kimura-Kuroda et al., 2007) and humans (Pocar et al., 2006; Roegge and Schantz 2006). PCBs can also contribute to the development of cancer in experimental animals (Carpenter, 2006; Knerr and Schrenk, 2006; Lehmann et al., 2007) and are classified as the probable carcinogens in humans (class 2A carcinogens according to the IARC classification) (Shields, 2006). "
ABSTRACT: Exposure to specific congeners of polychlorinated biphenyls (PCBs) can induce proinflammatory alterations, which may contribute to the formation of blood-borne tumor metastasis. The main aim of the present study was to establish an experimental model of PCB exposure in which PCBs are administered by oral gavage, which resembles the human exposure through the food chain. To determine structure-function relationship, we studied induction of inflammatory responses in the livers, lungs and brains of mice treated with PCB77 (a major coplanar PCB), PCB104 (a non-coplanar PCB with multiple ortho-chlorine substituents), and PCB153 (a major non-coplanar PCB) after a single gavage dose (150 µmol/kg body weight). The strongest expression of proinflammatory proteins occurred 24 h following the PCB administration independent of the class of PCB congeners. These data indicate that food-chain exposure to PCBs can induce proinflammatory mediators in organs that are potential targets for PCB-induced toxicity.Environmental Toxicology and Pharmacology 04/2008; 25(2):251-9. DOI:10.1016/j.etap.2007.10.020 · 2.08 Impact Factor