Polychlorinated Biphenyls Mixture Research Articles

Alteration of gene expression profiles in the brain of Japanese medaka ( Oryzias latipes) exposed to KC-400 or PCB126

Polychlorinated biphenyls (PCBs) are known as neurotoxic chemicals and possibly alter animal behavior. We previously reported that PCB-exposure induced abnormal schooling behavior in Japanese medaka ( Oryzias latipes). This abnormal behavior might be caused by the functional alteration of central or terminal nervous system. To understand the mechanism(s) of behavioral change by PCB-exposure, we analyzed the gene expression profiles in the brain of medaka exposed to 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) or a PCB mixture (Kanechlor-400: KC-400) using a cDNA microarray that we constructed. Twelve FLF-II strain medaka (six individuals per treatment) were dietary exposed to PCB126 (0.01 μg/g b.w./day) or KC-400 (1 μg/g b.w./day) for three weeks. For the control, six fish were fed a control diet. After the exposure period, fish were dissected, and the brain samples were collected. The samples from control fish were pooled and used as a common reference in the microarray experiment. Microarray data were normalized by the LOWESS method, and we screened the genes whose expression levels were altered more than 1.5-fold. Gene expression profiling showed 97 down-regulated and 379 up-regulated genes in the brain of medaka exposed to PCB126. KC-400 exposure suppressed 15 genes and induced 266 genes in medaka brain. Among these genes, the expression levels of 7 and 188 genes were commonly down- or up-regulated, respectively in both treatment groups. On the other hand, 31 gene expressions were significantly different between PCB126 and KC-400 treatment groups, and three out of 31 genes were received opposite effects. In addition, the microarray data showed that thyroid hormone-responsive genes were up-regulated by PCB-exposure, which may imply that PCBs or their metabolites mimic thyroid hormone effects in the brain of PCB-exposed medaka.

ELECTRON-MICROSCOPIC LOCALIZATION OF LIPOPHILIC CHEMICALS BY AN ANTIBODY-BASED DETECTION SYSTEM USING THE BLUE MUSSEL MYTILUS EDULIS AS A MODEL SYSTEM

Identification of lipophilic chemicals requires the development of new techniques to detect these compounds at the cellular and subcellular levels. To address this issue, we have developed a combinational protocol using antibodies directed against chemicals together with a multiple signal amplification system (catalyzed signal amplification/gold-substituted silver-intensified peroxidase) to detect the lipophilic compounds at their subcellular sites of accumulation by transmission electron microscopy. As a model organism, we exposed the blue mussel Mytilus edulis to the polycyclic aromatic hydrocarbon phenanthrene and the polychlorinated biphenyl mixture Aroclor 1254 for up to 10 d. The aim of these exposure experiments was to analyze the cellular targets and sites of accumulation in the digestive system by transmission electron microscopy. The endo-lysosomal system of digestive cells and mitochondria of epithelial cells appeared to be the preferred accumulation sites for the lipophilic compounds studied. The antibody-based approach to detect lipophilic chemicals provides an important insight into the pathways of uptake and accumulation as well as mechanisms of toxicity.

Polychlorinated biphenyl-induced oxidative stress in organotypic co-cultures: Experimental dopamine depletion prevents reductions in GABA

Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants that have been demonstrated to be toxic to the dopamine (DA) systems of the central nervous system. One proposed mechanism for PCB-induced DA neurotoxicity is inhibition of the vesicular monoamine transporter (VMAT); such inhibition results in increased levels of unsequestered DA and DA metabolism leading to oxidative stress. We have used an organotypic co-culture system of developing rat striatum and ventral mesencephalon (VM) to determine whether alterations in the vesicular storage of DA, resulting from PCB exposure and consequent induction of oxidative stress, leads to GABA and DA neuronal dysfunction. Twenty-four-hour exposure to an environmentally relevant mixture of PCBs reduced tissue DA and GABA concentrations, increased medium levels of DA and measures of oxidative stress in both the striatum and VM. Alterations in neurochemistry and increases in measures of oxidative stress were blocked in the presence of n-acetylcysteine (NAC). Although NAC treatment did not alter PCB-induced changes in DA neurochemistry, it did protect against reductions in GABA concentration. To determine whether alterations in the vesicular storage of DA were responsible for PCB-induced oxidative stress and consequent reductions in GABA levels, we depleted DA from the co-cultures using α-methyl- p-tyrosine (AMPT). AMPT reduced striatal and VM DA levels by 90% and 70%, respectively. PCB exposure, following DA depletion, neither increased levels of oxidative stress nor resulted in GABA depletion. These results suggest that PCB-induced alterations in the vesicular storage of DA, resulting in increased levels of unsequestered DA, leads to increased oxidative stress, depletion of tissue glutathione, and consequent reductions in tissue GABA concentrations.

Effects of perinatal coexposure to methylmercury and polychlorinated biphenyls on neurobehavioral development in mice

Methylmercury (MeHg) and polychlorinated biphenyls (PCBs) are environmental pollutants that cause neurobehavioral deficits in humans. Because exposures to MeHg and PCBs occur through fish consumption, it is necessary to clarify the effects of the interaction of the two pollutants. Therefore, we investigated the effects of perinatal exposure to MeHg and PCBs on the neurobehavioral development in mice. Female mice (C57BL/6Cr) were divided into four groups according to the type of exposure: (1) vehicle control, (2) MeHg alone, (3) PCBs alone, and (4) MeHg + PCBs. The MeHg-exposed groups were fed with a diet containing 5 ppm MeHg (as Hg), from 4 weeks before mating, throughout pregnancy, and lactation. The PCB-exposed groups were given a commercial mixture of PCBs, Aroclor 1,254, at 18 mg/kg body weight in corn oil by gavage every 3 days from day 5 after breeding and continued until postnatal day (PND) 20. Before weaning, an assessment of eye opening showed the interactive effects between MeHg and PCBs on PND 12: The coexposure group showed a similar response to the control group, whereas the MeHg- and PCB-exposed groups showed a high response than the former two groups. We also observed delay in development of grasp reflex by MeHg exposure on PNDs 12 and 14. When the offspring mice were 8 weeks old, the group exposed to PCBs alone showed increases in the frequencies of excrement defecation and urine traces in an open-field test. Analysis of the latency revealed the antagonistic interaction between the MeHg and PCBs: The latency increased by either MeHg or PCB exposure was decreased by coexposure. Treatment with MeHg decreased the distance walked by the mice, and MeHg interacted with PCBs. Moris' water maze test showed that the MeHg-treated mice took a long time to reach the submerged platform; however, this MeHg exposure showed no interaction with PCB exposure. The spontaneous locomotion activity of the mice was not affected by the chemical exposure at 9 weeks of age. These behavioral changes were not accompanied by any histopathological changes at the levels of the frontal cortex-caudoputamen, hippocampus-amygdala, brainstem and cerebellum. These results show that perinatal coexposure to MeHg and PCBs produces no additive or synergistic effects. This phenomenon needs to be further investigated.

Effects of inhibitors on anaerobic microbial consortium with enhanced dechlorination activity in polychlorinated biphenyl mixture

Characterization was carried out on the anaerobic microbial consortium with enhanced degradation activity toward polychlorinated biphenyls in Kanechlor-300 and Kanechlor-400 mixtures in a burnt soil (BS) culture. The addition of molybdate to the BS culture resulted in the accumulation of less-chlorinated biphenyls such as 4,4'-dichlorinated biphenyl and 2,3',4-trichlorinated biphenyl; however, no such accumulation occurred without molybdate supplementation. No significant effect was observed in individual congeners in the BS culture supplemented with 2-bromoethane sulfonic acid. Analyses involving both the polymerase chain reaction-denaturing gradient gel electrophoresis of partial 16S rRNA genes and respiratory quinones showed that the predominant microorganisms in the BS culture were anaerobic Firmicutes, while sulfate reducers of the phyla Deltaproteobacteria, Firmicutes and Chloroflexi were absent in the culture amended with the inhibitors. No positive correlation was observed between the dechlorination activity and a PCR-based detection of gene fragments of known dechlorinating bacteria. These results suggest that sulfate reducers played an important role in the enhanced anaerobic dechlorination of PCBs in the BS culture.

Effects of polychlorinated biphenyls (PCBs) on expression of neurotrophic factors in C6 glial cells in culture

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants that affect nervous system function. Glial cells are among the first lines of defense in the nervous system and are involved in activities, including production of neurotrophic factors, which maintain an environment optimally suited for neuronal function. In this study, we investigated the effects of a commercial mixture of PCBs, Aroclor 1254 (A1254), on neurotrophic factor secretion by C6 cells in culture. C6 cells were exposed to medium containing 10 ppm A1254, 0.1% dimethyl sulfoxide (DMSO = vehicle), or normal culture medium. Glial cell line-derived neurotrophic factor (GDNF) and nerve growth factor (NGF) protein were measured by enzyme-linked immunosorbant assay. GDNF mRNA was measured by real-time RT-PCR. The role of protein kinase C (PKC) signaling in A1254 effects was investigated using bisindolylmaleimide, a PKC antagonist. Exposure to A1254 increased NGF (8.8 × 10 −5 ± 8.2 × 10 −6 pg NGF/cell) and GDNF (1.0 × 10 −4 ± 6.7 × 10 −6 pg GDNF/cell) secretion compared to DMSO treated controls (5.0 × 10 −5 ± 7.5 × 10 −6 pg NGF/cell and 6.2 × 10 −5 ± 3.1 × 10 −6 pg GDNF/cell). The effect of A1254 was long-lived, as GDNF secretion was elevated following 5 days of exposure (4.1 × 10 −5 ± 1.7 × 10 −6 pg GDNF/cell in A1254 exposed cells vs. 2.9 × 10 −5 ± 2.3 × 10 −6 pg GDNF/cell in DMSO exposed cells). GDNF mRNA expression was also elevated following exposure to A1254 (1.14 ± 0.07 gene expression units in A1254 exposed cells vs. 0.8 ± 0.07 gene expression units in DMSO exposed cells). Bisindolylmaleimide was able to block the effects of A1254 on GDNF secretion. Thus, one potential mechanism by which PCBs may alter nervous system function is via disruption of neurotrophic factor expression by glial cells. The observation that neurotrophic factor expression was increased following exposure to PCB may suggest that glial cells increase expression of neuroprotective genes following exposure to potentially damaging agents such as PCBs.

Enhancement of PCB degradation by Burkholderia xenovorans LB400 in biphasic systems by manipulating culture conditions

Two-phase partitioning bioreactors (TPPBs) can be used to biodegrade environmental contaminants after their extraction from soil. TPPBs are typically stirred tank bioreactors containing an aqueous phase hosting the degrading microorganism and an immiscible, non-toxic and non-bioavailable organic phase functioning as a reservoir for hydrophobic compounds. Biodegradation of these compounds in the aqueous phase results in thermodynamic disequilibrium and partitioning of additional compounds from the organic phase into the aqueous phase. This self-regulated process can allow the delivery of large amounts of hydrophobic substances to degrading microorganisms. This paper explores the reactor conditions under which the polychlorinated biphenyl (PCB) degrader Burkholderia xenovorans LB400 can degrade significant amounts of the PCB mixture Aroclor(R) 1242. Aroclor(R) degradation was found to stall after approximately 40 h if no carbon source other than PCBs was available in the reactor. Sodium pyruvate was found to be a suitable carbon source to maintain microbial activity against PCBs and to function as a substrate for additional cell growth. Both biphenyl (while required during the inoculum preparation) and glucose had a negative effect during the Aroclor(R) degradation phase. Initial Aroclor(R) 1242 degradation rates in the presence of pyruvate were high (6.2 mg L(-1) h(-1)) and 85% of an equivalent concentration of 100 mg Aroclor(R) 1242 per L aqueous phase could be degraded in 48 h, which suggest that solvent extraction of PCBs from soil followed by their biodegradation in TPPBs might be a feasible remediation option.

The effect of dietary glycine on the hepatic tumor promoting activity of polychlorinated biphenyls (PCBs) in rats

Polychlorinated biphenyls (PCBs) are ubiquitious lipophilic environmental pollutants. Some of the PCB congeners and mixtures of congeners have tumor promoting activity in rat liver. The mechanism of their activity is not fully understood and is likely to be multifactorial. The aim of this study was to investigate if the resident liver macrophages, Kupffer cells, are important in the promoting activity of PCBs. The hypothesis of this study was that the inhibition of Kupffer cell activity would inhibit hepatic tumor promotion by PCBs in rats. To test our hypothesis, we studied the effects of Kupffer cell inhibition by dietary glycine (an inhibitor of Kupffer cell secretory activity) in a rat two-stage hepatocarcinogenesis model using 2,2′,4,4′,5,5′-hexachlorobiphenyl (PCB-153, a non-dioxin-like PCB) or 3,3′,4,4′-tetrachlorobiphenyl (PCB-77, a dioxin-like PCB) as promoters. Diethylnitrosamine (DEN, 150 mg/kg) was administered to female Sprague–Dawley rats, which were then placed on an unrefined diet containing 5% glycine (or casein as nitrogen control) starting two weeks after DEN administration. On the third day after starting the diets, rats received PCB-77 (300 μmol/kg), PCB-153 (300 μmol/kg), or corn oil by i.p. injection. The rats received a total of 4 PCB injections, administered every 14 days. The rats were euthanized on the 10th day after the last PCB injection, and the formation of altered hepatic foci expressing placental glutathione S-transferase (PGST) and the rate of DNA synthesis in these foci and in the normal liver tissue were determined. Glycine did not significantly affect foci number or volume. PCB-153 did not significantly increase the focal volume, but increased the number of foci per liver, but only in the rats not fed glycine; PCB-77 increased both the foci number and their volume in both glycine-fed and control rats. Glycine did not alter the PCB content of the liver, but did increase the activity of 7-benzyloxyresorufin O-dealkylase (BROD) in liver microsomes from PCB-153 treated rats. However, glycine did not affect the induction of ethoxyresorufin O-dealkylase activity by PCB-77 in liver microsomes. Glycine diminished hepatocyte proliferation in PGST-positive foci, but not in normal tissue. Overall these results do not support the hypothesis that dietary glycine inhibits the promoting activities of PCBs. The observations that PCB-153 increased the number of foci per liver in control rats but not glycine-fed rats and that dietary glycine reduced cell proliferation in PGST-positive foci, however, do not allow us to completely rule out a role for dietary glycine. But the data overall indicate that Kupffer cells likely do not contribute to the tumor promoting activities of PCB-77 and PCB-153.

The Comparison of Silica Gel-Alumina Sorbents for Separation of PAHs and PCBs

The aim of this research is to develop a silica gel and alumina column chromatography for separation of polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs) into two groups. This is achieved by optimizing the cut-off volume of eluting solvent and weight ratio of silica gel and alumina. In this process mixture of PAHs and PCBs divide in two groups and simultaneously other interferences like lipids and aliphatic compounds are removed. So the sample is prepared to be analyzed and quantified by HPLC. The main purpose of the research was to find a combination of sorbents for the column chromatography method that would permit the determination of many types of pollutants (PAHs, PCBs and aliphatic compounds) in a single run. Elution profiles for both the analytes and the interfering components were determined for several types of column chromatography sorbents (alumina, silica) and combination of them . The silica: alumina (5:5 g) column is suitable for the separation of PCBs and silica: alumina (5:10 g) is preferred for the separation of PAHs. The efficiency of the developed clean- up method was evaluated using real sediment sample.

Aroclor-1254 affects mRNA polyadenylation, translational activation, cell morphology, and DNA integrity of rat primary prostate cells

Environmental xenobiotics have been shown to act as endocrine disruptors and to be implicated in increased cancer susceptibility. In particular, there is a significant concern regarding the impact of these contaminants on prostate cancer development and progression. However, the mechanisms with which these contaminants exert their detrimental effects are yet unclear and need to be further elucidated. In the present study, we investigated the effects of Aroclor-1254, a mixture of more than 60 environmental pollutants belonging to the polychlorinated biphenyl family, on rat prostate primary cultures. The results obtained after 24-h exposure indicated the ability of this contaminant mixture to influence mRNA stability and length of the 3'-end poly(A)tail of Connexin-32, Connexin-43, and heat shock protein-70. Consistent with this observation, immunostaining experiments demonstrated the altered availability of the encoded proteins. We also focused our attention on possible effects of Aroclor-1254 on cell morphology and could detect ultrastructural changes with gap junction disruption, fusion of single cells into clusters, and different aspects of apoptosis that became evident when exposure to Aroclor-1254 was extended to 72 h. The effects on the nuclear compartment were confirmed by the results obtained with Comet assay that showed DNA decompression and double-strand breaks already after 24-h exposure. Taken together, these findings show a detrimental effect of Aroclor 1254 on rat prostate cells and indicate a possible association between exposure to polychlorinated biphenyl mixture and induction of transformation process in prostate cells.

Destruction and Removal of PCBs in Waste Transformer Oil by a Chemical Dechlorination Process

A practical and efficient disposal of PCBs (polychlorinated biphenyls) in waste transformer oil by a chemical dechlorination process has been reported. The transformer oil containing commercial PCB mixtures (Aroclor 1242, 1254 and 1260) was treated by the required amounts of PEG 600 (polyethylene glycol 600), potassium hydroxide (KOH) and aluminum (Al), along with different reaction temperatures and times. The reaction of PEG with PCBs under basic condition produces arylpolyglycols, the products of nucleophilic aromatic substitution. The relative efficiencies of PCB treatment process were assessed in terms of destruction and removal efficiency (DRE, %). Under the experimental conditions of PEG600/KOH/Al/100 o C/2hr, average DRE of PCBs was approximately 78%, showing completely removal of PCBs containing 7-9 chlorines on two rings of biphenyl which appear later than PCB no. 183 (2,2',3,4,4',5',6-heptaCB) in retention time of GC/ECD. However, when increasing the reaction temperature and time to 150 o C and 240 min, average DRE of PCBs including the most toxic PCBs (PCB no. 77, 105, 118, 123 and 169) in PCB family reached 99.99% or better, with the exception of PCB no. 5 and 8 (2,3-diCB and 2,4'-diCB). In studying the reaction of PEG with PCBs, it confirmed that the process led to less chlorinated PCBs through a stepwise process with the successive elimination of chlorines. The process also permits complete recovery of treated transformer oil through simple segregating procedures.

Effect of aroclor 1248 and two pure PCB congeners on phospholipase D activity in rat renal tubular cell cultures

This paper elucidates the effect of different polychlorinated biphenyls (PCBs) on the phospholipase D (PLD) activity in soluble and particulate fractions of rat renal proximal tubular culture cells. Treatment with Aroclor 1248 (a commercial PCB mixture) caused a marked increase in the activity of PLD in intact renal tubular cells. The PLD activity was increased by Aroclor 1248 in the particulate fraction while the enzyme activity was unaffected in the soluble fraction. This work also shows that PCB 153 (2,2',4,4',5,5'-hexachlorobiphenyl, a di-ortho-substituted nonplanar congener) can increase the activity of PLD only in the particulate fraction. The exposure of cell cultures to PCB 77 (3,3',4,4'-tetrachlorobiphenyl, a non-ortho-substituted planar congener) does not alter PLD activity. These results suggest that PCB effects are structure dependent. Therefore, in order to clarify the molecular mechanism of activation of PLD by PCBs, the contents of immunoreactive PLD were examined by immunoblot analysis. Renal tubular cells expressed a PLD protein of 120 kDa corresponding with the PLD1 mammalian isoform in both the particulate and the soluble fraction. Aroclor 1248, PCB 153, and PCB 77 do not induce changes in the levels of PLD protein. These data indicate that PCBs, particularly nonplanar congeners, increase PLD activity. Moreover, these changes could not be demonstrated in the enzyme content in rat renal tubular cell cultures.

Protective effects of insulin on polychlorinated biphenyls‐induced disruption of actin cytoskeleton in hippocampal neurons

Insulin receptors are widely distributed in the brain, and insulin improves learning and memory in some brain injury. Insulin elevates LIM kinase 1 (LIMK-1) activity and induces actin polymerization in some cells, while actin cytoskeleton dynamics mediated via LIMK-1/cofilin signal pathway is considered important to learning and memory formation. Our previous studies have shown that polychlorinated biphenyls (PCBs) disrupt the actin cytoskeleton by inhibiting LIMK-1/cofilin signaling pathway in the cultured hippocampal neurons. To determine potential neuronal protective effects by insulin, we administered insulin to the cultured hippocampal neurons after exposure to PCBs mixture Aroclor 1254 (A 1254). We found that insulin antagonized a loss of filamentous actin and the cytotoxicity induced by A 1254. Similarly, insulin restored the decrease of LIMK-1 and cofilin phosphorylation induced by A 1254. We concluded that insulin could protect neurons, probably partly by ameliorating filamentous actin cytoskeleton disruption mediated via the activation of LIMK-1/cofilin signal pathway in cultured hippocampal neurons after exposure to A 1254. The above protective effects in hippocampal neuron may have important implications in the treatment of PCBs-induced neurotoxicity and the mechanism by which insulin improves learning and memory. (c) 2007 Wiley Periodicals, Inc. Environ Toxicol 22: 152-158, 2007.

Monitoring Native Vegetation on a Dumpsite of PCB-Contaminated Soil

Composition of native vegetation on a polychlorinated biphenyls (PCB)-contaminated soil dumpsite at Lhenice, South Bohemia (Czech Republic), was determined and species variability in the accumulation of PCBs in plant biomass was investigated. Soil stripping contaminated by PCBs originated at a factory producing electrical transformers that mostly used the commercial PCB mixture Delor 103 and 106. The PCB content of soil in the most contaminated part of the dumpsite reached 153 mg kg−1 dry soil. Low diversity of plant species was found on the dumpsite. Results showed three grass species, Festuca arundinacea Schreb., Phalaroides arundinacea (L.) Rauschert., and Calamagrostis epigeios (L.) Roth., to be the major components of the vegetation and confirmed their high tolerance toward PCB contamination. The highest content of PCB in plant biomass—813.2 μg kg−1 dry biomass—was determined in Festuca aboveground biomass. For phytoextraction purposes especially, Festuca can be recommended due to its high biomass yield, but its bioconcentration factor was very low (0.006). Tripleurospermum maritimum (L.) Sch. Bip. and Cirsium arvense (L.) Scop. grew mainly at the margins of the most contaminated part of the dumpsite. The PCB content determined in their aboveground biomass—278.7 and 289.5 μg kg−1 dry biomass, respectively—was nonsignificantly lower compared to grass species Phalaroides and Calamagrostis. Salix (Salix viminalis L. and Salix caprea L.) was monitored among plant species composition at this site as a representative of woody species.

Polychlorinated Biphenyl-Induced Neurotoxicity in Organotypic Cocultures of Developing Rat Ventral Mesencephalon and Striatum

Polychlorinated biphenyls (PCBs) are persistent environmental contaminants that are highly toxic to the developing nervous system, particularly via their disruption of dopamine (DA) function. In order to characterize the effects of PCBs on the developing basal ganglia DA system, we utilized an organotypic coculture system of developing rat striatum and ventral mesencephalon (VM). Exposure of the cocultures to an environmentally relevant mixture of PCBs for 1, 3, 7, or 14 days reduced tissue DA concentrations and increased medium levels of DA, homovanillic acid, and 3,4-dihydroxyphenylacetic acid. PCB exposure also increased neuronal cell death in both the VM and the striatum and reduced the number of DA neurons in the VM. Decreases in both tyrosine hydroxylase and DA transporter protein expression were shown by Western blot analysis in PCB-exposed cocultures. There was also an increase in neuronal cell death, identified by Fluoro Jade B, prior to a reduction in the number of VM DA neurons; we hypothesize this increase to be partly due to a loss of gamma-aminobutyric acid (GABA) neurons. Indeed, Western blot analysis revealed up to a 50% reduction in both VM and striatal glutamic acid decarboxylase 65/67. Analysis of tissue PCB levels revealed that concentrations were at or below 10 ppm following all exposure paradigms. This coculture system provides an excellent model to examine the chronology of PCB-induced neurotoxic events in the developing basal ganglia. Our results suggest that PCB-induced neurotoxicity in the developing basal ganglia involves GABAergic neuronal dysfunction, in addition to PCBs' better-recognized effects on DA function. These findings have important implications for disease states such as Parkinson's disease and for developmental deficits associated with exposure to PCBs and toxicologically similar environmental contaminants.

Ontogenetic alterations in molecular and structural correlates of dendritic growth after developmental exposure to polychlorinated biphenyls.

ObjectivePerinatal exposure to polychlorinated biphenyls (PCBs) is associated with decreased IQ scores, impaired learning and memory, psychomotor difficulties, and attentional deficits in children. It is postulated that these neuropsychological deficits reflect altered patterns of neuronal connectivity. To test this hypothesis, we examined the effects of developmental PCB exposure on dendritic growth.MethodsRat dams were gavaged from gestational day 6 through postnatal day (PND) 21 with vehicle (corn oil) or the commercial PCB mixture Aroclor 1254 (6 mg/kg/day). Dendritic growth and molecular markers were examined in pups during development.ResultsGolgi analyses of CA1 hippocampal pyramidal neurons and cerebellar Purkinge cells indicated that developmental exposure to PCBs caused a pronounced age-related increase in dendritic growth. Thus, even though dendritic lengths were significantly attenuated in PCB-treated animals at PND22, the rate of growth was accelerated at later ages such that by PND60, dendritic growth was comparable to or even exceeded that observed in vehicle controls. Quantitative reverse transcriptase polymerase chain reaction analyses demonstrated that from PND4 through PND21, PCBs generally increased expression of both spinophilin and RC3/neurogranin mRNA in the hippocampus, cerebellum, and cortex with the most significant increases observed in the cortex.ConclusionsThis study demonstrates that developmental PCB exposure alters the ontogenetic profile of dendritogenesis in critical brain regions, supporting the hypothesis that disruption of neuronal connectivity contributes to neuropsychological deficits seen in exposed children.

Effects of aqueous exposure to polychlorinated biphenyls (Aroclor 1254) on physiology and behavior of smolt development of Atlantic salmon

Polychlorinated biphenyls (PCBs) are a widespread aquatic contaminant and are present in both wild and hatchery raised Atlantic salmon, Salmo salar. The possible sub-lethal alterations in smolt physiology and behavior due to PCB exposure of salmon have not been widely examined. In this study, we examined the effects of the PCB mixture Aroclor 1254 on survival and smolt development of Atlantic salmon. In separate experiments, fish were exposed as yolk-sac larvae or as juveniles just prior to the parr–smolt transformation in April to 1 μg l −1 (PCB-1) or 10 μg l −1 (PCB-10) aqueous Aroclor 1254 (A1254), or vehicle for 21 days. After exposure, yolk-sac larvae were reared at ambient conditions for 1 year, until the peak of smolting the following May. Juveniles were sampled immediately after exposure. Both groups were assessed for behavioral, osmoregulatory, and endocrine disruption of smolt development at the peak of smolting. PCB-1 and PCB-10 treated yolk-sac larvae exhibited significant increases in the rate of opercular movement after 14 and 21 days of exposure. At the peak of smolting, prior exposure as yolk-sac larvae to PCB-1 did not affect behavior, while PCB-10 dramatically decreased volitional preference for seawater. Neither concentration of A1254 had long-term effects on the osmoregulatory or endocrine parameters measured in animals exposed as yolk-sac larvae. Juvenile fish exposed to PCB-1 or PCB-10 during smolting exhibited a dose-dependent reduction in preference for seawater. Fish treated with the higher dose of A1254 also exhibited a 50% decrease in gill Na +,K +-ATPase activity and a 10% decrease in plasma chloride levels in freshwater. In addition, plasma triiodothyronine was reduced 35–50% and plasma cortisol 58% in response to exposure to either concentration; whereas plasma thyroxine, growth hormone, and insulin-like growth factor I levels were unaffected. These results indicate that the effects of exposure to A1254 may vary according to developmental stage. Exposure to A1254 in the freshwater environment can inhibit preparatory adaptations that occur during smolting, thereby reducing marine survival and sustainability of salmon populations.

PCB-degrading potential of aerobic bacteria enriched from marine sediments

The main objective of this work was to study catabolic potential of marine sediment bacteria in aerobic degradation of polychlorinated biphenyls (PCBs). Marine sediment samples were collected at urban areas of the Croatian Adriatic coast, and microcosm enrichment experiments were performed in seawater mineral salts (SMS) medium with the addition of biphenyl as the only carbon source. After two to four subcultures, all enriched mixed cultures demonstrated the capability to use biphenyl, indicating that biphenyl-utilizing bacteria are widespread in coastal marine sediments. PCB-degrading activity of the enrichment cultures as well as that of their biphenyl-utilizing members were further studied in SMS medium with the addition of PCB mixtures containing di- to heptachlorinated congeners. GC-MS analyses of the extracted cultures suggested that, although they differed in PCB-degrading capabilities, all of the enrichment cultures expressed activity toward at least some of the lower chlorinated congeners (di- to tetrachlorobiphenyls). Biphenyl-utilizing bacteria isolated from the most active PCB-degrading mixed cultures showed little taxonomic diversity (six out of seven isolates belonged to the genus Rhodococcus and one to the genus Sphingomonas). All isolated Rhodococcus strains (R. erythropolis and R. ruber) showed substantial PCB-degrading activity, suggesting that these bacteria might play an important role in aerobic PCB degradation in polluted marine sediment.

Depletion of selected polychlorinated biphenyl, dibenzodioxin, and dibenzofuran congeners in farmed rainbow trout ( Oncorhynchus mykiss): A hint for safer fish farming

Farmed fish can be exposed to persistent organic contaminants – such as polychlorinated biphenyls (PCBs), dibenzodioxins (PCDDs), and dibenzofurans (PCDFs) – via feed, this eventually resulting in accumulation levels of health concern. To study the correlation between feed contamination, chemical accumulation in fish muscle (fillet), and chemical depletion, an all-vegetal base (or blank) feed was prepared and fortified with a commercial PCB mixture (Aroclor 1254) and six PCDD and PCDF congeners (namely, 2,3,7,8-T 4CDD, 2,3,7,8-T 4CDF, 1,2,3,7,8-P 5CDD, 1,2,3,7,8-P 5CDF, O 8CDD, and O 8CDF) to reproduce realistic low, medium, and high contamination levels. After a 1-month exposure, trout ( Oncorhynchus mykiss) were fed with the blank feed and sacrificed every 0.5 months over a 3-month period from exposure end; fillet specimens were sampled at each time. In all groups, the average fish weight increased linearly through the observation period. The chemical diminishing patterns observed were due to the combined effect of clearance and growth dilution: for 10 PCB and four PCDD and PCDF congeners, patterns were described with an empirical one-compartment (fish muscle) model. The canonical pseudo-first-order kinetic equation used was also modified into the form C = [ C 0 exp (− k C t)] ( m W t + 1) −1 to distinguish between the contributions to depletion from clearance, exp (− k C t), and growth dilution, ( m W t + 1) −1. Most mean clearance half-life (HL C) estimates appear to be greater than 4 months, in a number of cases reaching magnitudes well over 10 months or even negative, thus clearly indicating a non-negligible contribution from a second compartment. Based on means and their 95% confidence intervals, the depletion HL D estimates of the 14 selected congeners seem to be comprised between 1.2–3.4 and 1.0–5.0 months, respectively: these values, accounting for both clearance and growth dilution, provide an indication of the relevance of a blank feed as a management option to reduce the overall PCB, PCDD, and PCDF content in farmed trout. Due to a lack of bioaccumulation, O 8CDD and O 8CDF yielded no results for evaluation, whereas for many PCB congeners results were insufficient for empirical modelling.

Toxicity Equivalency Values for Polychlorinated Biphenyl Mixtures

Toxicity Equivalency Values for Polychlorinated Biphenyl Mixtures