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Toxicants
Kinds of Toxicants Terms modified by Toxicants Selected AbstractsShort-term responses by the German cockroach, Blattella germanica, to insecticidal baits: behavioural observationsENTOMOLOGIA EXPERIMENTALIS ET APPLICATA, Issue 1 2002Stephen A. Jones Abstract Toxicants may cause insects to avoid a bait, and yet bait efficacy is dependent upon insects ingesting it in adequate quantities. Amounts ingested are, in turn, determined by meal frequency, meal durations and ingestion rate within meals, but to date no report has been made of these variables for domestic cockroaches. We report an experiment in which sixth instar German cockroach, Blattella germanica, nymphs were initially able to self-select their protein and carbohydrate intake independently, then daily at the start of the scotophase some insects had their choice of foods replaced by a single treatment food, which varied through the presence or absence of protein, carbohydrate, and insecticide. Insect behaviour was recorded for the following 5 h, and the data were subsequently subjected to bout analysis in order to identify discrete meals. The age of insects in days on first exposure to a treatment food (,age') and the amount of food eaten in the observation period were both recorded and included in the analysis. Amounts eaten were affected by insect age and food nutrient content, but not by the presence of insecticide. Toxicant effects were, however, seen on average meal duration and meal frequency, in interactions with age and food nutrient effects. These results suggest ways in which direct observations of behaviours may lead to improved bait design. [source] Structure,Activity Relationship Studies on Derivatives of Eudesmanolides from Inula helenium as Toxicants against Aedes aegypti Larvae and AdultsCHEMISTRY & BIODIVERSITY, Issue 7 2010Charles Abstract An Aedes aegypti larval toxicity bioassay was performed on compounds representing many classes of natural compounds including polyacetylenes, phytosterols, flavonoids, sesquiterpenoids, and triterpenoids. Among these compounds, two eudesmanolides, alantolactone, and isoalantolactone showed larvicidal activities against Ae. aegypti and, therefore, were chosen for further structure,activity relationship study. In this study, structural modifications were performed on both alantolactone and isoalantolactone in an effort to understand the functional groups necessary for maintaining and/or increasing its activity, and to possibly lead to more effective insect-control agents. All parent compounds and synthetic modification reaction products were evaluated for their toxic activities against Ae. aegypti larvae and adults. Structure modifications included epoxidations, reductions, catalytic hydrogenations, and Michael additions to the ,,, -unsaturated lactones. None of the synthetic isomers synthesized and screened against Ae. aegypti larvae were more active than isoalantolactone itself which had an LC50 value of 10.0,,g/ml. This was not the case for analogs of alantolactone for which many of the analogs had larvicidal activities ranging from 12.4 to 69.9,,g/ml. In general, activity trends observed from Ae. aegypti larval screening were not consistent with observations from adulticidal screening. The propylamine Michael addition analog of alantolactone was the most active adulticide synthesized with an LC50 value of 1.07,,g/mosquito. In addition, the crystal structures of both alantolactone and isoalantolactone were determined using CuK, radiation, which allowed their absolute configurations to be determined based on resonant scattering of the light atoms. [source] Mechanism of DNA damage by cadmium and interplay of antioxidant enzymes and agentsENVIRONMENTAL TOXICOLOGY, Issue 2 2007Veera L. D. Badisa Abstract Cadmium is an environmental toxicant, which causes cancer in different organs. It was found that it damages DNA in the various tissues and cultured cell lines. To investigate the mechanism of DNA damage, we have studied the effect of cadmium-induced DNA damage in plasmid pBR322 DNA, and the possible ameliorative effects of antioxidative agents under in vitro conditions. It was observed that cadmium alone did not cause DNA damage. However, it caused DNA damage in the presence of hydrogen peroxide, in a dose dependent manner, because of production of hydroxyl radicals. Findings from this study show the conversion of covalently closed circular double-stranded pBR 322 DNA to the open circular and linear forms of DNA when treated with 10 ,M cadmium and various concentrations of H2O2. The conversion was due to nicking in DNA strands. The observed rate of DNA strand breakage was dependent on H2O2 concentration, temperature, and time. Metallothionein I failed to prevent cadmium-induced DNA nicking in the presence of H2O2. Of the two antioxidant enzymes (catalase and superoxide dismutase) studied, only catalase conferred significant (50,60%) protection. EDTA and DMSO exhibited protection similar to catalase, while mannitol showed only about 20% protection against DNA damage. Ethyl alcohol failed to ameliorate cadmium-induced DNA strands break. From this study, it is plausible to infer that cadmium in the presence of hydrogen peroxide causes DNA damage probably by the formation of hydroxyl ions. These results may indicate that cadmium in vivo could play a major role in the DNA damage induced by oxidative stress. © 2007 Wiley Periodicals, Inc. Environ Toxicol 22: 144,151, 2007. [source] Toxicity evaluation of metal plating wastewater employing the Microtox® assay: A comparison with cladocerans and fishENVIRONMENTAL TOXICOLOGY, Issue 2 2001Kyungho Choi Abstract The relative sensitivity of the Microtox assay is closely related to the type of toxicant, and hence its utility in biomonitoring effluents is better evaluated on a case-by-case basis. The Microtox® assay, employing the marine bacterium Vibrio fischeri, was evaluated for its applicability in monitoring metal plating wastewater for toxicity. The results of the Microtox assay after 5, 15, and 30 min of exposure, were compared with data obtained from conventional whole effluent toxicity testing (WET) methods that employed Daphnia magna, Ceriodaphnia dubia, and the fathead minnow (Pimephales promelas). The Microtox assay produced notably comparable EC50 values to the LC50 values of the acute fathead minnow toxicity test (<0.5 order of difference). The Spearman's rank correlation analyses showed that the bacterial assay, regardless of exposure duration, correlated better with the acute fish than the daphnid results (p<0.05). These observations were consistent to other studies conducted with inorganic contaminants. The relative sensitivity of the 30-min Microtox assay was within the range of the two frequently used acute daphnid/fish toxicity tests. In conclusion, the Microtox assay correlated well with the acute fathead minnow data and is well suited for toxicity monitoring for these types of industrial wastes. © 2001 John Wiley & Sons, Inc. Environ Toxicol 16: 136,141, 2001 [source] Whole sediment toxicity identification evaluation tools for pyrethroid insecticides: III.ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 1 2009Temperature manipulation Abstract Since the toxicity of pyrethroid insecticides is known to increase at low temperatures, the use of temperature manipulation was explored as a whole-sediment toxicity identification evaluation (TIE) tool to help identify sediment samples in which pyrethroid insecticides are responsible for observed toxicity. The amphipod Hyalella azteca is commonly used for toxicity testing of sediments at a 23°C test temperature. However, a temperature reduction to 18°C doubled the toxicity of pyrethroids, and a further reduction to 13°C tripled their toxicity. A similar response, though less dramatic, was found for 1,1-bis(p -chlorophenyl)-2,2,2-trichloroethane (DDT), and dissimilar temperature responses were seen for cadmium and the insecticide chlorpyrifos. Tests with field-collected sediments containing pyrethroids and/or chlorpyrifos showed the expected thermal dependency in nearly all instances. The inverse relationship between temperature and toxicity provides a simple approach to help establish when pyrethroids are the principal toxicant in a sediment sample that could be used as a supplemental tool in concert with chemical analysis or other TIE manipulations. The phenomenon appears to be, in part, a consequence of a reduced ability to biotransform the toxic parent compound at cooler temperatures. The strong dependence of pyrethroid toxicity on temperature has important ramifications for predicting their environmental effects, and the standard test temperature of 23°C dramatically underestimates risk to resident fauna during the cooler months. [source] From organisms to populations: Modeling aquatic toxicity data across two levels of biological organizationENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 2 2006Sandy Raimondo Abstract A critical step in estimating the ecological effects of a toxicant is extrapolating organism-level response data across higher levels of biological organization. In the present study, the organism-to-population link is made for the mysid, Americamysis bahia, exposed to a range of concentrations of six toxicants. Organism-level responses observed were categorized as no effect, delayed reproduction, reduced overall reproduction, or both reduced overall reproduction and survival. Population multiplication rates of each toxicant concentration were obtained from matrix models developed from organism-level endpoints and placed into the four categories of organism-level responses. Rates within each category were compared with growth rates modeled for control populations. Population multiplication rates were significantly less than control growth rates only for concentrations at which overall reproduction and both reproduction and survival were significantly less than the control values on the organism level. Decomposition analysis of the significant population-level effects identified reduced reproduction as the primary contributor to a reduced population multiplication rate at all sublethal concentrations and most lethal concentrations. Mortality was the primary contributor to reduced population growth rate only when survival was less than 25% of control survival. These results suggest the importance of altered reproduction in population-level risk assessment and emphasizes the need for complete life-cycle test data to make an explicit link between the organism and population levels. [source] Comparing the solid phase and saline extract Microtox® assays for two polycyclic aromatic hydrocarbon-contaminated soilsENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 2 2004Carolyn M. Acheson Abstract The performance of remedial teatments is typically evaluated by measuring the concentration of specific chemicals. By adding toxicity bioassays to treatment evaluations, a fuller understanding of treatment performance is obtained. The solid phase Microtox® assay is a useful tool in characterizing the toxicity of contaminated soils and sediments. This study compares the performance of the solid phase and saline extract Microtox assays in two experiments using two soils contaminated with polycyclic aromatic hydrocarbons (PAHs). The first experiment, conducted to refine the solid phase assay procedures, evaluated sample holding times, sample replication, and reference toxicant controls. The effective concentration reducing light emission by 50% (EC50) of four samples was measured with eight replicates of each sample. Samples were stored for as long as two weeks without showing substantial changes in toxicity. For future studies, three replicates of each sample are recommended because that degree of replication yielded a statistical power of more than 95% in most samples. Phenol was a reliable reference toxicant with a mean EC50 of 21.76 and a 95% confidence interval of 15.6 to 27.9 mg/L. In a second experiment, the solid phase Microtox assay was compared to saline extract Microtox assays with mixing times ranging from 5 min to 16 h. The solid phase assay was more sensitive yielding EC50s 7 to 50 times lower than the extract EC50s. In addition, the saline extract assays displayed results that varied for mixing times of less than 2 h. Based on these two experiments, the solid phase Microtox test has proved to be a useful assay for measuring the toxicity of PAH-contaminated soils. [source] Effects of the androgenic growth promoter 17-,-trenbolone on fecundity and reproductive endocrinology of the fathead minnow,ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 6 2003Gerald T. Ankley Abstract Trenbolone acetate is a synthetic steroid that is extensively used in the United States as a growth promoter in beef cattle. The acetate is administered to livestock via slow-release implants; some is converted by the animal to 17-,-trenbolone, a relatively potent androgen receptor agonist in mammalian systems. Recent studies indicate that excreted 17-,-trenbolone is comparatively stable in animal waste, suggesting the potential for exposure to aquatic animals via direct discharge, runoff, or both. However, little is known concerning the toxicity of trenbolone to fish. Our goal was to assess the effects of 17-,-trenbolone on reproductive endocrinology of the fathead minnow (Pimephales promelas). An in vitro competitive binding study with the fathead minnow androgen receptor demonstrated that 17-,-trenbolone had a higher affinity for the receptor than that of the endogenous ligand, testosterone. Male and female fish were exposed for 21 d to nominal (target) concentrations of 17-,-trenbolone ranging from 0.005 to 50 ,g/L. Fecundity of the fish was significantly reduced by exposure to measured test concentrations , 0.027 ,g/ L. The 17-,-trenbolone was clearly androgenic in vivo at these concentrations, as evidenced by the de novo production in females of dorsal (nuptial) tubercles, structures normally present only on the heads of mature males. Plasma steroid (testosterone and ,-estradiol) and vitellogenin concentrations in the females all were significantly reduced by exposure to 17-,-trenbolone. The 17-,-trenbolone also altered reproductive physiology of male fathead minnows, albeit at concentrations much higher than those producing effects in females. Males exposed to 17-,-trenbolone at 41 ,g/L (measured) exhibited decreased plasma concentrations of 11-ketotestosterone and increased concentrations of ,-estradiol and vitellogenin. Overall, our studies indicate that 17-,-trenbolone is a potent androgen and reproductive toxicant in fish. Given the widespread use of trenbolone acetate as a growth promoter, and relative stability of its metabolites in animal wastes, further studies are warranted to assess potential ecological risk. [source] The relative sensitivity of four benthic invertebrates to metals in spiked-sediment exposures and application to contaminated field sedimentENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 4 2003Danielle Milani Abstract The relative sensitivity of four benthic invertebrates (Hyalella azteca, Chironomus riparius, Hexagenia spp., and Tubifex tubifex) was determined for Cd, Cu, and Ni in water-only and in spiked-sediment exposures. Survival (median lethal concentrations [LC50s] and the concentrations estimated to be lethal to 25% of test organisms [LC25s]), and endpoints for growth and reproduction (mean inhibitory concentrations [IC25s]) were compared. The sensitivities differed depending on the species and metal, although some trends emerged. In water-only exposures, H. azteca is the most sensitive species to cadmium and nickel, with mean LC50s of 0.013 and 3.6 mg/L, respectively; C. riparius is the most sensitive species to copper, with a mean LC50 of 0.043 mg/L. In the spiked-sediment exposures, the order in decreasing sensitivity to copper is Hyalella = Hexagenia < Chironomus < Tubifex for survival and growth/reproduction. For cadmium, the order in decreasing sensitivity is Hyalella = Chironomus < Hexagenia < Tubifex, and for nickel is Hyalella , Hexagenia < Chironomus < Tubifex. Chironomus riparius and Hexagenia spp. survival can be used to distinguish between toxicity caused by different metals. Species test responses in field-collected sediment (Collingwood Harbour, ON, Canada) were examined in an attempt to determine the causative agent of toxicity throughout, using the established species sensitivities. Sediment toxicity was categorized first by comparing species responses to those established for a reference database. Test responses in the field-collected sediment do not support causality by Cu, a suspected toxicant based on comparison of sediment chemistry with sediment quality guidelines. [source] Polycyclic aromatic hydrocarbon bioaccumulation by meiobenthic copepods inhabiting a superfund site: Techniques for micromass body burden and total lipid analysisENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 11 2002Susan L. Klosterhaus Abstract Microtechniques for polycyclic aromatic hydrocarbon (PAH) body burden and total lipid analysis were developed and applied to determine the first lipid-normalized bioaccumulation factors for a hydrophobic organic toxicant in a meiobenthic organism (0.063-0.500 mm) living in field-contaminated sediments. The total lipid microtechnique combines the standard Bligh-Dyer extraction method with a colorimetric quantification method for analysis of samples containing 1 to 50 ,g lipid. The microtechnique for body burden analysis quantifies PAHs from tissue samples containing as little as 10 pg PAH. Fluoranthene, benz[a]anthracene, and benzo[a]pyrene biota-sediment accumulation factors (BSAFs) were determined for the meiobenthic copepod Microarthridion littorale living in an estuarine U.S. Environmental Protection Agency Superfund site. Gravid female, nongravid female, and male BSAFs were 0.82, 0.54, and 0.36, respectively, for fluoranthene; 0.50, 0.44, and 0.40, respectively, for benz[a]anthracene; and 0.09, 0.12, and 0.15, respectively, for benzo[a]pyrene. Comparison of nonlipid-normalized bioaccumulation factors (BAFs) to BSAFs indicates that M. littorale bioaccumulated PAHs on a gram lipid basis. The BSAFs declined consistently with increasing PAH log Kow for all copepod sex and reproductive stages. Sex- and stage-specific comparisons of BSAFs suggest that differences in lipid content and quality may lead to differences in BSAF values depending on PAH molecular weight and/or hydrophobicity. [source] A test of the community conditioning hypothesis: Persistence of effects in model ecological structures dosed with the jet fuel jp-8ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 2 2000Wayne G. Landis Abstract The foundation of the community conditioning hypothesis, the persistence of effects, was tested in a series of microcosm experiments. Experiments were conducted with the water-soluble fraction of the turbine fuel JP-8 using the standard protocols for the standardized aquatic microcosm (SAM). A repeat trial was conducted using the SAM protocol but with a 126-d test period, twice the standard duration. The results were examined using a variety of conventional univariate, multivariate, and graphical techniques. The principal conclusions were as follows. Effects are persistent in these model ecological systems long after the degradation of the toxicant. Patterns of impacts are detectable at concentrations 15 times lower than an experimentally derived single-species EC50. The replicate experiments are not replicable in the specific, but the broad pattern of the disruption of algal- herbivore dynamics followed by more subtle effects are consistently repeated. The durability of the indirect effects and therefore the information about historical events appears to be a consistent feature of these microcosm systems. The identity of the treatment groups persists. The critical features of the community conditioning hypothesis,persistence of information within ecologicalsystems and the reappearance of patterns and therefore the nonequilibrium dynamics,are again confirmed. The implications of these findings for environmental toxicology, monitoring, and ecological risk assessment are discussed. [source] The individual tolerance concept is not the sole explanation for the probit dose-effect model,ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 2 2000Michael C. Newman Abstract Predominant methods for analyzing dose- or concentration-effect data (i.e., probit analysis) are based on the concept of individual tolerance or individual effective dose (IED, the smallest characteristic dose needed to kill an individual). An alternative explanation (stochasticity hypothesis) is that individuals do not have unique tolerances: death results from stochastic processes occurring similarly in all individuals. These opposing hypotheses were tested with two types of experiments. First, time to stupefaction (TTS) was measured for zebra fish (Brachydanio rerio) exposed to benzocaine. The same 40 fish were exposed during five trials to test if the same order for TTS was maintained among trials. The IED hypothesis was supported with a minor stochastic component being present. Second, eastern mosquitofish (Gambusia holbrooki) were exposed to sublethal or lethal NaCl concentrations until a large portion of the lethally exposed fish died. After sufficient time for recovery, fish sublethally exposed and fish surviving lethal exposure were exposed simultaneously to lethal NaCl concentrations. No statistically significant effect was found of previous exposure on survival time but a large stochastic component to the survival dynamics was obvious. Repetition of this second type of test with pentachlorophenol also provided no support for the IED hypothesis. We conclude that neither hypothesis alone was the sole or dominant explanation for the lognormal (probit) model. Determination of the correct explanation (IED or stochastic) or the relative contributions of each is crucial to predicting consequences to populations after repeated or chronic exposures to any particular toxicant. [source] Effects of a toxicant on population growth rates: sublethal and delayed responses in blowfly populationsFUNCTIONAL ECOLOGY, Issue 6 2001S. J. MOE Summary 1,Previous studies have shown that cadmium exposure of blowfly populations (Lucilia sericata[Meigen 1826]) results in reduced population growth rate, but also in higher individual mass, because of reduced competition for food. In this study, the discrepancy between the positive effect on individual growth and the negative effect on population growth is investigated, by measuring direct and delayed effects of cadmium in the adult stage. 2,Blowfly populations were exposed to cadmium through the diet in four treatment combinations: larval stage, adult stage, both stages or neither stage. The effects on accumulation of cadmium, survival, development time, mass and reproductive rate were measured. 3,Cadmium was accumulated from both stages. 4,Individuals exposed to cadmium in the larval stage had higher mean pupal and adult mass (because of reduced densities), but also reduced adult longevity and fecundity. 5,Adult longevity and fecundity were also reduced by cadmium exposure in the adult stage. 6,In stage-structured populations, the link between individual-level and population-level responses to a toxicant may be complicated by stage-specific sensitivities to the toxicant, by delayed responses in the adult stage to sublethal effects in the juvenile stage, and by density-dependent compensatory responses to toxicant-induced mortality. [source] Impact of inter-individual differences in drug metabolism and pharmacokinetics on safety evaluationFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2004J.L.C.M. Dorne Abstract Safety evaluation aims to assess the dose,response relationship to determine a dose/level of exposure for food contaminants below which no deleterious effect is measurable that is ,without appreciable health risk' when consumed daily over a lifetime. These safe levels, such as the acceptable daily intake (ADI) have been derived from animal studies using surrogates for the threshold such as the no-observed-adverse-effect-level (NOAEL). The extrapolation from the NOAEL to the human safe intake uses a 100-fold uncertainty factor, defined as the product of two 10-fold factors allowing for human variability and interspecies differences. The 10-fold factor for human variability has been further subdivided into two factors of 100.5 (3.16) to cover toxicokinetics and toxicodynamics and this subdivsion allows for the replacement of an uncertainty factor with a chemical-specific adjustment factor (CSAF) when compound-specific data are available. Recently, an analysis of human variability in pharmacokinetics for phase I metabolism (CYP1A2, CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4, hydrolysis, alcohol dehydrogenase), phase II metabolism (N-acetyltransferase, glucuronidation, glycine conjugation, sulphation) and renal excretion was used to derive pathway-related uncertainty factors in subgroups of the human population (healthy adults, effects of ethnicity and age). Overall, the pathway-related uncertainty factors (99th centile) were above the toxicokinetic uncertainty factor for healthy adults exposed to xenobiotics handled by polymorphic metabolic pathways (and assuming the parent compound was the proximate toxicant) such as CYP2D6 poor metabolizers (26), CYP2C19 poor metabolizers (52) and NAT-2 slow acetylators (5.2). Neonates were the most susceptible subgroup of the population for pathways with available data [CYP1A2 and glucuronidation (12), CYP3A4 (14), glycine conjugation (28)]. Data for polymorphic pathways were not available in neonates but uncertainty factors of up to 45 and 9 would allow for the variability observed in children for CYP2D6 and CYP2C19 metabolism, respectively. This review presents an overview on the history of uncertainty factors, the main conclusions drawn from the analysis of inter-individual differences in metabolism and pharmacokinetics, the development of pathway-related uncertainty factors and their use in chemical risk assessment. [source] Elevation of cyclin D1 following trimethyltin induced hippocampal neurodegenerationJOURNAL OF NEUROCHEMISTRY, Issue 2002R. N. Wine Previous work has suggested that a major contributor to neuronal cell death is the aberrant induction of the cell cycle process, as indicated by an up-regulation of cyclin D. In order to examine the temporal and spatial relationship of cyclin D in a model of acute neurodegeneration, the hippocampal toxicant, trimethyltin (TMT; 2.0 mg/kg), was administered to 21-day old CD,1 male mice and the level and cellular localization of cyclin D1 examined. Within 24 h following TMT, dentate granule cells of the hippocampus showed evidence of neuronal necrosis resulting in severe cell loss over a 3-day period. The pyramidal cell layer was spared with only sparse punctate neuronal necrosis. Microglia response was seen at 72 h with ameboid microglia present in the dentate and ramified microglia present in the pyramidal cell layer, contributing to the elevation seen in TNF-alpha mRNA levels. A transient elevation was seen in mRNA levels for cyclin D1 over 48,72 h post-TMT. Immunohistochemistry demonstrated a transient increase in staining for cyclin D1 in CA1 pyramidal neurons as early as 24 h. Punctate staining occurred in neurons throughout the dentate at 48 h. BrdU positive cells were present along the inner blades of the dentate in control animals. Following TMT exposure, an increase was seen in both the number of neurons stained and a diffusion of the staining pattern into the full dentate region. Thus, in TMT-induced neurodegeneration, cyclin D1 is not expressed in the vulnerable neurons but rather in neurons spared from degeneration. This expression pattern appears to not be linked to an increase in the cellular processes for proliferation as the majority of BrdU positive cells were present in the region of neuronal damage. [source] Ethanol Can Modify the Effects of Certain Free Radical-Generating Systems on AstrocytesALCOHOLISM, Issue 4 2004B. Gonthier Abstract: The central nervous system is vulnerable to oxidative stress, especially when a toxicant can modify the physiological balance between anti- and pro-oxidant mechanisms. Among brain cells, astrocytes seem less vulnerable than neurons, but their impairment can dramatically affect neurons because of their protective role toward neurons. Ethanol is able to stimulate the formation of reactive oxygen species and modify the activity of most of the antioxidant agents. However, ethanol can react with the OH· radical to form the ,-hydroxyethyl radical, which is considered to be less toxic. Ethanol also can stimulate H2O2 degradation through catalase activation. This study, therefore, sought to determine whether ethanol affected the sensitivity of astrocytes exposed to various free radical-generating systems. The cellular impact of such exposure was assessed by assays exploring cytotoxicity (i.e., NR (neutral red) and MMT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetiazolium bromide) reduction assays) and genotoxicity (comet assay) induced by these treatments. DNA alterations were evaluated by single-cell gel electrophoresis (comet assay), considered a precocious biomarker of intracellular alterations. After concomitant exposure to H2O2 and ethanol, the viability of astrocytes decreased significantly whereas the mean percentage of DNA in the tail increased, reflecting DNA damage (H2O2 was either directly added to the culture medium or endogenously produced from menadione). Ethanol also reduced the loss of viability and DNA alterations after exposure to OH· radicals produced by a Fenton system. The exposure to a xanthine/xanthine oxidase system had the same effect. [source] Inorganic arsenic as a developmental toxicant: In utero exposure and alterations in the developing rat lungsMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 5 2009Jay S. Petrick Abstract In the present study, we characterize the toxic effects of in utero arsenic exposure on the developing lung. We hypothesize that in utero exposure to inorganic arsenic through maternal drinking water causes altered gene and protein expression in the developing lung, indicative of downstream molecular and functional changes. From conception to embryonic day 18, we exposed pregnant Sprague-Dawley rats to 500 ppb arsenic (as arsenite) via the drinking water. Subtracted cDNA libraries comparing control to arsenic exposed embryonic lungs were generated. In addition, a broad Western blot analysis was performed to identify altered protein expression. A total of 59 genes and 34 proteins were identified as being altered. Pathway mapping and analysis showed that cell motility was the process most affected. The most likely affected pathway was alteration in integrin signaling through the ,-catenin pathway, altering c-myc. The present study shows that arsenic induces alterations in the developing lung. These data may be useful in the elucidation of molecular targets and biomarkers of arsenic exposure during lung development and may aid in understanding the etiology of arsenic induced adult respiratory disease and lung cancers. [source] Rodenticide grain bait ingredient acceptance by Norway rats (Rattus norvegicus), California ground squirrels (Spermophilus beecheyi) and pocket gophers (Thomomys bottae)PEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 7 2006Terrell P Salmon Abstract Vertebrate pest control in California is often accomplished through the use of rodenticide grain baits. These grain baits are composed of steam-rolled oats (SRO), a toxicant, an indicator dye and an oil combination. A series of tests were performed to determine the effects of various dye and oil formulations on acceptance of grain bait by Norway rats [Rattus norvegicus (Berk)], California ground squirrels [Spermophilus beecheyi (Richardson)] and pocket gophers (Thomomys bottae Eyd & Gerv). Seven different dyes, four oil formulations and clean (untreated) oats were tested for acceptance. The addition of the selected oils and dyes to grain resulted in no significant differences in consumption. This indicates that there is a wide variety of dyes that could be used in the formulation of rodenticides. These alternatives could aid in proper pesticide use, the deterrence of bait consumption by birds and possibly in ingredient adhesion to the finished bait. Copyright © 2006 Society of Chemical Industry [source] Survey of albumin purification methods for the analysis of albumin-organic toxicant adducts by liquid chromatography-electrospray ionization-tandem mass spectrometryPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 18 2005Carrie L. Young Abstract HSA has been shown to react with many organic toxicants to form adducts that are useful biomarkers for exposure. Albumin isolation is an important first step for the analysis of these protein-toxicant adducts. We tested several approaches to isolate albumin from serum treated with an electrophilic organic toxicant known to form adducts with albumin, i.e., sulfur mustard agent (HD) (2,2'-dichloroethyl sulfide), in order to evaluate these techniques as purification methods. To select the most efficient isolation strategy, methods were evaluated using gel electrophoresis, total protein quantitation, and peptide-adduct identification by MS. Results suggest that the albumin-rich fractions obtained can be used to identify exposure by quantitating the albumin adducts to electrophilic organic toxicants such as HD. The HiTrap Blue HP albumin isolation system appears to display the most promising results for purifying albumin to detect HD-adducts, exhibiting high purification efficiency, satisfactory albumin recovery, promising specificity, and a higher loading capacity for serum. [source] A Risk of Alzheimer's Disease and Aluminum in Drinking WaterPSYCHOGERIATRICS, Issue 4 2002Shunsuke Meshitsuka Abstract: The epidemiological studies on the relation between Alzheimer's disease and aluminum in drinking water are reviewed. In descriptive studies, case-control studies, and also cohort studies aluminum in drinking water turned out to be positive for the senile dementia of Alzheimer type. Negative results were obtained in the studies of presenile dementia or alminum levels lower than 0.1 mg/L. Aluminum is the third abundant element on earth, therefore, exposure to aluminum is inevitable in daily life. It is known that as over 95% of cases with Alzheimer's disease are sporadic, some environmental factors are expected to be etiological. Aluminum has been so far studied as a candidate for a neurotoxic factor. It is not known why attention has been given to only aluminum in drinking water as the cause of the neuro-degenerative disease other than aluminum in foods or medications, and how aluminum acts as a toxicant in brain. Nonetheless, reduction of aluminum in drinking water is recommended, as well as investigations on the mechanism of neurotoxicity of aluminum to find out the way to be free from the fear of aluminum. [source] Toxic effects of dexamethasone on mouse testicular germ cellsANDROLOGIA, Issue 4 2010M. Orazizadeh Summary Exposure to glucocorticoids (GCs) leads to numerous changes in various biological systems including the reproductive system. This work evaluated effects of dexamethasone (Dex), a widely used GC, on mouse testicular germ cells. Experimental groups (E1,E3) received one of the following treatments daily for 7 days: 4, 7 and 10 mg kg,1 Dex respectively. Control groups were treated with equivalent volumes of saline. Testicular histopathology, morphometric analysis and deoxy-UTP-digoxigenin nick end labeling (TUNEL) assessment were performed for evaluation of the toxic effects of Dex and detection of the apoptotic cells. The results showed that Dex induces histopathological alterations such as epithelial vacuolisation, atrophy and reduction in testicular spermatozoid. Morphometrical data showed that Dex significantly reduced tubular diameter and epithelial height (P < 0.05). Johnsen's scoring also showed poor spermatogenesis in E2 and E3 groups (P < 0.05). Apoptotic index of germ cells was significantly increased in E2 (18.9% versus 1.76%, P < 0.01) and E3 (24.6 versus 1.76%, P < 0.001) groups. It is concluded that Dex acts as testicular toxicant and that further studies are needed to establish its mechanism of action upon spermatogenesis. [source] A multicriteria ranking of organotin(IV) compounds with fungicidal propertiesAPPLIED ORGANOMETALLIC CHEMISTRY, Issue 10 2003Godwin A. Ayoko Abstract The application of multicriteria decision-making methods to the results of in vitro antifungal properties of organotin compounds of the type PhxSnXz (x = 2 or 3; X = O2CC6H4OH, O2CC6H4OCOCH3, Cl or O2CCH3; z = 1 or 2) and of free 2-hydroxybenzoic and 2-acetoxybenzoic acids against Aspergillus niger, Aspergillus flavus, Candida albicans, Penicillium citrinum, Trichophyton rubrum and Trichophyton violaceum have been described. Ranking information necessary to select one toxicant in preference to others and to assess the properties influencing the preference has been obtained. Patterns in the multivariate analyses suggest that cationic and anionic moieties of the toxicant play some roles in their fungicidal activities. The triphenyltin compounds were generally more active than their diphenyltin analogues, but the acetoxybenzoates were more active than the corresponding hydroxybenzoates, acetates or chlorides. Thus, triphenyltin acetoxybenzoate is up to 7.5 times as active as the corresponding acetate, which is commercially marketed as a fungicide. The results of the analyses have been discussed in the light of the mechanism of antifungal activity of organotin compounds and the potential of multivariate data analysis techniques to facilitate the screening and ranking of antifungal agents. Copyright © 2003 John Wiley & Sons, Ltd. [source] Acute tolerance of juvenile Florida pompano, Trachinotus carolinus L., to ammonia and nitrite at various salinitiesAQUACULTURE RESEARCH, Issue 9 2006Charles R Weirich Abstract The acute tolerance of juvenile Florida pompano Trachinotus carolinus L. (mean weight±SE=8.1±0.5 g) to environmental unionized ammonia-nitrogen (NH3 -N) and nitrite-nitrogen (NO2 -N) at various salinities was determined via a series of static exposure trials. Median-lethal concentrations (LC50 values) of NH3 -N and NO2 -N at 24, 48, and 96 h of exposure were calculated at salinities of 6.3, 12.5 and 25.0 g L,1 at 28 °C (pH=8.23,8.36). Tolerance of pompano to acute NH3 -N exposure was not affected by salinity, with 24, 48 and 96 h LC50 values ranging from 1.05 to 1.12, 1.00 to 1.08 and 0.95 to 1.01 mg NH3 -N L,1 respectively. Regarding NO2 -N, tolerance of pompano to this environmental toxicant was compromised at reduced salinities. Median-lethal concentrations of NO2 -N to pompano at 24, 48 and 96 h of exposure ranged from 67.4 to 220.1, 56.9 to 140.7 and 16.7 to 34.2 mg NO2 -N L,1 respectively. The results of this study indicate that juvenile Florida pompano are relatively sensitive to acute NH3 -N and NO2 -N exposure, and in the case of the latter, especially at lower salinities. [source] Carbon monoxide-induced axial skeletal dysmorphogenesis in the chick embryo,,BIRTH DEFECTS RESEARCH, Issue 4 2003Peter G. Alexander Abstract BACKGROUND Congenital axial skeletal defects affect two to three individuals per 1,000 live births. Without strong evidence for heritability, the cause is assumed to be multi-factorial. Carbon monoxide (CO), an increasingly prevalent environmental toxicant, is a potential environmental component in the etiology of these defects. The chick embryo is a useful model for the characterization and assessment of the mechanism(s) of action of basic developmental mechanisms. METHODS We have determined a critical period and dose for CO teratogenicity and established a model of CO-induced axial skeletal dysmorphogenesis in the chick embryo. The resulting phenotypes reveal a spectrum of axial skeletal defects ranging from minor defects of the vertebral canal and inter,vertebral discs, to thoraco,lumbar scoliosis, to a tailless phenotype reminiscent of caudal dysgenesis syndrome. These axial skeletal defects have been related to earlier developmental defects in somitogenesis, including errors in segmentation and epithelialization and the expression of the somitic epithelialization factor, Paraxis. We have examined patterns of cell death and apoptosis in CO exposed chick embryos to assess the target tissue(s) involved in the teratogenicity of CO. RESULTS With respect to the embryonic axis, the neural tube was found to be the most sensitive to CO-induced apoptosis, followed by the somitic mesoderm and Hensen's node. CONCLUSIONS We hypothesize that the somitic defects and the resulting axial skeletal dysmorphogenesis are caused by disrupted neural tube or ectoderm functions related to somite formation and maintenance. We also hypothesize that CO-induced dysmorphogenesis at this critical period of somitogenesis is caused by the overabundance of CO acting endogenously as a cellular signal, while coincidentally exerting its influence as a toxicant of oxygen delivery or utilization. Birth Defects Research (Part A) 67:219,230, 2003. Published 2003 Wiley-Liss, Inc. [source] Kinetics of the Action of Na2SeO3 on Bacillus subtilis Growth as Studied by MicrocalorimetryCHINESE JOURNAL OF CHEMISTRY, Issue 2 2002Yi Liu Abstract Microcalorimetric bioassay for acute cellular toxicity is based on metabolic heat production from cultured cells. The biological response to toxicants is the inhibition of the heat production rate in cells, and toxicity is expressed as the concentration of toxicant that is 50% effective in this inhibition (IC50). In mis paper, the effect of Na2SeO3 on Bacillus subtilis growth was investigated at 37 °C by microcalorimetry. The relationship between growth rate constants (k) and concentration of Na2SeO3 (c) shows a logarithmic normal distribution, and lC50 is 20.3 ,g/mL. All these thermokinetic information is readily obtained by an LKB 2277,204 heat conduction microcalorimeter. Microcalorimetry is a quantitative, inexpensive, and versatile method for toxicology research. [source] Genetic and environmental interactions on oral cancer in Southern ThailandENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2 2001Suparp Kietthubthew Abstract Many countries are interested in understanding the relationship between genetic susceptibility and their prevalent environmental cancers for disease prevention. In Thailand we conducted a population-based case-control study of 53 matched pairs to assess the risk of oral cancer in relation to genetic polymorphism of the glutathione-S-transferase genes (GSTM1 and GSTT1) in cigarette smokers, alcohol drinkers, and betel quid chewers. Interaction of the genes with other potential risk factors such as local bean consumption were also elucidated. Homozygous deletion of GSTM1 has a frequency of 56.6% (n = 30 over 53) among the patients and 30.2% (16/53) among the controls. This gene is associated with a 2.6-fold higher risk for development of oral cancer (95% CI 1.04,6.5). Among the null GSTM1 individuals, those who smoke, consume alcohol, and/or chew betel quid have a significantly increased risk for oral cancer with an odd ratio (OR) = 4.0 (95% CI = 1.2,13.7), OR = 7.2 (95% CI = 1.5,33.8), and OR = 4.4 (95% CI = 1.1,17.8), respectively. Interactions between any two of the lifestyle habits for oral cancer risk, however, are not found. The frequency of the GSTT1 null genotype is 34.0% (18/53) among the patients and 47.2% (25/53) among our controls. There is no association between the GSTT1 null allele and oral cancer risk. In conclusion, our study provides data to indicate that individuals who have homozygous deletion of the GSTM1 gene have increased risk for oral cancer. The risk increases further when these individuals are exposed to environmental toxicants such as chemicals in cigarette smoke, alcohol, and betel quid. These baseline data can be applied to a larger population-based study, both to verify the observation and to conduct mechanistic investigations. Environ. Mol. Mutagen. 37:111,116, 2001 © 2001 Wiley-Liss, Inc. [source] Coselection for microbial resistance to metals and antibiotics in freshwater microcosmsENVIRONMENTAL MICROBIOLOGY, Issue 9 2006Ramunas Stepanauskas Summary Bacterial resistances to diverse metals and antibiotics are often genetically linked, suggesting that exposure to toxic metals may select for strains resistant to antibiotics and vice versa. To test the hypothesis that resistances to metals and antibiotics are coselected for in environmental microbial assemblages, we investigated the frequency of diverse resistances in freshwater microcosms amended with Cd, Ni, ampicillin or tetracycline. We found that all four toxicants significantly increased the frequency of bacterioplankton resistance to multiple, chemically unrelated metals and antibiotics. An ampicillin-resistant strain of the opportunistic human pathogen Ralstonia mannitolilytica was enriched in microcosms amended with Cd. Frequencies of antibiotic resistance were elevated in microcosms with metal concentrations representative of industry and mining-impacted environments (0.01,1 mM). Metal but not antibiotic amendments decreased microbial diversity, and a weeklong exposure to high concentrations of ampicillin (0.01,10 mg l,1) and tetracycline (0.03,30 mg l,1) decreased microbial abundance only slightly, implying a large reservoir of antibiotic resistance in the studied environment. Our results provide first experimental evidence that the exposure of freshwater environments to individual metals and antibiotics selects for multiresistant microorganisms, including opportunistic human pathogens. [source] Histopathological alterations in the liver of the sharptooth catfish Clarias gariepinus from polluted aquatic systems in South AfricaENVIRONMENTAL TOXICOLOGY, Issue 2 2009M. J. Marchand Abstract There is a need for sensitive bio-monitoring tools in toxicant impact assessment to indicate the effect of toxicants on fish health in polluted aquatic ecosystems. Histopathological assessment of fish tissue allows for early warning signs of disease and detection of long-term injury in cells, tissues, or organs. The aim of this study was to assess the degree of histopathological alterations in the liver of C. gariepinus from two dams in an urban nature reserve, (Gauteng, South Africa). Two dams (Dam 1 and Dam 2) were chosen for their suspected levels of toxicants. Water and sediments were sampled for metal and potential endocrine disrupting chemical analysis. A quantitative and qualitative histology-based health assessment protocol was employed to determine the adverse health effects in fish. The analysis of blood constituents, fish necropsy, calculation of condition factors, and hepatosomatic indices were employed to support the findings of the qualitative and quantitative histological assessment of liver tissue. Assessment of the liver tissue revealed marked histopathological alterations including: structural alterations (hepatic cord disarray) affecting 27% of field specimens; plasma alterations (granular degeneration 98% and fatty degeneration 25%) of hepatocytes; an increase in melanomacrophage centers (32%); hepatocyte nuclear alterations (90%); and necrosis of liver tissue (14%). The quantitative histological assessment indicated that livers of fish collected from Dam 1 were more affected than the fish livers collected from Dam 2. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2009. [source] Application of DNA diffusion assay in earthworm coelomocytesENVIRONMENTAL TOXICOLOGY, Issue 2 2008A. A. Apte Abstract We have applied the DNA diffusion assay proposed by Singh (2000) Exp Cell Res 256:328,337, for quantitative estimation of apoptosis in earthworm coelomocytes, exposed to Chromium (VI) and cypermethrin as model toxicants in vitro. The DNA diffusion assay was originally described for mammalian cells. H2O2, Sodium ascorbate, and hyperthermia were used as positive controls in present study. Apoptosis such as DNA diffusion occurred in dose-dependent manner for Chromium (VI) and cypermethrin at very low concentration (1, 3, and 10 ppm for Chromium (VI) and 4, 8, and 16 ppm for cypermethrin). Three distinct patterns (apoptosis like DNA diffusion, necrosis, and normal) were observed in exposed and nonexposed cells. Present study is probably the first report of application of the DNA diffusion technique in earthworm coelomocytes. Findings of this study indicate that this assay has potential for use in invertebrate cells to differentiate between apoptosis and necrosis. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2008. [source] Response of the charophyte Nitellopsis obtusa to heavy metals at the cellular, cell membrane, and enzyme levelsENVIRONMENTAL TOXICOLOGY, Issue 3 2002Levonas Manusad, ianas Abstract The responses of the freshwater macroalga Nitellopsis obtusa to heavy metal (HM) salts of Hg, Cd, Co, Cu, Cr, and Ni were assessed at different levels: whole-cell mortality (96-h LC50), in vivo cell membrane (45-min depolarization of resting potential, EC50), and enzyme in plasma membrane preparations (K+, Mg2+ -specific H+ -ATPase inhibition, IC50). To measure ATPase activity, a novel procedure for isolation of plasma membrane,enriched vesicles from charophyte cells was developed. The short-term ATPase inhibition assay (IC50 from 6.0 × 10,7 to 4.6 × 10,4 M) was slightly more sensitive than the cell mortality test (LC50 from 1.1 × 10,6 to 2.6 × 10,3 M), and the electrophysiological test with the end point of 45-min depolarization of resting potential was characterized by less sensitivity for HMs (EC50 from 1.1 × 10,4 to 2.2 × 10,2 M). The variability of IC50 values assessed for HMs in the ATPase assays was close to that of LC50 values in the mortality tests (CVs from 33.5 to 83.5 and from 12.4% to 57.7%, respectively), whereas the EC50 values in the electrophysiological tests were characterized by CVs generally below 30%. All three end points identified two separate HM groups according to their toxicity to N. obtusa: Co, Ni, and Cr comprised a group of less toxic metals, whereas Hg, Cu, and Cd comprised a group of more toxic metals. However, the adverse effects within each group were discriminated differently. For example, the maximum difference between the highest and lowest LC50 for the group of less toxic metals in the long-term mortality test was approximately 60% of the response range, whereas the corresponding difference in IC50 values in the ATPase assay was 30%. In contrast, the LC50 values of the more toxic metals occupied only 10% of the response range, whereas the IC50 values were spread over 70%. Further investigation should be done of the underlying mechanism or mechanisms responsible for the observed differences in the dynamic range of a particular end point of the groups of toxicants of varying strength. © 2002 Wiley Periodicals, Inc. Environ Toxicol 17: 275,283, 2002; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/tox.10058 [source] | ||||||||||||||||||||||