Title: Toxicology Letters

Title: Toxicology Letters

ISO Abbreviated Title: Toxicol. Lett.

JCR Abbreviated Title: Toxicol Lett

ISSN: 0378-4274

Issues/Year: 12

Journal Country/Territory: Ireland

Language: English

Publisher: Elsevier Sci Ireland Ltd

Publisher Address: Customer Relations Manager, Bay 15, Shannon Industrial Estate Co, Clare, IR

Subject Categories:

Toxicology: Impact Factor 2.430, 15/75 (2005)

Risto, L., Vartiainen, T. and Komulainen, H. (1993), Formation of methemoglobin by 3-chloro-4-(dichloromethyl)-5-hydroxy-2 (5H)-furanone, MX, in rat erythrocytes in vitro. Toxicology Letters, 68 (3), 325-332.

Full Text: T\Tox Let68, 325.pdf

Abstract: Oxidative effects of 3-chloro-4-(dichloromethyl)-5-hydroxy-2 (5H)-furanone (MX), the principal bacterial mutagen in chlorinated drinking water were studied in rat erythrocytes. Upon incubation of rat blood with 14C-labelled MX (2 micrograms/ml), 42% of the radioactivity was found in plasma, 26% in erythrocyte cell membranes and 32% bound in hemoglobin. Although it was bound to hemoglobin, MX (1 mM) did not immediately affect the oxygen binding capacity of hemoglobin. MX (0.5 to 5 mM) decreased the portion of oxyhemoglobin and increased that of methemoglobin in erythrocytes suspended in buffer in a time-and concentration-dependent fashion. In the same concentration range MX did not stimulate proteolysis nor did it cause hemolysis in erythrocytes. The results indicate that MX binds to hemoglobin and stimulates oxidation of hemoglobin in erythrocytes but MX does not cause overt oxidative damage to erythrocytes.

Clark, N.W.E. and Chipman, J.K. (1995), Absorption of 3-chloro-4-(dichloromethyl)-5-hydroxy-2-[5H] furanone (MX) through rat small intestine in vitro. Toxicology Letters, 81 (1), 33-38.

Full Text: T\Tox Let81, 33.pdf

Abstract: The intestinal absorption of 3-chloro-4-(dichloromethyl)-5-hydroxy-2-[5H] furanone (MX), a highly mutagenic furanone found in chlorinated waters, was studied using an in vitro everted rat gut sac system, using reverse mutation in Salmonella typhimurium to detect mutagens transported from the mucosal to the serosal compartments. Absorption was measurable, but limited, with significant increase in bacterial revertants (serosal compartment) noted at a dose of 50 µg/ml MX (mucosal compartment, p < 0.05). Gut sac incubation with MX and glutathione (GSH, 1.0 mM) resulted in no detectable absorption of mutagens. Preincubation with diethylmaleate to deplete mucosal GSH resulted in increased absorption of MX-derived mutagens compared to controls (a significant induction of revertant colonies was noted at a dose of 25 µg/ml MX p < 0.05). Gut sac incubation with chlorinated fulvic acids resulted in no detectable absorption of mutagens. In vitro studies to assess the possibility of beta-lyase activation of the postulated MX-GSH conjugate showed no mutagenic activation.

Keywords: 3-Chloro-4-(Dichloromethyl)-5-Hydroxy-2-Furanone, Absorption, Mutagenicity, Humic Substances, Beta-Lyase, In Vitro, Mutagenic By-Products, Glutathione, Disinfection, Chlorination, Cancer, Water

Mumtaz, M.M. (1995), Risk assessment of chemical mixtures from a public health perspective. Toxicology Letters, 82-83, 527-532.

Full Text: T\Tox Let82-83, 527.pdf

Abstract: Health risk assessment is the practice of evaluating the degree of danger associated with chemical exposure, whether the exposure is intentional (pharmacologic agents, pesticides) or unintentional (industrial/automobile by-products). Chemical exposure can either be to a single chemical or to complex mixtures such as industrial effluents, municipal wastes, jet fuels, gasoline, or mixtures of drinking water contaminants. The mixtures can be simple or complex; partially or completely characterized; and stable or varying in composition. Three different approaches are often used in health risk assessment of chemical mixtures (51 FR 33992-34054). These 3 approaches consist of (a) use of data on the specific mixture of concern; (b) use of data on a similar mixture; and (c) use of data on each component of the mixture. The individual component-based approach is by far the most often used because it allows the individual risks from each component to be combined, usually by dose or response additivity, to calculate an overall risk for the mixture. In addition, several innovative methods, such as the toxicity equivalency factor, relative potency, and even the use of indicator chemicals, are also employed. More recently, a binary weight-of-evidence approach has been proposed to evaluate potential interactions between the various components and to integrate them into the overall toxicity assessment of the mixture. Because no single approach is suitable for assessing the health risk associated with all the exposure scenarios associated with the various types of mixtures, the use of professional judgment is still imperative in conducting health risk assessments.

Keywords: Chemical Mixtures, Toxicity Assessment, Chemical Interactions, Hazard Index, Public Health, Analgesia

Randow, F.F., Hübener, T. and Merkel, G. (1996), Hazards for the Rostock water supply from a tar-contaminated sediment in the river Warnow. Toxicology Letters, 88 (1-3), 355-358.

Full Text: T\Tox Let88, 355.pdf

Abstract: By the gas plant at Schwaan (a small city near Rostock), tar and other by-products were released into the river Warnow which supplies Rostock with drinking water 20 km downstream. The tar-contaminated river sediment contained phenols and polycyclic aromatic hydrocarbons (PAH), indicating a mutagenic potential. Investigations in the catchment area and on tributaries showed PAH contents up to about 10 ng/l in the water. The river sediment was found to be the sole PAH source. Although the PAH level is very low, sediment disturbances may produce an increase in concentrations. The consequences of such a worst case are difficult to estimate, even though the content of seston and humic substances in the river seems to reduce the PAH concentrations. Although this lowers the probability that increased PAH concentrations reach the Rostock water supply, the removal of the tar-contaminated sediment from the river is strongly recommended.

Černá, M., Pastorkoveá, A., Šmíd, J., Dobiáš, L. and Rössner, P. (1998), The use of YG bacterial tester strains for the monitoring of drinking water mutagenicity. Toxicology Letters, 96-97, 335-339.

Full Text: T\Tox Let96-97, 335.pdf

Abstract: The organic extract from the 50 drinking water specimens taken in four cities were tested for mutagenicity in the Ames test (plate incorporation assay) using the parent TA98 and TA100 strains, and derived YG1041 and YG1042 strains. Four dose levels of extractable organic matter (EOM) with duplicate plate per dose were used. Slopes (revertants/mg EOM) were calculated by the Bernstein linear regression rejection model using GeneTox Manager software. The mutagenicity observed in the conventional strains TA98 and TA100 did not reach the significant increase in all tested samples with the higher mutagenic response found in TA100-S9. With the YG1041 and YG1042 tester strains, the results obtained demonstrated the clear-cut direct dose-related mutagenicity response in all tested drinking water extracts. Compared with TA98 and TA100 strains, the numbers of YG induced revertants were approximately 20 times higher. The high sensitivity of the YG tester strains could facilitate the mutagenicity monitoring in drinking water extracts, and help reduce the volume of sample required. However, to identify the chemical contaminants in drinking water responsible for the mutagenicity further studies are required.

Ruan, Y., Peterson, M.H., Wauson, E.M., Gelineau-Van Waes, J., Finnell, R.H. and Vorce, R.L. (2000), Folic acid protects SWV/Fnn embryo fibroblasts against arsenic toxicity. Toxicology Letters, 117 (3), 129-137.

Full Text: T\Tox Let117, 129.pdf

Abstract: It has been proposed that arsenic exerts its toxic effects, in part, by perturbing cellular methyl metabolism. Based on the hypothesis that folic acid treatment will attenuate the cytotoxic and growth inhibitory effects of arsenic, SWV/Fnn embryo fibroblasts were cultured in media supplemented with Various concentrations of folic acid during treatment with sodium arsenite or dimethylarsinic acid (DMA). It was found that folic acid protects SWV/Fnn embryo fibroblasts from sodium arsenite and DMA cytotoxicity in a dose-dependent manner. In contrast, folic acid supplementation has no effect on toxicity resulting from treatment with ethanol or staurosporine. suggesting that folic acid is not generally protective against necrosis and apoptosis. Although folic acid protects against acute arsenic toxicity, this agent shows a modest and delayed ability to attenuate the growth inhibitory effect of arsenic on these cells. These results support a model in which perturbations of methyl metabolism contribute to the acute cytotoxicity of arsenic. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.

Keywords: Arsenic, Folic Acid, Cytotoxicity, DMA, Arsenite, Neural-Tube Defects, Drinking-Water, Gene-Expression, Developmental Toxicity, Blackfoot Disease, Sodium Arsenite, Skin-Lesions, West-Bengal, Cancer, Taiwan

? Rodríguez, V.M., Jiménez-Capdeville, M.E. and Giordano, M. (2003), The effects of arsenic exposure on the nervous system. Toxicology Letters, 145 (1), 1-18,

Full Text: 2003\Tox Let145, 1.pdf

Abstract: Arsenic (As) is a common environmental contaminant widely distributed around the world. Human exposure to this metalloid comes from well water and contaminated soil, from fish and other sea organisms rich in methylated arsenic species, and from occupational exposure. It has been reported that human arsenic exposure causes several health problems such as cancer, liver damage, dermatosis, and nervous system disturbances such as polyneuropathy, EEG abnormalities and, in extreme cases, hallucinations, disorientation and agitation. Although there is evidence that arsenic exposure has a toxic effect on the nervous system there are few studies that address this issue. The purpose of this review is to describe what is presently known about the effects of arsenic compounds on the nervous system in humans and rodents and to discuss its possible mechanisms of action. (C) 2003 Elsevier Ireland Ltd. All fights reserved.

Keywords: Arsenic, Neurotoxicity, Behavior, Nervous System, Neurotransmitter, Barre-Like Syndrome, Sodium Arsenite, Enzymatic Methylation, Urinary-Excretion, Gene-Expression, Drinking-Water, Permeability Transition, Environmental Exposure, Developmental Toxicity, Induced Apoptosis

? Miró, Ò., Montori, E., Ramos, X., Galicia, M. and Nogu, S. (2009), Trends in research activity in toxicology and by toxicologists in seven European countries. Toxicology Letters, 189 (1), 1-4.

Full Text: 2009\Tox Let189, 1.pdf

Keywords: Bibliometric Analysis, Impact, Oil Syndrome, Policy, Publications, Research, Spanish Scientific Production