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Oral Toxicity (oral + toxicity)
Kinds of Oral Toxicity Selected AbstractsOral toxicity of the cyanobacterial toxin cylindrospermopsin in mice: Long-term exposure to low dosesENVIRONMENTAL TOXICOLOGY, Issue 6 2006A. Sukenik Abstract The hepatotoxin cylindrospermopsin, a sulfated-guanidinium alkaloid with substituted dioxypyrimidine (uracil) moiety, was isolated from several cyanobacteria species. The acute toxicity of cylindrospermopsin was well established based on intraperitoneal and oral exposure; however, only a few long-term subacute exposure studies were performed to permit a reliable guideline value for cylindrospermopsin in drinking water. In the study reported herein, female and male mice were exposed to cylindrospermopsin in their drinking water. Cylindrospermopsin-containing, Aphanizomenon ovalisporum (cyanobacterium)-free medium was provided as the only source of drinking water, whereas a control group was given a fresh medium for cyanobacteria as drinking water. Over a period of 42 weeks, experiment groups were exposed to cylindrospermopsin concentration, gradually increased from 100 to 550 ,g L,1 (daily exposure ranged between 10 and 55 ,g kg,1 day,1). Body and organ weights were recorded, and serum and hematology analyses were performed 20 and 42 weeks after the beginning of the experiment. The most pronounced effect of cylindrospermopsin was elevated hematocrit levels in both male and female mice after 16 weeks of exposure to cylindrospermopsin. The observed changes in the hematocrit level were accompanied by deformation of red blood cells, which were changed into acanthocyte. Based on these results, a daily cylindrospermopsin dose of 20 ,g kg,1 day,1 (equivalent to 200 ,g L,1) is proposed as the lowest-observed-adverse-effect level for both male and female mice. © 2006 Wiley Periodicals, Inc. Environ Toxicol 21: 575,582, 2006. [source] Oral toxicity of the cyanobacterial toxin cylindrospermopsin in male Swiss albino mice: Determination of no observed adverse effect level for deriving a drinking water guideline valueENVIRONMENTAL TOXICOLOGY, Issue 2 2003A. R. Humpage Abstract The cyanobacterial toxin cylindrospermopsin (CYN) is a frequent contaminant of freshwaters throughout the world, including those that are sources of drinking water. The first cases of human poisoning attributed to this toxin occurred from a treated drinking water supply in Queensland, Australia, in 1979. The toxin causes extensive damage to the liver, kidneys, spleen, heart, and other organs. It is known to be a potent protein synthesis inhibitor, but there is mounting evidence for genotoxicity and that it metabolizes to even more toxic forms. As part of a risk assessment process leading to a guideline for a safe drinking water level for this toxin, we performed a series of experiments to determine a no-observed-adverse-effect level (NOAEL) for this toxin. In the first trial male mice were exposed to CYN-containing cyanobacterial extract in their drinking water (0,657 ,g CYN kg,1 day,1) for 10 weeks. In the second trial mice received purified CYN by daily gavage (0,240 ,g CYN kg,1 day,1) for 11 weeks. Body and organ weights were recorded; urine, serum, and hematology analyses were performed; and histopathological examination of tissues was carried out. Body weights were significantly increased at low doses (30 and 60 ,g kg,1 day,1) and decreased at high doses (432 and 657 ,g kg,1 day,1). Liver and kidney weights were significantly increased at doses of 240 ,g kg,1 day,1 and 60 ,g kg,1 day,1, respectively. Serum bilirubin levels were significantly increased and bile acids significantly decreased at doses of 216 ,g kg day,1 and greater. Urine total protein was significantly decreased at doses above 60 ,g kg,1 day,1. The kidney appeared to be the more sensitive organ to this toxin. If it is assumed that increased organ weights and changes in functional capacity are responses to an underlying toxic effect, then the NOAEL based on this data is 30 ,g kg,1 day,1, which, with standard calculations and uncertainty factors, provides a proposed guideline safety value of 1 ,g/L in drinking water. © 2003 Wiley Periodicals, Inc. Environ Toxicol 18: 94,103, 2003. [source] Insecticidal activity of scorpion toxin (ButaIT) and snowdrop lectin (GNA) containing fusion proteins towards pest species of different ordersPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 1 2010Elaine C Fitches Abstract BACKGROUND: The toxicity of a fusion protein, ButalT/GNA, comprising a venom toxin (ButaIT) derived from the red scorpion, Mesobuthus tamulus (F.), and Galanthus nivalis agglutinin (GNA), was evaluated under laboratory conditions against several pest insects. Insecticidal activity was compared with SFI1/GNA, a fusion comprising a venom toxin (SFI1) derived from the European spider Segestria florentina (Rossi) and GNA, which has been previously demonstrated to be effective against lepidopteran and hemipteran pests, and to GNA itself. RESULTS: Injection assays demonstrated that both fusion proteins were toxic to lepidopteran larvae, dipteran adults, coleopteran adults and larvae and dictyopteran nymphs. ButalT/GNA was more toxic than SFI1/GNA in all cases. GNA itself made a minor contribution to toxicity. Oral toxicity of ButalT/GNA towards lepidopteran pests was confirmed against neonate Spodoptera littoralis (Boisd.), where incorporation at 2% dietary protein resulted in 50% mortality and > 85% reduction in growth compared with controls. ButaIT/GNA was orally toxic to Musca domestica L. adults, causing 75% mortality at 1 mg mL,1 in aqueous diets and, at 2 mg g,1 it was orally toxic to Tribolium castaneum (Herbst.), causing 60% mortality and a 90% reduction in growth. CONCLUSIONS: Toxicity of the ButaIT/GNA recombinant fusion protein towards a range of insect pests from different orders was demonstrated by injection bioassays. Feeding bioassays demonstrated the potential use of the ButaIT/GNA fusion protein as an orally active insecticide against lepidopteran, dipteran and coleopteran pests. These experiments provide further evidence that the development of fusion protein technology for the generation of new, biorational, anti-insect molecules holds significant promise. © Crown Copyright 2009. Reproduced with permission of Her Majesty's Stationery Office. Published by John Wiley & Sons, Ltd. [source] Effects of selected insecticides on Diadegma semiclausum (Hymenoptera: Ichneumonidae) and Oomyzus sokolowskii (Hymenoptera: Eulophidae), parasitoids of Plutella xylostella (Lepidoptera: Plutellidae)INSECT SCIENCE, Issue 3 2005MUHAMMAD HASEEB Abstract Field doses of six selected insecticides were tested against the immature (pupae) and mature (adult) stages of Diadegma semiclausum (Hellén) and Oomyzus sokolowskii (Kurdjumov), parasitoids of the diamondback moth, Plutella xylostella (L.). Effects of contact toxicity (direct spraying) of the six insecticides on emergence of parasitoids were found negligible on both species except permethrin which caused 37.5% mortality. All adults of both parasitoid species died 24 hours after exposure to chlorfenapyr, emamectin benzoate and permethrin. In contrast, the three insect growth regulators (IGRs), chlorfluazuron, flufenoxuron and teflubenzuron, were found harmless to both species, and adult mortality of both parasitoid species was 0,16.7%. However, parasitism by the females of both parasitoid species was severely impaired when the females were offered the three IGR diluted solutions for 24 hours. Effects of oral toxicities of the IGRs on longevity of both parasitoids after 12 hours exposure were found to be significantly different between males and females. Compatibility of tested insecticides with D. semiclausum and O. sokolowskii and integration of compatible insecticides with these parasitoids in integrated pest management programs of crucifers are discussed. [source] Estimating the probability of bird mortality from pesticide sprays on the basis of the field study recordENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 7 2002Pierre Mineau Abstract The outcome of avian field studies was examined to model the likelihood of mortality. The data were divided into clusters reflecting the type of pesticide application and bird guilds present on site. Logistic regression was used to model the probability of a bird kill. Four independent variables were tested for their explanatory power: a variable reflecting acute oral toxicity and application rate; a variable reflecting the relative oral to dermal toxicity of the pesticides; Henry's law constant; and a variable reflecting possible avoidance of contaminated food items, the hazard factor (HF). All variables except for HF significantly improved model prediction. The relative dermal to oral toxicity, especially, was shown to have a major influence on field outcome and clearly must be incorporated into future avian risk assessments. The probability of avian mortality could be calculated from a number of current pesticide applications and the conclusion was made that avian mortality occurs regularly and frequently in agricultural fields. [source] Effects of contact, oral and persistent toxicity of selected pesticides on Cotesia plutellae (Hym., Braconidae), a potential parasitoid of Plutella xylostella (Lep., Plutellidae)JOURNAL OF APPLIED ENTOMOLOGY, Issue 1 2002M. Haseeb Cotesia plutellae (Kurd.) is an important larval parasitoid of Plutella xylostella (L.). Effects of contact, oral and persistent toxicity of field doses of selected pesticides on immature and mature stages of this useful wasp were determined in controlled conditions. Contact toxicity tests showed that cartap 75% SG, chlorfenapyr 10% F, emamectin benzoate 1% EC, permethrin 20% EC, chlorfluazuron 5% EC, flufenoxuron 10% EC, and teflubenzuron 5% EC were found to be selective against the cocoon stage. In contrast, contact toxicity of four insecticides viz., cartap 75% SG, chlorfenapyr 10% F, emamectin benzoate 1% EC, permethrin 20% EC were found to be moderately to extremely toxic (80% to 100% lethal) to wasp stage. Effects of oral toxicity of three IGRs on wasp stage were somewhat selective. However, beneficial performance of wasps seems to be adversely affected as host parasitism was recorded as being significantly different (P < 0.05) in comparison with control. A persistent toxic effect of insecticides via cabbage leaves discs against female wasps showed that cartap 75% SG was moderately persistent (16,30 days). While chlorfenapyr 10% F and emamectin benzoate 1% EC were recorded slightly to be persistent (5,10 days) and permethrin seems to be short lived (< 5 days). Implications of tested products in IPM of cabbage are discussed. [source] Acute oral toxicity of colchicine in rats: effects of gender, vehicle matrix and pre-exposure to lipopolysaccharideJOURNAL OF APPLIED TOXICOLOGY, Issue 5 2007Paddy L. Wiesenfeld Abstract The oral toxicity of a single administration by gavage (10, 20 or 30 mg kg,1 body weight) of colchicine (COL) was determined in young, mature male and female Sprague-Dawley rats. The effect of COL was evaluated in the presence or absence of additional treatment variables that included vehicle and lipopolysaccharide (LPS) pre-exposure. The vehicle for COL was either Half and Half cream (H & H) or saline, and each group included pretreatment with either saline or a low, minimally toxic dose (83 µg kg,1 body weight) of LPS. Colchicine toxicity in both male and female age-matched rats was characterized by progressively more severe dose-related clinical signs of toxicity. These included mortality, decreased body weight and feed intake during the first several days after dosing, with recovery thereafter in surviving animals. There were differences in the severity of the toxic response to COL between male and female rats. The most notable sex-related difference was in COL lethality. Female rats were two times more susceptible to the lethal effects of COL than male rats. Saline or H & H delivery vehicles did not result in any apparent qualitative or quantitative differences in COL toxicity. LPS pretreatment significantly potentiated COL lethality in both males and females, although the potentiation in males was greater than in females. LPS pretreatment modestly increased the COL induced anorexic effect in surviving males, but not in surviving female animals. LPS did not appear to modulate either the body weights or clinical signs of COL induced toxicity in surviving males or females. Copyright © 2007 John Wiley & Sons, Ltd. [source] One-year dog toxicity study of D-002, a mixture of aliphatic alcoholsJOURNAL OF APPLIED TOXICOLOGY, Issue 3 2001Celia Alemán Abstract D-002 is a mixture of high-molecular-weight aliphatic alcohols, obtained from bees wax (Apis mellifera), with mild anti-inflammatory properties and effective anti-ulcer activities demonstrated in experimental models. This study investigated the oral toxicity of D-002 administered for 1 year to beagle dogs. Twenty-four beagle dogs (12 males and 12 females) were distributed randomly in three experimental groups (four animals per group): a control and two treated groups received D-002 at 50 and 250 mg kg,1 (7 days/week) by gastric gavage. Overall, D-002 was well tolerated throughout the study. No signs or symptoms of toxicity were observed, and no mortality occurred during the study. All groups showed similar weight gain and food consumption. No hematological, blood biochemical or histopathological disturbances attributable to treatment were observed. This study shows no drug-related toxicity induced by long-term administration of up to 250 mg kg,1 D-002 to beagle dogs. Copyright © 2001 John Wiley & Sons, Ltd. [source] Gastroprotective activity of ferruginol in mice and rats: effects on gastric secretion, endogenous prostaglandins and non-protein sulfhydrylsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 2 2008Carlos Areche The gastroprotective mechanism of the natural diterpene ferruginol was assessed in mice and rats. The involvement of gastric prostaglandins (PGE2), reduced glutathione, nitric oxide or capsaicin receptors was evaluated in mice either treated or untreated with indometacin, N-ethylmaleimide (NEM), N-nitro-L-arginine methyl ester (L-NAME) or ruthenium red, respectively, and then orally treated with ferruginol or vehicle. Gastric lesions were induced by oral administration of ethanol. The effects of ferruginol on the parameters of gastric secretion were assessed in pylorus-ligated rats. Gastric PGE2 content was determined in rats treated with ferruginol and/or indometacin. The reduction of gastric glutathione (GSH) content was determined in rats treated with ethanol after oral administration of ferruginol, lansoprazole or vehicle. Finally, the acute oral toxicity was assessed in mice. Indometacin reversed the gastroprotective effect of ferruginol (25 mg kg,1) but not NEM, ruthenium red or L-NAME. The diterpene (25 mg kg,1) increased the gastric juice volume and its pH value, and reduced the titrable acidity but was devoid of effect on the gastric mucus content. Ferruginol (25, 50 mg kg,1) increased gastric PGE2 content in a dose-dependent manner and prevented the reduction in GSH observed due to ethanol-induced gastric lesions in rats. Single oral doses up to 3 g kg,1 ferruginol did not elicit mortality or acute toxic effects in mice. Our results showed that ferruginol acted as a gastroprotective agent stimulating the gastric PGE2 synthesis, reducing the gastric acid output and improving the antioxidant capacity of the gastric mucosa by maintaining the GSH levels. [source] Toxicity and nicotinic acetylcholine receptor interaction of imidacloprid and its metabolites in Apis mellifera (Hymenoptera: Apidae)PEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 7 2001Ralf Nauen Abstract Acute oral and contact toxicity tests of imidacloprid, an insecticide acting agonistically on nicotinic acetylcholine receptors (nAChR), to adult honeybees, Apis mellifera L var carnica, were carried out by seven different European research facilities. Results indicated that the 48-h oral LD50 of imidacloprid is between 41 and >81,ng per bee, and the contact LD50 between 49 and 102,ng per bee. The ingested amount of imidacloprid-containing sucrose solution decreased with increasing imidacloprid concentrations and may be attributed to dose-related sub-lethal intoxication symptoms or to antifeedant responses. Some previously reported imidacloprid metabolites occuring at low levels in planta after seed dressing, ie olefine-, 5-OH- and 4,5-OH-imidacloprid, showed lower oral LD50 values (>36, >49 and 159,ng per bee, respectively) compared with the concurrently tested parent molecule (41,ng per bee). The urea metabolite and 6-chloronicotinic acid (6-CNA) exhibited LD50 values of >99,500 and >121,500,ng per bee, respectively. The pharmacological profile of the [3H]imidacloprid binding site in honeybee head membrane preparations is consistent with that anticipated for a nAChR. IC50 values for the displacement of [3H]imidacloprid by several metabolites such as olefine, 5-OH-, 4,5-OH-imidacloprid, urea and 6-CNA were 0.45, 24, 6600, >100,000, and >100,000,nM, respectively. Displacement of [3H]imidacloprid by imidacloprid revealed an IC50 value of 2.9,nM, thus correlating well with the observed acute oral toxicity of the compounds in honeybees. Neurons isolated from the antennal lobe of A mellifera and subjected to whole-cell voltage clamp electrophysiology responded to the application of 100,µM acetylcholine with a fast inward current of between 30 and 1600 pA at ,70,mV clamp potential. Imidacloprid and two of the metabolites (olefine- and 5-OH-imidacloprid) acted agonistically on these neurons, whereas the others did not induce currents at test conencentrations up to 3,mM. The electrophysiological data revealed Hill coefficients of approximately 1, indicating a single binding site responsible for an activation of the receptor and no direct cooperativity or allosteric interaction with a second binding site. © 2001 Society of Chemical Industry [source] Risk posed to honeybees (Apis mellifera L, Hymenoptera) by an imidacloprid seed dressing of sunflowersPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 3 2001Richard Schmuck Abstract In a greenhouse metabolism study, sunflowers were seed-treated with radiolabelled imidacloprid in a 700,g,kg,1 WS formulation (Gaucho® WS 70) at 0.7,mg AI per seed, and the nature of the resulting residues in nectar and pollen was determined. Only the parent compound and no metabolites were detected in nectar and pollen of these seed-treated sunflower plants (limit of detection <0.001,mg,kg,1). In standard LD50 laboratory tests, imidacloprid showed high oral toxicity to honeybees (Apis mellifera), with LD50 values between 3.7 and 40.9,ng per bee, corresponding to a lethal food concentration between 0.14 and 1.57,mg,kg,1. The residue level of imidacloprid in nectar and pollen of seed-treated sunflower plants in the field was negligible. Under field-growing conditions no residues were detected (limit of detection: 0.0015,mg,kg,1) in either nectar or pollen. There were also no detectable residues in nectar and pollen of sunflowers planted as a succeeding crop in soils which previously had been cropped with imidacloprid seed-treated plants. Chronic feeding experiments with sunflower honey fortified with 0.002, 0.005, 0.010 and 0.020,mg,kg,1 imidacloprid were conducted to assess potential long-term adverse effects on honeybee colonies. Testing end-points in this 39-day feeding study were mortality, feeding activity, wax/comb production, breeding performance and colony vitality. Even at the highest test concentration, imidacloprid showed no adverse effects on the development of the exposed bee colonies. This no-adverse-effect concentration of 0.020,mg,kg,1 compares with a field residue level of less than 0.0015,mg,kg,1 (,=, limit of detection in the field residue studies) which clearly shows that a sunflower seed dressing with imidacloprid poses no risk to honeybees. This conclusion is confirmed by observations made in more than 10 field studies and several tunnel tests. © 2001 Society of Chemical Industry [source] Acute oral toxicity of Yersinia pseudotuberculosis to fleas: implications for the evolution of vector-borne transmission of plagueCELLULAR MICROBIOLOGY, Issue 11 2007David L. Erickson Summary Yersinia pestis diverged from Yersinia pseudotuberculosis, 20 000 years ago, during which time it evolved to be transmitted by fleas. In comparing the ability of these closely related species to infect the rat flea Xenopsylla cheopis, we found that Y. pseudotuberculosis, unlike Y. pestis, is orally toxic to fleas. Fleas showed signs of acute toxicity, including diarrhoea, immediately after feeding on blood containing Y. pseudotuberculosis in response to protein toxin(s) produced by the bacteria. Adherence of Y. pseudotuberculosis to the midgut and large intracellular vacuoles in midgut epithelial cells were detected during the first 24 h after infection. The insect pathogen Photorhabdus luminescens and its TcdA1 and TcdB1-TccC1 insecticidal toxin complexes were similarly toxic to fleas, implicating the toxin complex (tc) genes also present in Yersinia species. However, the Y. pestis and Y. pseudotuberculosis TcaAB and TcaC-TccC proteins were non-toxic to fleas, and Y. pseudotuberculosis mutants deleted of tc genes retained acute toxicity. Our results indicate that loss of one or more insect gut toxins was a critical step in the recent evolution of flea-borne transmission in the genus Yersinia. Changes in the tc insecticidal genes do not appear to have been responsible, but may have had other effects on Yersinia,flea interactions. [source] | |||||||||||||