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At least 19 recordsLinked to original sources
PubMed1998

The use of microsomal in vitro assay to study phase I biotransformation of chlorobornanes (Toxaphene) in marine mammals and birds. Possible consequences of biotransformation for bioaccumulation and genotoxicity.

The factors determining the bioaccumulation of lipophilic compounds in wildlife are often poorly understood, partly because it is difficult to do in vivo experiments with animals such as marine mammals and birds. To evaluate the role of phase I biotransformation in the bioaccumulation process of chlorobornanes (toxaphene), this was studied in in vitro assays with hepatic microsomes of animals that could be sampled shortly after death. The capacity of microsomes to metabolise a technical toxaphene mixture decreased in the order Phoca vitulina (harbour seal) >> Lagenorhynchus albirostris (whitebeaked dolphin) approximately equal to Diomedea immutabilis (Laysan albatross) > Physeter macrocephalus (sperm whale). Harbour seal microsomes metabolised the chlorobornane (CHB) congeners CHB-32 and CHB-62; whitebeaked dolphin and Laysan albatross microsomes only metabolised CHB-32. Metabolism of CHB-26 and CHB-50 was never observed. The negative chemical ionisation (NCI-) mass spectra of some of the hydroxylated metabolites were obtained. The number of peaks in the toxaphene residues of wildlife extracts decreased in the order of increasing in-vitro biotransformation capacity. Thus, the results of the in vitro assays and residue analysis were in accordance, although assays with microsomes of more individuals of the same species are required for a more general conclusion at the species level. Finally, the effect of in vitro biotransformation was evaluated in terms of the genotoxic potential using the Mutatox assay. Only technical toxaphene and CHB-32 were genotoxic in the direct assay, whereas the addition of rat S9 fraction or microsomes of harbour seal and albatross decreased the genotoxic response. Thus, organisms with a low ability to metabolise chlorobornanes, such as whales, may be most affected by the carcinogenic properties of toxaphene. A hypothetical reaction which fits the experimental results is discussed. Based on these results it is concluded that in vitro assays with microsomes of wildlife animals which died a natural cause can act as a valuable tool to assess the occurrence and effects of phase I metabolism. Some precautions are discussed, that should be taken to reduce the chance of false negative results.

Animals↗
PubMed1986

[Study of promutagen biotransformation in the Ames test. IV. The effect of transplanted tumors on the biotransformation of various antineoplastic agents].

The effect of transplantation of rat tumours Jensen sarcoma, sarcoma 45, sarcoma M-1, as well as of inoculation of rat normal connective tissue on the processes of biotransformation of antitumour preparations cyclophosphane (CP), thiophosphamide, prospidine and of model compound nitrosomorpholine (NM) was studied. The study was accomplished by means of the Ames test with indicator bacterial strain Salmonella typhimurium TA 1950 in relation to the reactions of the 1st and the 2nd phases of xenobiotics metabolism. It was shown that the presence of tumours leads to inhibition of both metabolic activation processes of the promutagens NM and CP and the conjugation reactions of genetically active metabolites of these compounds with reduced glutathione. Genetic danger is supposed to be increased during application of antitumour preparations, the mutagenic activity of which is due to the activity of their metabolites. It is noted that the most essential effect on biotransformation processes of NM and CP was exhibited by sarcoma M-1, the most important changes of the biotransformation processes of promutagens being observed in the initial period of pathologic process, i.e. on the 3rd day after inoculation. Transplantation of the normal connective tissue of rats had no effect on reactions of both the 1st and the 2nd phase of metabolism of the promutagens studied.

Animals↗
PubMed1981

Terpenoids biotransformation in mammals III: Biotransformation of alpha-pinene, beta-pinene, pinane, 3-carene, carane, myrcene, and p-cymene in rabbits.

The biotransformation of (+)-, (-)-, and (+-)-alpha-pinenes, (-)-beta-pinene (nopinene), (-)-cis-pinane, (+)-3-carene, (-)-cis-carane, myrcene, and p-cymene in rabbits was investigated. The major metabolites were as follows: (-)-trans-verbenol from (+)-, (-)-, and (+/-)-alpha-pinenes; (-)-10-pinanol and (-)-1-p-menthene-7,8-diol from (-)-beta-pinene; (-)-alpha-terpineol and (-)-trans-sobrerol from (-)-cis-pinane; (-)-m-mentha-4,6-dien-8-ol, 3-caren-9-ol, (-)-3-carene-9-carboxylic acid, and 3-carene-9,10-dicarboxylic acid from (+)-3-carene; carane-9,10-dicarboxylic acid from (-)-cis-carane; and myrcene-3(10)-glycol, myrcene-1,2-glycol, uroterpenol, and p-cymene-9-carboxylic acid from p-cymene. These metabolisms include allylic oxidation, epoxidation, stereoselective gem-dimethyl hydroxylation and its oxidation, cleavage of a conjugated double bond by epoxidation, and regioselective oxidation, some of which are not found usually in chemical reactions, and due to which various new compounds were determined. This biotransformation of the monoterpene hydrocarbons gave some insect pheromones in high yield.U

Acyclic Monoterpenes↗
PubMed1987

[Biotransformation and pharmacokinetics of bamipine in rats. 1. biotransformation].

Biotransformation and Pharmacokinetics of Bamipine in Rats/1st Communication: Biotransformation studies. The metabolism of the antihistaminic N-phenyl-N-benzyl-4-amino-1-methylpiperidine (bamipine) was investigated after oral application in Wistar rats. The major metabolites in the urine were the ether glucuronides of N-p-hydroxy-phenyl-N-benzyl-4-amino-1-methylpiperidine and of N-p-hydroxyphenyl-N-benzyl-4-amino-piperidine. Unchanged drug was not detected. In vitro studies showed, in good correlation with in vivo studies, a oxidative demethylation of bamipin.

Animals↗
PubMed1979

Terpenoid biotransformation in mammals. II: Biotransformation of dl-camphene in rabbits.

The biotransformation of dl-camphene in rabbits was investigated. Four neutral metabolites, 6-exo-hydroxycamphene, 10-hydroxycamphene, and diastereoisomers of camphene-2,10-glycol, were identified and two alcohols, 7-hydroxycamphene and 3-hydroxytricyclene, were estimated by IR, UV, NMR, and mass spectra and chemical degradations. The formation of these compounds can be explained through a homoallylic oxidation or an epoxide formation.

Animals↗
PubMed2002

Recent results of biotransformation of drugs: investigation of the in vitro biotransformation of thalidomide using a dual cyclodextrin system in capillary electrophoresis.

A previously developed capillary electrophoresis method for the simultaneous separation and enantioseparation of thalidomide (TD) and its hydroxylated metabolites was extended to one additional biotransformation product. The dual chiral selector system using native beta-cyclodextrin (beta-CD) and the negatively charged sulfobutyl-beta-CD (SBE-beta-CD) was slightly modified up to a concentration of 12 mg/ml running buffer of each CD. The carrier mode in which these buffer additives transport the neutral compounds to the detector as well as the use of a polyacrylamide-coated capillary were necessary to achieve reproducible enantioseparations of all eight analytes.

Animals↗
PubMed1977

Studies on biotransformation of lysozyme. III. Comparative studies on biotransformation of exogenous and endogenous lysozyme in rats.

Exogenous hen lysozyme or endogenous rat lysozyme labeled with 131I was intravenously injected to rats with the same dosage, respectively, and the uptake and degradation of injected 131I-labeled rat lysozyme in liver and kidney were studied in comparison with those of 131I-labeled hen lysozyme. 1. Although the serum levels of both enzymes injected were almost indentical during the first 6 h, the liver uptake of 131I-labeled hen lysozyme was 2.2-fold more than that of 131I-labeled rat lysozyme at the peak time of 5 min after injection. The uptake and clearance of 131I-labeled rat lysozyme in the kidney were exclusively slow as compared with those of 131I-labeled hen lysozyme. 2. The intracellular distribution in the liver and kidney were examined by the differential centrifugation after injection of each lysozyme. The protein-bound radioactivity of each subcellular fraction was found to be the highest in the 12 000 X g (10 min) fraction in the liver and the 19 600 X g (20 min) fraction in the kidney. The relative specific activity of 12 000 X g fraction of the liver after injection increased with the time lapse. On the other hand, the relative specific activity of 105 000 X g (1 h) fraction of the liver attained a maximum within 5 min after injection and thereafter decreased. It was assumed that the mechanism of the uptake of injected 131I-labeled rat lysozyme in the liver and kidney was similar to that of 131I-labeled hen lysozyme. 3. The degradation of exogenous or endogenous lysozyme in subcellular particles was examined. From the effect of pH, activator and inhibitor on the degradation, the proteolytic enzyme to degrade the injected 131I-labeled hen lysozyme was indicated to be mainly cathepsin BL, with the optimal pH of about 5.0, and the injected 131I-labeled rate lysozyme was mainly degraded by cathepsin D, with the optimal pH of about 3.5 The in vitro degradation of exogenous and endogenous lysozymes showed a tendency similar to the in vivo clearance from the liver and kidney.

Animals↗
PubMed1986

Terpenoid biotransformation in mammals. IV Biotransformation of (+)-longifolene, (-)-caryophyllene, (-)-caryophyllene oxide, (-)-cyclocolorenone, (+)-nootkatone, (-)-elemol, (-)-abietic acid and (+)-dehydroabietic acid in rabbits.

The metabolism of (+)-longifolene, (-)-caryophyllene, (-)-caryophyllene oxide, (-)-cyclocolorenone, (+)-nootkatone, (-)-elemol, (-)-abietic acid and (+)-dehydroabietic acid was studied in rabbits. Each of these sesquiterpenoids was converted to primary, secondary or tertiary alcohols, among which the primary alcohol was predominant. A vinylic methyl group and an exomethylene group were easily hydroxylated and converted to a glycol via an epoxide in many cases. Eight new metabolites were determined by chemical and spectroscopic methods.

Abietanes↗
PubMed1983

[Biotransformation und pharmacokinetics of beta-methyl[1,1'-biphenyl]-4-propanenitrile (LU 20884) in rats. Studies on biotransformation].

The metabolism of the antiphlogistic beta-methyl[1,1'-biphenyl]-4-propanenitrile (LU 20884) was investigated in urine after oral application in male Wistar-rats. Metabolite with the major share was alpha-hydroxy-4'-methoxy-alpha-methyl[1,1'-biphenyl]- 4-aceticacidmethylester, which could be identified by mass and 1H-NMR spectroscopy as derivative of diazomethane. Furthermore the following metabolites could be detected as 4'-methoxy-beta-methyl[1,1'-biphenyl]-4-propanoicmethylester and propanenitrile.

Animals↗
PubMed1982

[Biotransformation and pharmacokinetics of mesoionic didehydro-4-methyl-5-phenyl-1,3,4-thiadiazolidine-2-thione (LU 2443). Studies on its biotransformation in rats].

The metabolism of the antiepileptic mesoionic didehydro-4-methyl-5-phenyl-1,3,4-thiadiazolidine-2-thione (LU 2443) was investigated after p.o. application in rats. The main metabolite was benzoic acid, besides the unchanged material and hippuric acid the spasmodically compounds N-methyl-benzamide and mesionic didehydro-4-methyl-5-phenyl-1,3,4-thiadiazolidine-2-one were detectable. In-vitro experiments could be demonstrated that LU 2443 was not demethylated by biochemical oxidation, and LU 2443 was also very stable against metabolizing influences by enteric bacteria.

Animals↗
PubMed1989

Differential biotransformation of glyceryl trinitrate by red blood cell-supernatant fraction and pulmonary vein homogenate.

We have demonstrated previously that glyceryl trinitrate (GTN) undergoes biotransformation to two glyceryl dinitrate (GDN) metabolites in the human red blood cell-supernatant fraction (RBC-SF) by hemoglobin-mediated and sulfhydryl-dependent enzymatic mechanisms. In the present study, we have shown that biotransformation of GTN in rabbit RBC-SF yields a glyceryl-1,2-dinitrate (1,2-GDN)/glyceryl-1,3-dinitrate (1,3-GDN) ratio of 5.3. Following inhibition of hemoglobin-mediated biotransformation of GTN by carbon monoxide (CO), the 1,2-GDN/1,3-GDN ratio was 2.1. Following inhibition of sulfhydryl-dependent biotransformation by N-ethylmaleimide (NEM), the 1,2-GDN/1,3-GDN ratio was 30.0. We have demonstrated previously that for GTN-induced vasodilation of isolated bovine pulmonary vein (BPV), the 1,2-GDN/1,3-GDN ratio was 7.1, which indicated that a hemoprotein-dependent process was involved in GTN biotransformation. To determine if this was the case, the biotransformation of GTN (0.51 microM) was studied in BPV homogenates; 31.1 pmol GDN/mg BPV protein was formed in 20 min. The 1,2-GDN/1,3-GDN ratio was 1.1, which indicated that hemoprotein-mediated biotransformation did not occur. This conclusion was supported by the fact that CO did not inhibit GTN biotransformation. GTN biotransformation by BPV homogenate was inhibited 62% by NEM, 89% by boiling of the homogenate, and almost completely by boiling plus NEM. These results indicated that biotransformation of GTN by the BPV homogenate involved in a combination of enzymatic and nonenzymatic processes that were mostly sulfhydryl dependent. It is concluded that the mechanism for GTN biotransformation in isolated intact BPV, which yielded preferential formation of 1,2-GDN, was rendered nonfunctional upon tissue homogenization.

Animals↗
PubMed2006

Bioaccumulation and biotransformation of chiral triazole fungicides in rainbow trout (Oncorhynchus mykiss).

There are very little data on the bioaccumulation and biotransformation of current-use pesticides (CUPs) despite the fact that such data are critical in assessing their fate and potential toxic effects in aquatic organisms. To help address this issue, juvenile rainbow trout (Oncorhynchus mykiss) were exposed to dietary concentrations of a mixture of chiral triazole fungicides (bromuconazole, cyproconazole, metconazole, myclobutanil, penconazole, propiconazole, tebuconazole, tetraconazole, and triadimefon) and a chiral legacy pesticide [alpha-hexachlorocyclohexane (alpha-HCH)] to study the bioaccumulation and biotransformation of these CUPs. Fish accumulated all triazoles rapidly during the 8 day uptake phase, and was followed by rapid elimination, which was estimated by taking accelerated sampling times during the 16 day depuration period. Half-lives (t1/2s) and times to 95% elimination (t95s) ranged from 1.0 to 2.5 and 4.5 to 11.0 days, respectively. Chiral analysis suggested no significant selectivity in biotransformation for most of the compounds based on statistically unaltered enantiomer fractions (EFs) in the fish compared to food values; exceptions were a change in EF of myclobutanil and changes in diastereomer fractions (DFs) of propiconazole and cyproconazole. No biotransformation was observed for alpha-HCH based on consistent EFs in the fish throughout the experiment and a t1/2 (15.8 days) that fell within the 95% confidence interval of a log K(ow)-log t1/2 relationship developed for assessing biotransformation of organic contaminants. This relationship did show that biotransformation accounted for the majority (ranging from 59.9 to 90.4%) of the elimination for all triazoles, and that triazole compounds with oxygen and hydroxyl functional groups were more easily biotransformed. This research indicated that chiral analysis may potentially miss biotransformation of CUPs and other potential non-persistent organic contaminants and shows the utility of the log K(ow)-log t1/2 relationship as a mechanistic tool for quantifying biotransformation. Based on the rapid biotransformation of the triazoles, future research should focus on formation of metabolites and their fate and possible effects in the environment.

Animals↗
PubMed1992

Effects of antibacterial agents on in vitro ovine ruminal biotransformation of the hepatotoxic pyrrolizidine alkaloid jacobine.

Ingestion of pyrrolizidine alkaloids, naturally occurring plant toxins, causes illness and death in a number of animal species. Senecio jacobaea pyrrolizidine alkaloids cause significant economic losses due to livestock poisoning, particularly in the Pacific Northwest. Some sheep are resistant to pyrrolizidine alkaloid poisoning, because ovine ruminal biotransformation detoxifies free pyrrolizidine alkaloids in digesta. Antibacterial agents modify ruminal fermentation. Pretreatment with antibacterial agents may account for some animal variability in resistance to pyrrolizidine alkaloid toxicosis, and antibacterial agents can also be used for characterizing ruminal pyrrolizidine alkaloid-biotransforming microflora. The objective of this study was to evaluate the effects of antibacterial agents on biotransformation of a predominant S. jacobaea pyrrolizidine alkaloid, jacobine, in ovine ruminal contents. Ovine ruminal jacobine biotransformation was tested in vitro with 20 independent antibacterial agents. Low amounts of rifampin and erythromycin prevented jacobine biotransformation. Chlortetracycline, lasalocid, monensin, penicillin G, and tetracycline were slightly less effective at inhibiting jacobine biotransformation. Bacitracin, crystal violet, kanamycin, and neomycin were moderately inhibitory against jacobine biotransformation. Brilliant green, chloramphenicol, gramicidin, nalidixic acid, polymyxin B SO4, sodium azide, streptomycin, sulfisoxazole, and vancomycin had little to no effect on jacobine biotransformation. The antibiotics that were most effective at inhibiting biotransformation were those that are active against gram-positive bacteria. Therefore, gram-positive bacteria are most likely critical members of the jacobine-biotransforming consortia.

Animals↗
PubMed1999

Pharmacokinetics and biotransformations of oxaliplatin in comparison with ormaplatin following a single bolus intravenous injection in rats.

PURPOSE: Traditionally ultrafilterable Pt has been used to estimate the body exposure to platinum drugs. However, previous studies have shown that ultrafilterable Pt consists of both cytotoxic and inert biotransformation products of platinum drugs. Therefore, it has been proposed that pharmacokinetic parameters of the parent drug and its cytotoxic biotransformation products are more likely to be correlated with the drug toxicity and efficacy than those of ultrafilterable Pt. Oxaliplatin and ormaplatin are likely to form very similar biotransformation products in vivo based on previous studies. However, ormaplatin causes severe and irreversible neurotoxicity while oxaliplatin causes moderate and reversible neurotoxicity. To evaluate the hypothesis that the neurotoxicity is associated with the pharmacokinetics of active biotransformation products, we investigated the biotransformations and pharmacokinetics of oxaliplatin and ormaplatin in rats at equimolar doses. METHODS: 3H-oxaliplatin and 3H-ormaplatin were administered to Wistar male rats through single bolus i.v. injections (20 micromol/kg). Blood was sampled from 3.5 min to 360 min and centrifuged at 2000 g to separate the plasma from red blood cells (RBCs). The RBCs were sonicated and centrifuged at 13000 g to separate the cytosol from the membrane fraction. Both plasma and RBC cytosol were filtered through YMT30 membranes (Mr = 30000 kDa), and the ultrafiltrates were analyzed using a single column HPLC technique to identify and quantitate the biotransformation products. The pharmacokinetics of oxaliplatin, ormaplatin, and their biotransformation products were characterized utilizing the curve stripping and nonlinear least-squares fitting program RSTRIP. RESULTS: The decays of total, plasma, plasma ultrafilterable (PUF), RBC-bound, and plasma protein-bound Pt-dach (only Pt species with an intact dach carrier ligand were quantitated in this study) were described by biphasic curves. No significant kinetic differences between oxaliplatin and ormaplatin were observed for total, plasma, and PUF Pt-dach in the initial alpha decay phase. However, Pt-dach bound to plasma proteins fourfold more quickly for ormaplatin than for oxaliplatin, and the AUC for Pt-dach bound to plasma proteins was twofold higher for ormaplatin than for oxaliplatin. The concentration of RBC-bound Pt-dach was highest at the initial time-point of 3.5 min for both drugs, which suggested a very rapid RBC uptake. The binding of Pt-dach to RBCs was slightly greater initially for ormaplatin than for oxaliplatin. However, the RBC-bound Pt-dach decayed more rapidly for ormaplatin (t(1/2alphaRBC) = 5.1 min) than for oxaliplatin (t(1,2alphaRBC) = 15.3 min). Thus the AUC(RBC) was slightly greater for oxaliplatin than for ormaplatin. The AUC was also slightly greater for oxaliplatin than for ormaplatin for the Pt-dach associated with the RBC membrane and RBC cytosolic proteins. However, there was no significant difference between oxaliplatin and ormaplatin for Pt-dach in the RBC cytosolic ultrafiltrate. There was also no significant difference in the AUCpuf between oxaliplatin and ormaplatin. Both oxaliplatin and ormaplatin produced the same types of major plasma biotransformation products including Pt(dach)Cl2, Pt(dach)(Cys)2, Pt(dach)(GSH)2, Pt(dach)(GSH), Pt(dach)(Met), and free dach. The decays of oxaliplatin, ormaplatin, and their biotransformation products were described by biphasic curves. (ABSTRACT TRUNCATED)

Animals↗
PubMed2003

Effects of the headspace gas composition on anaerobic biotransformation of o-, m-, and p-toluic acid in sediment slurries.

Composition of the headspace gas affected the biotransformation pattern of toluic acid isomers in anoxic sediment slurries. Under an N2 atmosphere, o- and m-, and p-toluic acid (20-25 mg L(-1)) were biotransformed in 100 days, 77 days, and 148 days, respectively, with a lag period of 50 days, 49 days, and 50 days, respectively. Under a CO2 atmosphere, the same toluic acid isomers were biotransformed by the sediment microorganisms in 16-25 days without a lag period. CO2 thus increased the biotransformation rates. The presence of H2, on the other hand, decreased the biotransformation rates: in most cases, adding H2 gas (5% and 20% to the N2 and CO2 atmospheres, respectively) not only increased the lag period but also decreased the maximum biotransformation rates. These effects were especially noticeable for the N2 atmosphere. Under N2, the maximum biotransformation rates of the toluic acid isomers were in the order o-toluic acid > m-toluic acid > p-toluic acid. However, under CO2, the maximum biotransformation rates were reversed, i.e., p-toluic acid > m-toluic acid > o-toluic acid. The presence of the methanogen inhibitor bromoethanesulfonic acid (BESA) slowed the biotransformation rates of p-toluic acid, and this together with the population dynamics of the acetogenic bacteria in the sediment slurries, suggested that acetogenic bacteria were involved in the degradation pathway. However, their exact role remains unclear.

Benzoates↗
PubMed1991

Comparisons of tetrachloro(d,l-trans)1,2-diaminocyclohexane-platinum(IV) biotransformations in the plasma of Fischer 344 rats at therapeutic and toxic doses.

Plasma biotransformations of tetrachloro(d,l-trans)1,2-diaminocyclohexaneplatinum(IV) (tetraplatin) were determined in vivo at both therapeutic (3 mg/kg) and toxic (12 mg/kg) doses in Fischer 344 rats. Tetraplatin was rapidly converted to dichloro(d,l-trans)1,2-diaminocyclohexaneplatinum(II) [PtCl2(dach)]. This conversion was complete at the earliest time measured (7.5 min) at the therapeutic dose, but some unreacted tetraplatin was detectable in the circulation at the toxic dose. Three other major biotransformation products were observed in plasma: (d,l-trans)1,2-diaminocyclohexaneaquachloroplatinum(II) [Pt(H2O)(Cl)(dach)]+, the Pt-methionine complex, and another biotransformation product tentatively identified as either the Pt-cysteine or Pt-ornithine complex. Several other minor plasma biotransformation products were detected. Two of these were most likely formed intracellulary from tetraplatin. Two or more other platinum complexes appeared to lack the diaminocyclohexane carrier ligand and were most likely formed intracellulary by trans-labilization of the carrier ligand. Tetraplatin, PtCl2(dach), and [Pt(H2O)(Cl)(dach)]+ all rapidly disappeared from the circulation. The other biotransformation products were persistent through at least 3 h and could be responsible for the delayed toxicity of tetraplatin. Although some minor differences were observed between tetraplatin biotransformations at the toxic vs therapeutic doses, most biotransformation products were simply present at much greater concentrations at the toxic dose than at the therapeutic dose. Thus, our data suggest that dose-dependent differences in tetraplatin toxicity are probably attributable to the amount, rather than the type, of biotransformation products present in the plasma.

Animals↗
PubMed2006

Biotransformation of polychlorinated biphenyls (PCBs) and bioformation of hydroxylated PCBs in fish.

Hydroxylated PCBs (OH-PCBs) are a class of organic contaminants that have been found recently in the plasma of Great Lakes fish, the source of which is either bioformation from PCBs or accumulation from the environment. To address the potential for fish to biotransform PCBs and bioform OH-PCBs juvenile rainbow trout (Oncorhynchus mykiss; approximately 80 g) were exposed to dietary concentrations of an environmentally relevant mixture of PCBs. Eight OH-PCBs were found in the plasma of rainbow trout after 30 days of exposure to the PCBs, the relative pattern of which was similar to those observed in wild lake trout (Salvelinus namaycush) from Lake Ontario. Hydroxylated-PCBs were not found (detection limit 0.02 pg/g) in the food or control (not PCB-exposed) fish. A curvilinear logt(1/2)-logK(ow) relationship for recalcitrant PCBs was found, similar to previously reported relationships, although t(1/2) values were longer and shorter than studies using smaller fish or cooler temperatures, respectively. A number of PCB congeners fell below the logt(1/2)-logK(ow) relationship providing the first estimates of non-chiral PCB biotransformation rates in fish. Enantioselective degradation of the chiral congeners PCBs 91 and 136, also indicated biotransformation. Biotransformation of PCBs was structure-dependent with greater biotransformation of PCBs with vicinal hydrogen atoms in the meta/para positions, suggesting CYP 2B-like biotransformation. Other chiral congeners with a meta/para substitution pattern showed no enantioselective degradation but were biotransformed based on the logt(1/2)-logK(ow) relationship. The results of this study demonstrate that laboratory held rainbow trout can biotransform a number of PCB congeners and that bioformation is likely an important source of OH-PCBs in wild salmonids of the Great Lakes.

Animals↗