TY  - JOUR
AB  - The accumulation of lipid droplets in hepatocytes is a key feature of drug-induced liver injury (DILI) and can be induced by a subset of hepatotoxic compounds. In the present study, we optimized and evaluated an in vitro technique based on the fluorescent dye Nile Red, further named Nile Red assay to quantify lipid droplets induced by the exposure to chemicals. The Nile Red assay and a cytotoxicity test (CTB assay) were then performed on cells exposed concentration-dependently to 60 different compounds. Of these, 31 were known to induce hepatotoxicity in humans, and 13 were reported to also cause steatosis. In order to compare in vivo relevant blood concentrations, pharmacokinetic models were established for all compounds to simulate the maximal blood concentrations (Cmax) at therapeutic doses. The results showed that several hepatotoxic compounds induced an increase in lipid droplets at sub-cytotoxic concentrations. To compare how well (1) the cytotoxicity test alone, (2) the Nile Red assay alone, and (3) the combination of the cytotoxicity test and the Nile Red assay (based on the lower EC10 of both assays) allow the differentiation between hepatotoxic and non-hepatotoxic compounds, a previously established performance metric, the Toxicity Separation Index (TSI) was calculated. In addition, the Toxicity Estimation Index (TEI) was calculated to determine how well blood concentrations that cause an increased DILI risk can be estimated for hepatotoxic compounds. Our findings indicate that the combination of both assays improved the TSI and TEI compared to each assay alone. In conclusion, the study demonstrates that inclusion of the Nile Red assay into in vitro test batteries may improve the prediction of DILI compounds.
AU  - Brecklinghaus, T.*
AU  - Albrecht, W.*
AU  - Duda, J.*
AU  - Kappenberg, F.*
AU  - Gründler, L.*
AU  - Edlund, K.*
AU  - Marchan, R.*
AU  - Ghallab, A.*
AU  - Cadenas, C.*
AU  - Rieck, A.*
AU  - Vartak, N.*
AU  - Tolosa, L.*
AU  - Castell, J.V.*
AU  - Gardner, I.*
AU  - Halilbasic, E.*
AU  - Trauner, M.*
AU  - Ullrich, A.*
AU  - Zeigerer, A.
AU  - Demirci Turgunbayer, Ö.*
AU  - Damm, G.*
AU  - Seehofer, D.*
AU  - Rahnenführer, J.*
AU  - Hengstler, J.G.*
C1  - 65952
C2  - 53000
SP  - 33-46
TI  - In vitro/in silico prediction of drug induced steatosis in relation to oral doses and blood concentrations by the Nile Red assay.
JO  - Toxicol. Lett.
VL  - 368
PY  - 2022
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Skin affections after sulfur mustard (SM) exposure include erythema, blister formation and severe inflammation. An antidote or specific therapy does not exist. Anti-inflammatory compounds as well as substances counteracting SM-induced cell death are under investigation. In this study, we investigated the benzylisoquinoline alkaloide berberine (BER), a metabolite in plants like berberis vulgaris, which is used as herbal pharmaceutical in Asian countries, against SM toxicity using a well-established in vitro approach. Keratinocyte (HaCaT) mono-cultures (MoC) or HaCaT/THP-1 co-cultures (CoC) were challenged with 100, 200 or 300 mM SM for 1 h. Post-exposure, both MoC and CoC were treated with 10, 30 or 50 mu M BER for 24 h. At that time, supernatants were collected and analyzed both for interleukine (IL) 6 and 8 levels and for content of adenylate-kinase (AK) as surrogate marker for cell necrosis. Cells were lysed and nucleosome formation as marker for late apoptosis was assessed. In parallel, AK in cells was determined for normalization purposes. BER treatment did not influence necrosis, but significantly decreased apoptosis. Anti-inflammatory effects were moderate, but also significant, primarily in CoC. Overall, BER has protective effects against SM toxicity in vitro. Whether this holds true should be evaluated in future in vivo studies.
AU  - Dimitrov, S.
AU  - Gouttefangeas, C.*
AU  - Besedovsky, L.*
AU  - Jensen, A.T.R.*
AU  - Chandran, P.A.*
AU  - Rusch, E.*
AU  - Businger, R.*
AU  - Schindler, M.*
AU  - Lange, T.*
AU  - Born, J.
AU  - Rammensee, H.-G.*
C1  - 53763
C2  - 45002
CY  - Elsevier House, Brookvale Plaza, East Park Shannon, Co, Clare, 00000, Ireland
SP  - E5536-E5545
TI  - Activated integrins identify functional antigen-specific CD8+ T cells within minutes after antigen stimulation.
JO  - Toxicol. Lett.
VL  - 115
IS  - 24
PB  - Elsevier Ireland Ltd
PY  - 2018
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Di-(2-propylheptyl) phthalate (DPHP) is used as a plasticizer for polyvinyl chloride products. A tolerable daily intake of DPHP of 0.2 mg/kg body weight has been derived from rat data. Because toxicokinetic data of DPHP in humans were not available, it was the aim of the present work to monitor DPHP and selected metabolites in blood and urine of 6 male volunteers over time following ingestion of a single DPHP dose (0.7 mg/kg body weight). Concentration-time courses in blood were obtained up to 24 h for DPHP, mono-(2-propylheptyl) phthalate (MPHP), mono-(2-propyl-6-hydroxyheptyl) phthalate (OH-MPHP), and mono-(2-propyl-6-oxoheptyl) phthalate (oxo-MPHP); amounts excreted in urine were determined up to 46 h for MPHP, OH-MPHP, oxo-MPHP, and mono-(2-propyl-6-carboxyhexyl) phthalate (cx-MPHP). All curves were characterized by an invasion and an elimination phase the kinetic parameters of which were determined together with the areas under the concentration-time curves in blood (AUCs). AUCs were: DPHP > MPHP > oxo-MPHP > OH-MPHP. The amounts excreted in urine were: oxo-MPHP > OH-MPHP> > cx-MPHP > MPHP. The AUCs of MPHP, oxo-MPHP, or OH-MPHP could be estimated well from the cumulative amounts of urinary OH-MPHP or oxo-MPHP excreted within 22 h after DPHP intake. Not considering possible differences in species-sensitivity towards unconjugated DPHP metabolites, it was concluded from a comparison of their AUCs in DPHP-exposed humans with corresponding earlier data in rats that there is no increased risk of adverse effects associated with the internal exposure of unconjugated DPHP metabolites in humans as compared to rats when receiving the same dose of DPHP per kg body weight.
AU  - Klein, D.
AU  - Kessler, W.
AU  - Pütz, C.
AU  - Semder, B.
AU  - Kirchinger, W.*
AU  - Langsch, A.*
AU  - Gries, W.*
AU  - Otter, R.*
AU  - Gallien, A.K.E.*
AU  - Wurzenberger, X.*
AU  - Filser, J.G.
C1  - 53520
C2  - 44898
CY  - Po Box 211, 1000 Ae Amsterdam, Netherlands
SP  - 105-115
TI  - Single ingestion of di-(2-propylheptyl) phthalate (DPHP) by male volunteers: DPHP in blood and its metabolites in blood and urine.
JO  - Toxicol. Lett.
VL  - 294
PB  - Elsevier Science Bv
PY  - 2018
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Klein, D.
AU  - Kessler, W.
AU  - Pütz, C.
AU  - Semder, B.
AU  - Kirchinger, W.
AU  - Langsch, A.*
AU  - Gries, W.*
AU  - Otter, R.*
AU  - Gallien, A.K.E.*
AU  - Wurzenberger, X.*
AU  - Filser, J.G.
C1  - 54158
C2  - 45330
CY  - Elsevier House, Brookvale Plaza, East Park Shannon, Co, Clare, 00000, Ireland
SP  - 105
TI  - Corrigendum to “Single ingestion of di-(2-propylheptyl) phthalate (DPHP) by male volunteers: DPHP in blood and its metabolites in blood and urine” [Toxicol. Lett. 294 (2018) 105–115].
JO  - Toxicol. Lett.
VL  - 296
PB  - Elsevier Ireland Ltd
PY  - 2018
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Ethylene (ET) is the largest volume organic chemical. Mammals metabolize the olefin to ethylene oxide (EO), another important industrial chemical. The epoxide alkylates macromolecules and has mutagenic and carcinogenic properties. In order to estimate the EO burden in mice, rats, and humans resulting from inhalation exposure to gaseous ET or EO, a physiological toxicokinetic model was developed. It consists of the compartments lung, richly perfused tissues, kidneys, muscle, fat, arterial blood, venous blood, and liver containing the sub-compartment endoplasmic reticulum. Modeled ET metabolism is mediated by hepatic cytochrome P450 2E1, EO metabolism by hepatic microsomal epoxide hydrolase or cytosolic glutathione S-transferase in various tissues. EO is also spontaneously hydrolyzed or conjugated with glutathione. The model was validated on experimental data collected in mice, rats, and humans. Modeled were uptake by inhalation, wash-in-wash-out effect in the upper respiratory airways, distribution into tissues and organs, elimination via exhalation and metabolism, and formation of 2-hydroxyethyl adducts with hemoglobin and DNA. Simulated concentration-time courses of ET or EO in inhaled (gas uptake studies) or exhaled air, and of EO in blood during exposures to ET or EO agreed excellently with measured data. Predicted levels of adducts with DNA and hemoglobin, induced by ET or EO, agreed with reported levels. Exposures to 10000 ppm ET were predicted to induce the same adduct levels as EO exposures to 3.95 (mice), 5.67 (rats), or 0.313 ppm (humans). The model is concluded to be applicable for assessing health risks from inhalation exposure to ET or EO.
AU  - Filser, J.G.
AU  - Klein, D.
C1  - 51677
C2  - 43397
CY  - Clare
SP  - 54-79
TI  - A physiologically based toxicokinetic model for inhaled ethylene and ethylene oxide in mouse, rat, and human.
JO  - Toxicol. Lett.
VL  - 286
PB  - Elsevier Ireland Ltd
PY  - 2017
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Neu, E.*
AU  - Michailov, M.C.*
AU  - Foltin, V.*
AU  - Senn, T.*
AU  - Welscher, U.*
AU  - Foltinova, J.*
AU  - Graw, J.
AU  - Hofstetter, A.*
AU  - Hohlbrugger, G.*
AU  - Madersbacher, H.*
AU  - Weissenbacher, E.R.*
AU  - Weiss, D.G.*
C1  - 53253
C2  - 44440
CY  - Clare
SP  - S305-S305
TI  - On importance of pathophysiology for an integrative toxicology.
JO  - Toxicol. Lett.
VL  - 280
PB  - Elsevier Ireland Ltd
PY  - 2017
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - There is potential for oral exposure of humans to styrene (ST) such as from migration of residual levels in polystyrene food containers. After absorption, ST is metabolised to styrene-7,8-oxide (SO), an alkylating epoxide. Hence, a comparison of blood burdens of SO resulting from oral exposures to ST was made with SO burdens possibly warranting genotoxic concern. A validated physiological toxicokinetic model was used for the assessment. Model calculations predicted for exposures to ST that maximum concentrations of SO in venous blood of rats and humans should not exceed 0.33 mg/ml and 0.036μg/ml, respectively, because of saturation of the SO formation from ST. The daily area under the concentration-time curve of SO in venous blood (AUCSO) was directly proportional to the dose of ST (mg/kg body weight; BW), independent of the exposure route (inhalation or oral exposure). In resting humans, the daily AUCSO was about half that in rats at the same amount of ST/kg BW (calculated up to 100mg ST/kg BW in humans). Taking into account the results of cytogenetic studies in ST-exposed rats, it was deduced that no genotoxic effects of SO are to be expected in ST-exposed humans, at least up to a daily amount of 100mg ST/kg BW, which is equivalent to 100 times the amount originating from the Overall Migration Limit for ST migrating from food contact plastics in the EU. Therefore, no potential genotoxic concern is predicted for ST uptake from food packaging, based on the reported combined measured and modelled data.
AU  - Filser, J.G.
AU  - Gelbke, H.P.*
C1  - 47840
C2  - 39513
CY  - Clare
SP  - 11-28
TI  - An evaluation of concentrations of styrene-7,8-oxide in rats and humans resulting from exposure to styrene or styrene-7,8-oxide and potential genotoxicity.
JO  - Toxicol. Lett.
VL  - 247
PB  - Elsevier Ireland Ltd
PY  - 2016
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Di-(2-propylheptyl) phthalate (DPHP) does not act as a reproductive toxicant or endocrine disruptor in contrast to other phthalates. Considering adverse effects of phthalates to be linked to their metabolism, it was the aim of the present study to investigate in the rat the blood burden of DPHP and its metabolites as a basis for understanding the toxicological behavior of DPHP. Rats were administered single oral doses of DPHP of 0.7 and 100mg/kg body weight. Concentration-time courses of DPHP and metabolites were monitored in blood. The areas under the concentration-time curves in blood (AUCs), normalized for the dose of DPHP, showed the following order: DPHP
AU  - Klein, D.
AU  - Kessler, W.
AU  - Semder, B.
AU  - Pütz, C.
AU  - Lichtmannegger, J.
AU  - Otter, R.*
AU  - Filser, J.G.
C1  - 49169
C2  - 41691
CY  - Clare
SP  - 80-86
TI  - Di-(2-propylheptyl) phthalate (DPHP) and its metabolites in blood of rats upon single oral administration of DPHP.
JO  - Toxicol. Lett.
VL  - 259
PB  - Elsevier Ireland Ltd
PY  - 2016
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Mertes, F.
AU  - Uciechowski, P.*
AU  - Loa, A.*
AU  - Rink, L.*
AU  - Schramm, K.*
C1  - 51477
C2  - 43134
CY  - Clare
SP  - S176-S176
TI  - Ready to use EROD assay by cryo-preserved cells and quantification by standard addition method.
JO  - Toxicol. Lett.
VL  - 258
PB  - Elsevier Ireland Ltd
PY  - 2016
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Bellomo, F.
AU  - Habel, N.C.
AU  - Crosera, M.*
AU  - Lenz, A.-G.
AU  - Filon, F.L.*
AU  - Stöger, T.
C1  - 32441
C2  - 35056
CY  - Clare
SP  - S239
TI  - An in vivo and in vitro comparative study of silver nanoparticles toxicity in the lung.
JO  - Toxicol. Lett.
VL  - 229
PB  - Elsevier Ireland Ltd
PY  - 2014
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Bengalli, R.D.*
AU  - Gualtieri, M.*
AU  - Mantecca, P.*
AU  - Urani, C.*
AU  - Camatini, M.*
AU  - Stöger, T.
C1  - 32442
C2  - 35055
CY  - Clare
SP  - S187
TI  - In vitro lung models for testing NPs effects: A case study on zinc oxide toxicity.
JO  - Toxicol. Lett.
VL  - 229
PB  - Elsevier Ireland Ltd
PY  - 2014
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - The application of physiologically-based toxicokinetic (PBTK) modelling in route-to-route (RtR) extrapolation of three cosmetic ingredients, coumarin, hydroquinone and caffeine is shown in this study. In particular, the oral no-observed-effect-level (NOEL) doses of these chemicals are extrapolated to their corresponding dermal values by comparing the internal concentrations resulting from oral and dermal exposure scenarios. The PBTK model structure has been constructed to give a good simulation performance of biochemical processes within the human body. The model parameters are calibrated based on oral and dermal experimental data for the Caucasian population available in the literature. Particular attention is given to modelling the absorption stage (skin and gastrointestinal tract) in the form of several sub-compartments. This gives better model prediction results when compared to those of a PBTK model with a simpler structure of the absorption barrier. In addition, the role of quantitative structure-property relationships (QSPRs) in predicting skin penetration is evaluated for the three substances with a view to incorporating QSPR-predicted penetration parameters in the PBTK model when experimental values are lacking. Finally, PBTK modelling is used, first to extrapolate oral NOEL doses derived from rat studies to humans, and then to simulate internal systemic/liver concentrations - Area Under Curve (AUC) and peak concentration- resulting from specified dermal and oral exposure conditions. Based on these simulations, AUC-based dermal thresholds for the three case study compounds are derived and compared with the experimentally obtained oral threshold (NOEL) values.
AU  - Gajewska, M.*
AU  - Worth, A.*
AU  - Urani, C.*
AU  - Briesen, H.*
AU  - Schramm, K.-W.
C1  - 31076
C2  - 34138
CY  - Clare
SP  - 189-202
TI  - Application of physiologically-based toxicokinetic modelling in oral-to-dermal extrapolation of threshold doses of cosmetic ingredients.
JO  - Toxicol. Lett.
VL  - 227
IS  - 3
PB  - Elsevier Ireland Ltd
PY  - 2014
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Habel, N.C.
AU  - Kutschke, D.
AU  - Eickelberg, O.
AU  - Meiners, S.
AU  - Stöger, T.
C1  - 32440
C2  - 35057
CY  - Clare
SP  - S192-S193
TI  - Critical role of interleukin 1 for the initiation and resolution of pulmonary inflammation induced by carbon nanomaterials.
JO  - Toxicol. Lett.
VL  - 229
PB  - Elsevier Ireland Ltd
PY  - 2014
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Ulutas, O.K.*
AU  - Cok, I.*
AU  - Darendeliler, F.*
AU  - Aydin, B.*
AU  - Coban, A.*
AU  - Henkelmann, B.
AU  - Schramm, K.-W.
C1  - 32443
C2  - 35054
CY  - Clare
SP  - S92
TI  - Blood endocrine disruptor levels in cryptorchidic newborns.
JO  - Toxicol. Lett.
VL  - 229
PB  - Elsevier Ireland Ltd
PY  - 2014
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Selenium is a metalloid of considerable interest in the human from both a toxicological and a nutritional perspective, with a very narrow safe range of intake. Acute selenium intoxication is followed by adverse effects on the nervous system with special clinical relevance, while the neurotoxicity of long-term overexposure is less characterized and recognized. We aimed to address this issue from a public health perspective, focusing on both laboratory studies and the few epidemiologic human studies available, with emphasis on their methodological strengths and limitations. The frequently overlooked differences in toxicity and biological activity of selenium compounds are also outlined. In addition to lethargy, dizziness, motor weakness and paresthesias, an excess risk of amyotrophic lateral sclerosis is the effect on the nervous system which has been more consistently associated with chronic low-level selenium overexposure, particularly to its inorganic compounds. Additional research efforts are needed to better elucidate the neurotoxic effects exerted by selenium overexposure.
AU  - Vinceti, M.*
AU  - Mandrioli, J.*
AU  - Borella, P.*
AU  - Michalke, B.
AU  - Tsatsakis, A.*
AU  - Finkelstein, Y.*
C1  - 28501
C2  - 33430
CY  - Clare
SP  - 295-303
TI  - Selenium neurotoxicity in humans: Bridging laboratory and epidemiologic studies.
JO  - Toxicol. Lett.
VL  - 230
IS  - 2
PB  - Elsevier Ireland
PY  - 2014
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Ntziachristos, V.
AU  - Razansky, D.
C1  - 27667
C2  - 32792
SP  - S51
TI  - Revolutionizing biomedical optical imaging with multispectral optoacoustic tomography (MSOT).
JO  - Toxicol. Lett.
VL  - 221
PB  - Elsevier Ireland
PY  - 2013
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - The important industrial chemical 1,3-butadiene (BD; CAS Registry Number: 106-99-0) is a potent carcinogen in B6C3F1 mice and a weak one in Sprague-Dawley rats. This difference is mainly attributed to the species-specific burden by the metabolically formed 1,2:3,4-diepoxybutane (DEB). However, only limited data exist on the DEB blood burden of rodents at BD concentrations below 100ppm. Considering this, DEB concentrations were determined in the blood of mice and rats immediately after 6h exposures to various constant concentrations of BD of between about 1 and 1200ppm. Immediately after its collection, blood was injected into a vial that contained perdeuterated DEB (DEB-D(6)) as internal standard. Plasma samples were prepared and treated with sodium diethyldithiocarbamate that derivatized metabolically produced DEB and DEB-D(6) to their bis(dithiocarbamoyl) esters, which were then analyzed by high performance liquid chromatography coupled with an electrospray ionization tandem mass spectrometer. DEB concentrations in blood versus BD exposure concentrations in air could be described by one-phase exponential association functions. Herewith calculated (±)-DEB concentrations in blood increased in mice from 5.4nmol/l at 1ppm BD to 1860nmol/l at 1250ppm BD and in rats from 1.2nmol/l at 1ppm BD to 92nmol/l at 200ppm BD, at which exposure concentration 91% of the calculated DEB plateau concentration in rat blood was reached. This information on the species-specific blood burden by the highly mutagenic DEB helps to explain why the carcinogenic potency of BD in rats is low compared to that in mice.
AU  - Csanády, G.A.
AU  - Steinhoff, R.
AU  - Riester, M.B.
AU  - Semder, B.
AU  - Pütz, C.
AU  - Li, Q.*
AU  - Richter, N.*
AU  - Kessler, W.
AU  - Klein, D.*
AU  - Filser, J.G.
C1  - 6611
C2  - 28966
SP  - 286-290
TI  - 1,2:3,4-Diepoxybutane in blood of male B6C3F1 mice and male Sprague-Dawley rats exposed to 1,3-butadiene.
JO  - Toxicol. Lett.
VL  - 207
IS  - 3
PB  - Elsevier
PY  - 2011
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Hirn, S.
AU  - Tian, F.
AU  - Takenaka, S.
AU  - Kostarellos, K.*
AU  - Kreyling, W.G.
AU  - Stöger, T.
C1  - 47043
C2  - 40476
SP  - S46
TI  - Dynamics of pulmonary inflammation caused by isometric carbon nanoparticles or fibrous carbon nanotubes.
JO  - Toxicol. Lett.
VL  - 205
PY  - 2011
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Propylene oxide (PO) concentrations >or=300 ppm induced cell proliferation and tumors in rat nasal respiratory epithelium (NRE). Cell proliferation was suggested to result from depletion of glutathione (GSH) in NRE. In order to substantiate this hypothesis, cell proliferation - measured by bromodeoxyuridine incorporation into DNA of the epithelium lining middle septum, dorsal medial meatus, and medial and lateral surfaces of the nasoturbinate in transverse nasal sections taken immediately posterior to the upper incisor teeth - and water-soluble non-protein thiol (NPSH) in NRE were determined after exposing male Fischer 344 rats to 50 ppm, 100 ppm, 200 ppm, or 300 ppm PO (6 h/day, 3 days). Both parameters were also investigated after treating rats for 3 days with diethylmaleate (DEM; 2 x 250 mg/kg/day or 500 + 150 mg/kg/day) or buthionine sulfoximine (BSO; 500 mg/kg/day). Exposure to 50 ppm PO and treatment with 2 x2 50 mg/kg/day DEM resulted in NPSH levels approximating 50% and 80% of the level in untreated controls, respectively. Cell proliferation did not increase. After exposures to >or= 100 ppm PO or treatment with BSO or 500 + 150 mg/kg/day DEM, NPSH was depleted to
AU  - Khan, M.D.H.
AU  - Klein, D.
AU  - Mossbrugger, I.
AU  - Oesterle, D.
AU  - Csanády, G.A.
AU  - Quintanilla-Martinez, L.
AU  - Filser, J.G.
C1  - 701
C2  - 26316
CY  - Clare
SP  - 203-210
TI  - Is propylene oxide induced cell proliferation in rat nasal respiratory epithelium mediated by a severe depletion of water-soluble non-protein thiol?
JO  - Toxicol. Lett.
VL  - 185
IS  - 3
PB  - Elsevier
PY  - 2009
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Ethylene glycol (EG) is a widely used liquid. Limited data are published regarding inhaled EG and no data regarding transdermal EG uptake in humans. In order to gain information on the quantitative fate of EG, four male volunteers inhaled between 1340 and 1610mumol vaporous (13)C-labeled EG ((13)C(2)-EG) for 4h. Separately, three of these subjects were epidermally exposed for up to 6h to liquid (13)C(2)-EG (skin area 66cm(2)). Plasma concentrations and urinary amounts of (13)C(2)-EG were determined by gas chromatography with mass selective detection. Additionally, plasma was assayed for (13)C-labeled glycolic acid ((13)C(2)-GA) and urine for (13)C(2)-GA and (13)C-labeled oxalic acid ((13)C(2)-OA). Both EG metabolites were nephrotoxic in animals and humans and embryotoxic in rodents. (13)C-labels enabled to differentiate from also determined endogenous EG, glycolic acid (GA), and oxalic acid (OA). Of (13)C(2)-EG inhaled, 5.5+/-3.0%, 0.77+/-0.15%, and 0.10+/-0.12% were detected in urine as (13)C(2)-EG, (13)C(2)-GA, and (13)C(2)-OA, respectively. The skin permeability constant of liquid EG was 2.7x10(-5)+/-0.5x10(-5)cm/h. Of the dose taken up transdermally, 8.1+/-3.2% and up to 0.4% were excreted in urine as (13)C(2)-EG and (13)C(2)-GA, respectively. It is calculated that equally long-lasting exposure to 10ppm vaporous EG or wetting of both hands by liquid EG leads to about the same body burden by EG and metabolites. The amounts of GA and OA excreted daily in urine as a result of exposure (8h/day) to 10ppm EG are about 15% and 2%, respectively, of those excreted from naturally occurring endogenous GA and OA.
AU  - Upadhyay, S.
AU  - Carstens, J.
AU  - Klein, D.*
AU  - Faller, T.H.
AU  - Halbach, S.
AU  - Kirchinger, W.
AU  - Kessler, W.
AU  - Csanády, G.A.
AU  - Filser, J.G.
C1  - 639
C2  - 25318
SP  - 131-141
TI  - Inhalation and epidermal exposure of volunteers to ethylene glycol: Kinetics of absorption, urinary excretion, and metabolism to glycolate and oxalate.
JO  - Toxicol. Lett.
VL  - 178
IS  - 2
PB  - Elsevier
PY  - 2008
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - To evaluate an adequate strategy for biological monitoring of aluminium (Al), a group of 62 Al welders (age in 1999: 23-51 years, median 35 years) was surveyed annually from 1999 to 2003 by determination of pre- and post-shift Al in urine and plasma. Biomonitoring was supplemented by personal air measurements of the total dust concentration. The welders' internal exposure was compared to the exposure of 60 non-exposed assembly workers (age in 1999: 21-51 years, median: 36 years) who were surveyed in 1999, 2001 and 2003. Having a nearly constant dust exposure, median concentrations of Al in urine (Al in plasma) of the welders decreased from 40.1 μg/g to 19.8 μg/g creatinine (8.7 to 4.6 μg/l). For the control group the median levels of Al in urine (plasma) ranged from 4.8 μg/g to 5.2 μg/g creatinine (2.4-4.3 μg/l) indicating a higher sensitivity for the marker Al in urine. No systematic differences have been found between pre- and post-shift internal exposure. This might be caused by the slow elimination kinetics and low systemic bioavailability of Al. A correlation analysis did not yield close relationships between dust exposure, Al in plasma and Al in urine underlining the importance of biomonitoring for assessment of Al exposure. © 2005 Elsevier Ireland Ltd. All rights reserved.
AU  - Rossbach, B.*
AU  - Buchta, M.*
AU  - Csanády, G.A.
AU  - Filser, J.G.
AU  - Hilla, W.*
AU  - Windorfer, K.*
AU  - Stork, J.*
AU  - Zschiesche, W.*
AU  - Gefeller, O.*
AU  - Pfahlberg, A.*
AU  - Schaller, K.H.*
AU  - Egerer, E.*
AU  - Pinzón, L.C.*
AU  - Letzel, S.*
C1  - 4776
C2  - 23882
SP  - 239-245
TI  - Biological monitoring of welders exposed to aluminium.
JO  - Toxicol. Lett.
VL  - 162
IS  - 2-3
PY  - 2006
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Viluksela, M.*
AU  - Raasmaja, A.*
AU  - Lebofsky, M.*
AU  - Stahl, B.U.*
AU  - Rozman, K.K.
C1  - 2549
C2  - 22232
SP  - 133-142
TI  - Tissue-specific effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the activity of 5'-deiodinases I and II in rats.
JO  - Toxicol. Lett.
VL  - 147
PY  - 2004
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Csanády, G.A.
AU  - Kessler, W.
AU  - Hoffmann, H.D.*
AU  - Filser, J.G.
C1  - 9842
C2  - 20838
SP  - 75-102
TI  - A toxicokinetic model for styrene and its metabolite styrene-7,8-oxide in mouse, rat and human with special emphasis on the lung.
JO  - Toxicol. Lett.
VL  - 138
PY  - 2003
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Filser, J.G.
AU  - Kessler, W.
AU  - Csanády, G.A.
C1  - 9843
C2  - 21160
SP  - 273-276
TI  - Response to letter to editor. 
JO  - Toxicol. Lett.
VL  - 144
PY  - 2003
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Concerns of a tumorigenic risk of styrene (ST) originate from the findings that styrene (ST) is metabolized to the genotoxic, intermediate styrene-7,8-oxide (SO). Therefore, it was hypothesized that results of animal long-term studies with ST and SO together with the SO tissue burden are sufficient for conducting a 'worst case' estimate of the tumorigenic risk of ST. On this basis we predicted the excess human lifetime risk for lung tumors (p(HPS)) and the highest possible risk for other systemic tumors (p(HPS)) resulting from daily intake of ST via food and ambient air. As measures for p(EXL) the mean lifetime concentration of SO in the transitional zone of the lung and for p(HPS) the mean lifetime concentration of SO in blood were calculated using a physiological toxicokinetic model. For a daily oral intake of 12 mug ST, p(EXL) was obtained to be between 5 x 10(-9) and 2 x 10(-8) and p(HPS) to be between 7 x 10(-9) and 2 x 10(-8). Lifetime risks calculated for continuous exposure to 3 mug/m(3) ST in ambient air were between 8 x 10(-7) and 3 x 10(-6). (P-EXL) and between 2 x 10(-8) and 4 x 10(-8) (p(HPS)). Although these values indicate very low risks, the actual risks are expected to be even by far smaller. This is discussed in detail for lung tumorigenesis.
AU  - Filser, J.G.
AU  - Kessler, W.
AU  - Csanády, G.A.
C1  - 9844
C2  - 20381
SP  - 1-18
TI  - Estimation of a possible tumorigenic risk of styrene from daily intake via food and ambient air.
JO  - Toxicol. Lett.
VL  - 126
PB  - Elsevier
PY  - 2002
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - The mammalian xenobiotic-metabolizing sulfotransferases are cytosolic enzymes, which form a gene superfamily (SULT). Ten distinct human SULT forms are known. Two SULT forms represent splice variants, the other forms are encoded by separate genes. Common functional polymorphisms of the transcribed region are known for two of the forms. We have expressed 16 separate rat and human SULTs as well as some of their allelic variants, in Salmonella typhimurium TA1538 and/or V79 cells, which are target cells of commonly used mutagenicity assays. The expressed SULTs activated numerous compounds to mutagens in both assay systems. However, some promutagens were activated by only one or several of the human SULTs. Pronounced differences in promutagen activation were also detected between orthologous rat and human SULTs, and between allelic variants of human SULTs.
AU  - Glatt, H.*
AU  - Engelke, C.E.*
AU  - Pabel, U.*
AU  - Teubner, W.*
AU  - Jones, A.L.*
AU  - Coughtrie, M.W.*
AU  - Andrae, U.
AU  - Falany, C.N.*
AU  - Meinl, W.*
C1  - 23965
C2  - 31413
SP  - 341-348
TI  - Sulfotransferases: Genetics and role in toxicology.
JO  - Toxicol. Lett.
VL  - 112-113
PB  - Elsevier Science
PY  - 2000
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - The cytotoxicity of polycyclic and monocyclic nitroarenes was tested in cell lines V79/NH, H411EC3/G-, 5L and BWI-J, which are distinguished by their specific expression of xenobiotic metabolizing enzymes. The results show that polycyclic nitroarenes differentially affect the test cell lines suggesting that some compounds, such as 1,3-dinitropyrene, are activated by cytochrome P4501A1, others, such as 1,6-dinitropyrene, by reductase(s) and acetyltransferase. No such cell specific responses were seen for 13 monocyclic nitroarenes tested. This group of chemicals apparently is activated by an enzyme(s) other than the polycyclic nitroarenes tested.
AU  - Perchermeier, M.M.
AU  - Kiefer, F.
AU  - Wiebel, F.J.
C1  - 39988
C2  - 38954
SP  - 53-57
TI  - Toxicity of monocyclic and polycyclic nitroaromatic compounds in a panel of mammalian test cell lines.
JO  - Toxicol. Lett.
VL  - 72
IS  - 1-3
PY  - 1994
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Up to now only few experimental data for total deposition of inhaled aerosol particles are available for children. In this study 29 healthy children aged between 3 and 14 years volunteered for the determination of 1 μm, 2 μm and 3 μm particles for spontaneous and controlled breathing. It turns out that total deposition values for children are higher than for adults.The effect is significant for all particle sizes (Kruskal-Wallis). For the applied breathing patterns deposition decreases as a function of body height. For inhalation risk assessments the number of particles deposited per unit time (deposition rate) rather than the deposition per breath has to be taken. During spontaneous breathing at rest the deposition rate is on average higher for children than for adults.
AU  - Schiller-Scotland, C.F.*
AU  - Hlawa, R.*
AU  - Gebhart, J.
C1  - 34066
C2  - 37971
SP  - 137-144
TI  - Experimental data for total deposition in the respiratory tract of children.
JO  - Toxicol. Lett.
VL  - 72
IS  - 1-3
PY  - 1994
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Morphologic changes were observed in nasal cavities of beagle dogs after long-term exposure to a respirable sulfur(IV) aerosol at a concentration equivalent to a sulfur dioxide (SO2) concentration of 0.6 mg/m3. The changes were characterized by a thickened epithelial layer resulting from epithelial proliferation, by a loss of secretory material, and by moderate mononuclear cell infiltration.
AU  - Takenaka, S.
AU  - Fürst, G.M.
AU  - Heilmann, P.
AU  - Heini, A.
AU  - Heinzmann, U.*
AU  - Karg, E.W.
AU  - Murray, A.B.*
AU  - Ruprecht, L.*
AU  - Heyder, J.
C1  - 40067
C2  - 38349
SP  - 145-150
TI  - Morphologic effects of a sulfur(IV) aerosol on the nasal cavity of beagle dogs.
JO  - Toxicol. Lett.
VL  - 72
IS  - 1-3
PY  - 1994
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Rozman, J.
AU  - Rozman, K.K.
C1  - 20690
C2  - 13908
SP  - 253-257
TI  - Intraluminal Hexadecane Enhances Large Intestinal Excretion of Tissue Hexachlorobenzene in Rats (Liquid paraffins; halogenated hydrocarbons; non-biliary, intestinal excretion).
JO  - Toxicol. Lett.
VL  - 16
PY  - 1993
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - We have investigated the importance of nitronate formation from 2-nitropropane (2-NP) for the oxidative metabolism and the genotoxicity of 2-NP in 2sFou rat hepatoma cells. Treatment of the cells with 2-NP for up to 3 h resulted in the time-dependent appearance of nitrite in the culture medium and in a weak induction of DNA repair synthesis. Both nitrite formation and repair induction were markedly enhanced in cells exposed to the anionic form of 2-NP, propane 2-nitronate. These observations suggest that propane 2-nitronate, rather than 2-NP itself, is oxidized by the liver cells to yield a DNA-damaging product. The results also indicate that the nitro/nitronate equilibration in intact liver cells is slow, suggesting that nitronate formation represents the rate-limiting step in the metabolic activation of 2-NP.
AU  - Dalke, C.
AU  - Andrae, U.
C1  - 40679
C2  - 38891
SP  - 149-157
TI  - Propane 2-nitronate is more rapidly denitrified and is more genotoxic than 2-nitropropane in cultured rat hepatoma cells.
JO  - Toxicol. Lett.
VL  - 61
IS  - 2-3
PY  - 1992
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Klein, D.
AU  - Scholz, P.
AU  - Drasch, G.A.
AU  - Müller-Höcker, J.
AU  - Summer, K.H.
C1  - 18265
C2  - 11486
SP  - 61-67
TI  - Metallothionein, Copper and Zinc in Fetal and Neonatal Human Liver: Changes During  Development.
JO  - Toxicol. Lett.
VL  - 56
PY  - 1991
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Total and cytosolic zinc (Zn) and copper (Cu), cytosolic metallothionein (MT) and the Cu-load of MT were investigated in fetal (22, 24 and 32 gestational weeks) and neonatal (2-15 months) human liver. Whereas the fraction of cytosolic Zn remained constant at 66% of the total independent of the stage of development, the fraction of cytosolic Cu increased from 26% in preterm liver to about 100% within 12 months postnatally. The MT content was higher in fetal than in neonatal liver. There was a linear correlation (r = 0.996) between cytosolic MT and Zn in both fetal and neonatal liver but not between MT and Cu. In contrast to fetal liver, the Cu-load of MT in neonatal liver seems to be determined by the Zn/Cu ratio in the cytosol. The results suggest that MT is involved in the regulation of Cu and Zn metabolism during fetal and neonatal development.
AU  - Klein, D.A.
AU  - Scholz, P.
AU  - Drasch, G.A.
AU  - Müller-Höcker, J.
AU  - Summer, K.H.
C1  - 40756
C2  - 38922
SP  - 61-67
TI  - Metallothionein, copper and zinc in fetal and neonatal human liver: Changes during development.
JO  - Toxicol. Lett.
VL  - 56
IS  - 1-2
PY  - 1991
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Stahl, B.U.
AU  - Alper, R.H.
AU  - Rozman, K.K.
C1  - 19116
C2  - 12172
SP  - 65-72
TI  - Depletion of Brain Serotonin does not alter 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced  Starvation Syndrome in the Rat.
JO  - Toxicol. Lett.
VL  - 59
PY  - 1991
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) was investigated for its toxicity in 5L-cells, descendants of the hepatoma line H4IIEC3. TCDD reduced the proliferation of 5L-cells by about 50%, with half-maximum inhibition at 0.1-0.3 nM concentrations. As shown by flow cytometric analysís, TCDD blocked the entry of 5L-cells into the S-phase, but did not hinder their progression through S and G2/M to the G1 phase. There was a marked increase in cell volume concomitant with the inhibition of growth. Both effects became apparent as early as 4-8 h after TCDD exposure. The parental line H4IIEC3/G- and the variant lines H4IIEC3/T, p4 and H5 were insensitive to the growth-inhibitory effect of TCDD. In view of the rapid onset of effects which can readily be detected and quantitated, 5L-cells offer a highly useful system for analysing the mechanism of action of TCDD at the cellular level.
AU  - Wiebel, F.J.
AU  - Klose, U.
AU  - Kiefer, F.
C1  - 40790
C2  - 38881
SP  - 161-169
TI  - Toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in vitro: H4IIEC3-derived 5L hepatoma cells as a model system.
JO  - Toxicol. Lett.
VL  - 55
IS  - 2
PY  - 1991
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - This study was aimed at monitoring N-acetyltransferase activities of continuous cell lines, which differ in their sensitivity to the toxic effects of nitroaromatic compounds. Transferase activities were measured toward the acetyl acceptors sulfamethazine and p-aminobenzoic acid in partially purified preparation of cytosols. Cell lines such as hamster V79, BHK, rat hepatoma H4IIEC3G- or fibroblast 208F, which are sensitive to 1,6-dinitropyrene (1,6-DNP), possess high transferase activities ranging from 120-270 nmol/min × mg protein. In contrast, human lung cells NCI-H322, mouse and rat hepatoma cells BW1J and H5, respectively, which are resistant to 1,6-DNP contain no or low transferase activity of less than 15 nmol/min × mg. There was no apparent correlation between 1,6-DNP sensitivity and acetyltransferase levels in a few cell lines, e.g. rat hepatoma HTC, 2sFou and 5L, which express intermediate transferase activities ranging from 25-50 nmol/min × mg protein. The results suggest that acetylation is an essential step in activating 1,6-DNP to toxic products in mammalian cells.
AU  - Srivastava, A.K.
AU  - Wiebel, F.J.
C1  - 41691
C2  - 36472
SP  - 71-76
TI  - Arylamine N-acetyltransferase activities in cell lines of mouse, rat, hamster and man differing in their sensitivity to 1,6-dinitropyrene.
JO  - Toxicol. Lett.
VL  - 54
IS  - 1
PY  - 1990
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - V79 Chinese hamster lung cells expressed low but significant aryl hydrocarbon hydroxylase activities when treated with an inducer of cytochrome P-450I, such as benz[a]anthracene or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), together with aminophylline. Inducibility by polycyclic aromatic hydrocarbons and inhibition by a specific monoclonal antibody indicated that the observed enzyme activity was mediated by cytochrome P-450I. Intact V79 cells pretreated with TCDD and aminophylline for 24 h metabolized benzo[a]pyrene to phenolic products with accumulated linearly in the growth medium for at least the same time period. Exposure of V79 cells to 10 μM benzo[a]pyrene and aminophylline for 72 h reduced subsequent cell growth by about 40%. The results demonstrate that V79 cells, under specific conditions, express PAH-inducible cytochrome P-450I and are capable of activating benzo[a]pyrene to cytotoxic products.
AU  - Kiefer, F.
AU  - Wiebel, F.J.
C1  - 42200
C2  - 38201
SP  - 265-273
TI  - V79 Chinese hamster cells express cytochrome P-450 activity after simultaneous exposure to polycyclic aromatic hydrocarbons and aminophylline.
JO  - Toxicol. Lett.
VL  - 48
IS  - 3
PY  - 1989
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Rozman, K.K.
AU  - Muzi, G.
AU  - Gorski, J.R.
C1  - 17437
C2  - 10011
TI  - Mode of Metabolism is Altered in 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD)-treated Rats.
JO  - Toxicol. Lett.
PY  - 1988
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Weber, W.D.
AU  - Haart, T.W.
AU  - Rozman, K.K.
C1  - 20719
C2  - 13938
SP  - 241-248
TI  - Effect of 2,3,7,8,-Tetrachlorodibenzo-p-Dioxin (TCDD) on Thermogenesis in Brown Adipose Tissue of Rats (Norepinephrine; pair-feeding; GDP binding; thyroxine; insulin; corticosterone).
JO  - Toxicol. Lett.
VL  - 39
PY  - 1987
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Pyruvate efficiently protected V79 Chinese hamster cells against the lethal effects of hydrogen peroxide. Protection was also provided by other α-ketoacids, such as α-ketobutyrate, α-ketoglutarate and α-ketoadipate, although higher concentrations were required. The corresponding β-ketoacids had no effect. The results indicate that pyruvate and other α-ketoacids possess antioxidant activity in vitro and, probably, in vivo.
AU  - Andrae, U.
AU  - Singh, J.
AU  - Ziegler-Skylakakis, K.
C1  - 42295
C2  - 36215
SP  - 93-98
TI  - Pyruvate and related α-ketoacids protect mammalian cells in culture against hydrogen peroxide-induced cytotoxicity.
JO  - Toxicol. Lett.
VL  - 28
IS  - 2-3
PY  - 1985
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Rozman, K.K.
C1  - 20680
C2  - 13898
SP  - 5-12
TI  - Phase II Enzyme Induction Reduces Body Burden of Heptachlor in Rats (Pesticide; Decontamination; Kinetics; Trans-stilbene Oxide).
JO  - Toxicol. Lett.
VL  - 20
PY  - 1984
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - 14C-labelled sodium dodecylbenzene sulfonate (DBS) was administered daily in the diet at a concentration of 1.4 mg/kg to male rats for 5 weeks. From the total uptake (1.213 ± 0.08 mg/animal) of DBS, 81.8% was excreted during the dosing period; 52.4% in feces and 29.4% in urine. Low levels of [14C]DBS-derived residues were detected in all tissues analyzed on day 35 of the experiment. Following 1 week on normal diet only 7.8% of the nominally stored amount of 14C was found in the excreta. Single i.p. application of 0.385 mg [14C]DBS/rat (2.26 ± 0.15 mg/kg body wt.) resulted in a total elimination of 94.5% within 10 days. 84.7% of the dose was eliminated in the first 24 h. All fecal and renal [14C]DBS-derived activity consisted of highly polar metabolites.
AU  - P. Lay, J.
AU  - Klein, W.
AU  - Korte, F.
C1  - 41571
C2  - 38353
SP  - 187-192
TI  - Elimination- and biodistribution studies of [14C]dodecylbenzene sulfonate in rats, following low dosing in the daily diet and a single i.p. administration.
JO  - Toxicol. Lett.
VL  - 17
IS  - 1-2
PY  - 1983
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Rozman, J.
AU  - Rozman, K.K.
AU  - Smith, S.G.
C1  - 20691
C2  - 13909
SP  - 171-175
TI  - Relationsship of Body Weight to Disposition of Hexachlorobenzene in Rats (Urinary; fecal; execution; hexachlorobenzene; liver; kidney; adipose tissue concentration).
JO  - Toxicol. Lett.
VL  - 18
PY  - 1983
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Male rats of various body weights were dosed twice with [14C]hexachlorobenzene (50 mg/kg, p.o.) in olive oil by gavage on 2 consecutive days. During 2 weeks after dosage, cumulative excretion into urine was about 1% of the dose and unrelated to body weight. Cumulative excretion into feces was 30 ± 10% of the dose and decreased with increasing body weight. In contrast, the concentration of hexachlorobenzene in urine, feces, kidney, liver and adipose tissue 14 days after dosing was higher in larger than in smaller animals. However, the relative concentration, i.e. the concentration of hexachlorobenzene in urine, feces or tissue divided by the concentration of hexachlorobenzene in adipose tissue, eliminated most of the variability among individual animals. This allows direct comparison of dispositional data of animals with greatly differing body burdens.
AU  - Rozman, T.A.
AU  - Rozman, K.K.
AU  - Smith, G.S.
C1  - 33149
C2  - 35550
SP  - 171-175
TI  - Relationship of body weight to disposition of hexachlorobenzene in rats.
JO  - Toxicol. Lett.
VL  - 18
IS  - 1-2
PY  - 1983
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - In young adult female rats with a cecal stoma, administration of hexadecane into the stomach (750 or 500 mg) and into the ligated colon (250 mg) enhanced 2- to 3-fold the intestinal excretion of [14C]hexachlorobenzene. Apparent sites of increased transferral from the blood into luminal contents were (caudal) ileum, cecum and colon. Presence of nonabsorbed hexadecane in luminal contents seems to be a prerequisite for the effects. Results support previous reports that enhancement of intestinal excretion of lipophilic chemicals by liquid paraffins takes place in the large intestine.
AU  - Rozman, T.A.
AU  - Rozman, K.K.
C1  - 41842
C2  - 38630
SP  - 253-257
TI  - Intraluminal hexadecane enhances large intestinal excretion of tissue hexachlorobenzene in rats.
JO  - Toxicol. Lett.
VL  - 16
IS  - 3-4
PY  - 1983
SN  - 0378-4274
ER  - 

TY  - JOUR
AB  - Administration of [14C]chlorferron in a single oral dose of 0.5 and 20 mg/kg body weight to female rats resulted in a urinary excretion of > 74% of the given dose during the first 24 h. Approx. 8% of the dose was eliminated in faeces within 7 days. 7 days after dosing, very low levels of [14C]chlorferron-derived residues were detected in all analyzed organs. These findings indicated that chlorferron was absorbed from the gastro-intestinal tract in appreciable quantities, but was rapidly excreted mainly via the urine with small amounts only in the faeces.
AU  - Malik, J.K.
AU  - Lay, J.P.
AU  - Klein, W.
AU  - Korte, F.
C1  - 41888
C2  - 38687
SP  - 449-452
TI  - Elimination pattern and biodistribution of [14C]chlorferron in rats.
JO  - Toxicol. Lett.
VL  - 7
IS  - 6
PY  - 1981
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Rozman, K.K.
AU  - Rozman, T.A.
AU  - Greim, H.A.
C1  - 40950
C2  - 40381
SP  - P.40
TI  - The mechanism of intestinal elimination of hexachlorobenzene and its enhancement by hexadecane in the rat.
JO  - Toxicol. Lett.
VL  - 6
IS  - SPEC.
PY  - 1980
SN  - 0378-4274
ER  - 

TY  - JOUR
AU  - Rozman, T.A.
AU  - Rozman, K.K.
AU  - Greim, H.A.
C1  - 33168
C2  - 35629
SP  - 41
TI  - Quantitative determination of intestinal and biliary elimination of hexachlorobenzene in untreated and mineral oil treated rhesus monkeys with complete biliary bypasses.
JO  - Toxicol. Lett.
VL  - 6
PY  - 1980
SN  - 0378-4274
ER  -