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Isolation and partial characterization of PCB and PAH-degrading bacterial consortia from contaminated sites in Stephenville and Argentia, Island of Newfoundland /Squires-Parsons, Deborah V., January 2005 (has links)
Thesis (M.Sc.)--Memorial University of Newfoundland, 2005. / Restricted until October 2006. Bibliography: leaves 99-106.
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Toxicity and metabolism of alkyl-polycyclic aromatic hydrocarbons in fishTurcotte, Dominique 29 August 2008 (has links)
Alkyl-polycyclic aromatic hydrocarbons (alkyl-PAHs) constitute more than 90% of the total PAHs in crude oil and are the main constituents toxic to fish. Little characterization of alkyl-PAHs has been reported and is needed to predict the effects of crude oil following spills.
The objectives of this thesis were: (1) to evaluate the toxicity of alkyl-phenanthrenes and alkyl-anthracenes to the early life-stages of medaka (Oryzias latipes) using the partition controlled delivery of toxicants (PCD); (2) to investigate the effect of light on alkyl-anthracene toxicity; (3) to further characterize the PCD method; (4) to better understand alkyl-PAH mechanisms of toxicity; and (5) to identify the major phase I and phase II alkyl-PAH metabolites in rainbow trout (Oncorhynchus mykiss) and in medaka by both in vitro and in vivo methods.
It was determined that the toxicity of both series of alkyl-PAHs increased with the number of carbon substituents on the rings. Some alkyl-PAHs had EC50 values lower than the value from conventional semi-static exposure methods. These values were below the water solubility limit, consistent with the ability of PCD to correct for values from nominal concentrations above solubility. PCD provided stable concentrations for up to 17 days but could not always compensate for losses of alkyl-anthracenes by photodegradation.
Both series of alkyl-PAHs were toxic through different mechanisms that resulted from their physical and chemical properties. Alkyl-phenanthrenes such as 7-isopropyl-1-methylphenanthrene (retene) were more toxic to medaka embryos than phenanthrene. The appearance of blue sac disease suggested toxicity enhancement through the aryl hydrocarbon receptor pathway. Alkyl-anthracenes were toxic by narcosis in the absence of light and by phototoxicity in the presence of light. The photoproducts of alkyl-anthracenes were not toxic to fish.
The in vitro phase I metabolism by rainbow trout CYP1a enzymes and in vivo phase II metabolism in rainbow trout produced alkyl-anthracenes metabolites substituted mainly on the ring system. The phase II in vivo metabolites of alkyl-phenanthrenes in medaka larvae were substituted mainly on their alkyl chains. For all alkyl-PAHs, a predominance of glucuronide conjugates was identified in the phase II metabolites.
This characterization of the toxicity of alkyl-PAHs may contribute to predicting the toxicity of crude oil based on its composition. / Thesis (Ph.D, Chemistry) -- Queen's University, 2008-08-29 14:18:10.308
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N-(2'-deoxyguanosine-8-YL)-N-acetyl-2-aminofluorene induced translesion synthesis events in E. Coli: role of Y-family error-prone polymerases and the DNA sequence context /Nokhbeh, M. Reza January 1900 (has links)
Thesis (Ph. D.)--Carleton University, 2004. / Includes bibliographical references (p. 193-221). Also available in electronic format on the Internet.
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Studies of polycyclic aromatic hydrocarbons in Dungeness crabs : biomonitoring, physiologically based toxicokinetic model, and human health risk assessment /Eickhoff, Curtis Van. January 1900 (has links)
Thesis (Ph.D.) - Simon Fraser University, 2004. / Theses (Dept. of Biological Sciences) / Simon Fraser University.
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Antioxidant enzyme response in rainbow trout (Oncorhynchus mykiss) after subchronic exposure to an environmentally-relevant polycyclic aromatic hydrocarbon mixture /Norby, Tyler S. January 1900 (has links)
Thesis (M.S.)--Oregon State University, 2008. / Printout. Includes bibliographical references (leaves 40-46). Also available on the World Wide Web.
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Spectrofluorometric and Solubility Studies of Polycyclic Aromatic Hydrocarbons in Hydrogen Bonded Binary Solvent MixturesPowell, Joyce R., 1968- 05 1900 (has links)
The purpose of this dissertation is to investigate the behavior of polycyclic aromatic hydrocarbons (PAHs) in binary solvent systems and determine and/or develop predictive mathematical expressions for describing solutions in which hydrogen-bonding occurs.
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Use Of An Activated Magnesium/cosolvent System For The Desorption And Degradation Of Polycyclic Aromatic Hydrocarbons And Their Oxygenated Derivatives In Contaminated SoilsElie, Marc 01 January 2012 (has links)
The contamination of soils, with polycyclic aromatic hydrocarbons (PAHs), remains a widespread environmental concern. In the past two decades, many physical, chemical and biological methods have been developed and evaluated for the degradation of PAHs. However, due to their low aqueous solubility, high sorption affinity, hydrophobicity and recalcitrance, the environmental remediation of PAHs in soil continues to be economically challenging. In addition to PAH contamination, the presence of oxygenated derivatives of PAHs (OPAHs), in soils, has increasingly become a concern due to their greater toxic properties compared to parent PAH compounds. To date, no investigations on OPAH-remediation methods have been presented in the literature. The use of zero-valent metals (ZVMs) has been reported for several halogenated contaminants in solution systems, but the effectiveness of ZVM to degrade sorbed PAHs and OPAHs has been rarely addressed. This present research focuses on the development of a combined technique for the feasible desorption and degradation of PAHs and OPAHs in soils. PAH and OPAH degradation efficiency, using activated magnesium (Mg) metal combined with an ethanol-ethyl lactate cosolvent (1:1 ratio), was initially examined in soil-free systems. This metal/cosolvent system demonstrated adequate degradation (above 80%) for high-molecularweight (HMW) PAHs, which were subsequently converted into hydroaromatic compounds; while OPAHs were degraded and converted into hydroxylated or hydrogenated derivatives. Further soil-free studies revealed that the degradation rate was affected by the surface or reactive iv sites of the metal and that optimum degradation efficiency were obtained with Mg ball milled with graphite (Mg/C). In a bench-scale feasibility test, the efficacy of this system was assessed on a soil spiked with a mixture of three HMW PAHs compounds and three OPAHs compounds with amounts ranging from 0.033 mmol to 0.060 mmol. The experimental results show that 2 mL of an ethanol-ethyl lactate solvent mixture resulted in 58% to 85% extraction efficiency for the selected contaminants in 1 g of spiked soil, followed by 64 - 87% degradation efficiency of the extracted contaminants with 4.11 mmol of the activated metal. This activated-Mg/cosolvent system can be considered as a promising alternative method for ex situ remediation of PAH and OPAH-contaminated soils.
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ASSESSMENT OF POLYCYCLIC AROMATIC HYDROCARBON BIOAVAILABILITY FROM SOIL USING THE JUVENILE SWINE MODEL2016 January 1900 (has links)
Polycyclic aromatic hydrocarbons (PAHs) are common soil contaminants due to their lipophilic nature which limits partitioning to water or air. Soil properties such as organic carbon can affect PAH release from soil, and thus affect PAH bioavailability of ingested soil. Risk assessment of PAHs in soil generally assumes equal bioavailability of PAHs ingested in soil compared to PAHs ingested in reference dose media, leading to environmental cleanup guidelines that are potentially too conservative. This research intended to use the juvenile swine model to assess PAH bioavailability from impacted soil to better inform bioavailability estimates for risk assessment. This was done by assessing PAH bioavailability from single and repeated exposure to PAHs in different spiked exposure media, assessing PAH bioavailability from soil collected from PAH impacted sites, and assessing biomarkers of exposure and effect following PAH exposure.
The effect of exposure duration on bioavailability was assessed because people are usually chronically exposed to PAHs, rather than acutely exposed, as most bioavailability studies are performed, and chronic exposure may lead to increases in xenobiotic metabolizing enzymes and transporters which may affect bioavailability. This research found that exposure duration did not significantly affect anthracene and benzo[a]pyrene bioavailability (p>0.075), but exposure media did (p<0.004). These results suggest that exposure medium has a more important effect on bioavailability than exposure duration, and also bioavailability calculated from a single exposure is appropriate for use in risk assessment.
Bioavailability from 24 naturally impacted soils was assessed to determine which soil characteristics had the greatest effect on PAH bioavailability. Area under the curve (AUC) measurements for benzo[a]pyrene (BaP) and anthracene in swine blood after oral exposure from a soil matrix for benzo[a]pyrene and anthracene in soils had s very poor relationship with soil concentrations in soils collected from impacted sites (r2<0.15), but a very strong relationship with soil concentrations from spiked artificial soils (r2<0.95). As spiked soils had much higher concentrations of PAH, these results suggest there is a point of departure in soil concentrations where internal exposure becomes linearly related to soil concentration. Point of departure modeling indicates that this point occurs at soil PAH concentrations greater than 1,900 mg kg-1. Thus, risk assessment can assume a constant exposure to PAHs at soil concentrations lower than the point of departure. Comparison of terminal rate constants from intravenous (IV) exposure to PAHs and oral exposure to PAHs in a soilmatrix suggest that flip-flop kinetics occur in swine, where absorption occurs at a slower rate than elimination. Flip-flop kinetics likely explains the lack of relationship between real world soil concentrations and area under the curve measurements as absorption is the rate limiting step of elimination.
Biomarkers of exposure and effect were assessed in swine liver and ileum tissue, as well as blood following single and subchronic exposure to PAHs to determine if relationships could be drawn between exposure magnitude and duration and biomarker formation. Biomarkers included cytochrome P450 (P450) 1A1, 1A2, and 1B1 expression and activity as biomarkers of exposure and DNA adducts, carbonylated proteins, and micronucleated reticulocytes as biomarkers of effect. Biomarkers of exposure were not affected by exposure magnitude or duration, indicating that they would serve best as exposure markers rather than indicators of bioavailability or other effects. However, DNA adduct and protein carbonyl formation was significantly affected by exposure duration (p<0.045), but micronuclei formation was not. The micronuclei results suggest the liver was effective at clearing PAHs to non-toxic metabolites at the study doses, while tissue biomarkers of effect may correlate more effectively with exposure iv
length and magnitude of dose. This work indicates that PAH bioavailability from soil is lower than 100%, but additional work needs to be done to determine soil characteristics that affect bioavailability and to determine a bioavailability value relative to reference material.
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MECHANISMS OF RESISTANCE TO HALOGENATED AND NON-HALOGENATED AHR LIGANDS IN CHRONICALLY CONTAMINATED KILLIFISH POPULATIONSArzuaga, Xabier 01 January 2004 (has links)
Chronically contaminated killifish from Newark Bay (NB) NJ, and New Bedford Harbor (NBH) MA, have developed resistance to halogenated aromatic hydrocarbons that bind to and activate the aryl hydrocarbon receptor (AHR). To study the mechanisms of resistance, adult killifish were exposed to halogenated and non-halogenated AHR ligands and enzymatic and toxicological endpoints were measured in adult and embryonic fish.
The chlorinated and non-chlorinated AHR ligands 3,34,4-tetrachlorobiphenyl (PCB77) and benzo-a-pyrene (B[a]P) induced cytochrome P450 1A (CYP1A) in reference site, but not in NB killifish. Expression of CYP3A (not part of the AHR gene battery) was inducible only in Flax Pond killifish. Basal expression of the phase II enzyme glutathione-s-transferase (GST) was higher in NB killifish. These results suggest that NB killifish are resistant to CYP1A induction by chlorinated and non-chlorinated AHR ligands. Higher basal GST activity observed in NB killifish could be protective against toxicity caused by contaminants found in this site. Activation of AHR and induction of CYP1A, by AHR ligands has been associated with the toxic effects caused by these chemicals. To determine the association between resistance to CYP1A induction and the toxicity caused by AHR ligands, CYP1A activity, developmental deformities and reactive oxygen species (ROS) production were measured in reference site and contaminated (NB and NBH) killifish embryos exposed to AHR ligands. 3,34,45-pentachlorobiphenyl (PCB126) and 3-methylcholantherene (3-MC) induced CYP1A, and ROS production in reference site embryos. NB and NBH embryos were resistant to PCB126 induction of CYP1A, but responded to 3-MC. Killifish embryos from NB and NBH were resistant to PCB126 induced deformities. PCB126 and 3-MC did not increase ROS production in NB or NBH killifish embryos. Alpha-naphthoflavone (ANF) (an AHR/CYP1A inhibitor) blocked PCB126 mediated deformities and CYP1A induction in reference site embryos, but increased ROS production. The P450 inhibitor, piperonyl butoxide (PBO) was able to block PCB126 mediated induction of CYP1A activity and ROS production. These results suggest that PCB126 induced deformities are dependent on activation of AHR and CYP1A induction. In chronically contaminated killifish populations, loss of sensitivity to coplanar PCBs and PAHs could be through reduced expression of AHR, or altered DNA sequence or methylation status of the CYP1A gene promoter. Hepatic AHR expression, measured by photoaffinity labeling, was lower in NB killifish than reference site animals, suggesting that NB killifish express less AHR protein. DNA sequence analysis did not reveal considerable differences between contaminated and reference site populations, however additional DNA fragments were observed in some promoters but not in others. The methylation of the CYP1A promoters was studied using methylation sensitive restriction enzymes and no differences were detected between reference site and NB killifish. Treatment with the DNA methyltransferase inhibitor AzaC did not restore CYP1A induction by PCB126 in NB killifish. These studies suggest that resistance to activation of AHR and induction of xenobiotic activating enzymes (CYP1A and CYP3A) in combination with increased expression of conjugating enzymes (GST) protects chronically contaminated killifish against these chemicals.
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Diethylnitrosamine, ethylnitrosourea, and dimethylbenz(a)anthracene DNA binding studies in the rainbow troutVan Winkle, Samina 11 August 1988 (has links)
Dimethylbenz (a) anthracene (EMBA), a carcinogen that requires
metabolic activation to produce active metabolites capable of
binding to DNA, has been studied in the trout and other fish.
Polycyclic aromatic hydrocarbons (PAH) are of importance as they
are ubiquitous in the environment and their carcinogenic effects
in fish from contaminated waters are an important indication of
the pollution risks to man. Since such pollution risk assessment
presents the involvement of multiple agents, the study of the
modulation of PAH-DNA binding produced by other agents is
important. In this study the effect, of dietary pretreatment at
500 ppm, 100 ppm and 2000 ppn, using BNF, Aroclor 1254, or
indole-3-carbinol (I3C) respectively on DMBA-DNA binding was
examined. To study the effect of age on sensitivity to DMBA-DNA
binding, adult trout and fry were used in two separate studies.
The fish were fed treatment diet for at least two weeks. Fry were then injected with [³H] DMBA, at 22.4 μCi/3.9 x 10⁻² μmole/fish and adult trout at 284 μCi/1.58 μmole/fish. Liver DNA
was isolated, purified and binding of radioactivity to DNA was
examined and computed as the covalent binding index (CBI). Mean
CBI for control dietary group vising adult trout was 1000 fold
lower than for fry. Statistical analysis of covalent binding
index for the treatment groups revealed that a statistically
significant (p < 0.05) inhibition in DNA-DMBA binding response
in adult trout and fry was produced fcy the DNF dietary treatment
only.
Diethylnitrosamine (DENA), a potent hepatocarcinogen in
several animal species belongs also to the class of compounds
that require metabolic activation. Dietary treatment and
continuous exposure of trout to the carcinogen in water, have
produced hepatocellular carcinctnas. The water exposure also
produced a dose related DNA ethylation of the O⁶ position of
guanine, believed to be the promutagenic adduct produced after
DENA exposure. This study examines two other routes of exposure
to DENA, in vitro hepatocyte incubations and i.p. injection.
Adult trout and fry were injected with [³H] DENA. Adult fish
received 3.3, 16.5, and 33 mg/kg DENA, and fry received 10, 50
and 100 mg/kg. Hepatocyte incubation was performed with doses up
to 220 μM [³H] DENA, or 1 mM unlabelled DENA. DNA from fish
livers and from hepatocyte pellets was isolated, purified and
examined for radioactive binding of the DENA metabolites or in
the case of the unlabelled DENA, was analyzed for O⁶ and N7
adduct using an HPIC technique with fluorescence detection. O⁶-EtG adduct after DENA exposure, in DNA of hepatocytes obtained
from trout pretreated with beta-naphthoflavone (BNF, a known
inducer of cytodhrcme P-450 dependent enzyme activities involved
in the activation of xenobiotics) was below the limits of
detection of the HPDC-fluorescenoe detection procedure used. To
examine further if the lack of DNA binding and absence of the
O⁶-EtG adduct was due to rapid repair, the persistence of O⁶-EtG
after exposure to 40 nM ethylnitrosourea (ENU, a direct
ethylating agent) was studied in hepatocytes at 2, 4, and 5
hours after treatment. The activity of the alkyltransferase
protein involved in the repair of alkylguanines also was
determined using liver extracts from adult rainbow trout. The
studies did not reveal a significantly high rate of repair. It
is concluded that i.p. injection and in vitro hepatocyte
incubations are not a good method for studying the kinetics of
activation and DNA binding of DENA in the rainbow trout. The
i.p. route may lead to substantial loss of the dose of the
carcinogen administered and hepatocyte incubations are limited
by the toxic effects of increasing carcinogen concentration. The
reasons mentioned above, coupled with low levels of metabolism
of nitrosamines in trout results in the inability to detect and
study the appearance, persistence and repair of the O⁶-EtG
adduct. / Graduation date: 1989
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