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At least 181 records · Page 10Linked to original sources
PubMed2005

Experimental study on the toxicity of imidacloprid given in syrup to honey bee (Apis mellifera) colonies.

Two groups of eight honey bee colonies were fed with two different concentrations of imidacloprid in saccharose syrup during summer (each colony was given 1 litre of saccharose syrup containing 0.5 microg litre(-1) or 5 microg litre(-1) of imidacloprid on 13 occasions). Their development and survival were followed in parallel with control hives (unfed or fed with saccharose syrup) until the end of the following winter. The parameters followed were: adult bee activity (number of bee entering the hive and pollen carrying activity), adult bee population level, capped brood area, frequency of parasitic and other diseases, mortality, number of frames with brood after wintering and a global score of colonies after wintering. The only parameters linked to feeding with imidacloprid-supplemented saccharose syrup when compared with feeding with non-supplemented syrup were: a statistically non-significant higher activity index of adult bees, a significantly higher frequency of pollen carrying during the feeding period and a larger number of capped brood cells. When imidacloprid was no longer applied, activity and pollen carrying were re-established at a similar level for all groups. Repeated feeding with syrup supplemented with imidacloprid did not provoke any immediate or any delayed mortality before, during or following the next winter, whereas such severe effects are described by several French bee keepers as a consequence of imidacloprid use for seed dressing in neighbouring cultures. In any case, during the whole study, mortality was very low in all groups, with no difference between imidacloprid-fed and control colonies. Further research should now address several hypotheses: the troubles described by bee keepers have causes other than imidacloprid; if such troubles are really due to this insecticide, they may only be observed either when bees consume contaminated pollen, when no other sources of food are available, in the presence of synergic factors (that still need to be identified), with some particular races of bees or when colonies are not strong and healthy.

Animals↗
PubMed2005

Time-concentration-mortality modeling of the synergistic interaction of Beauveria bassiana and imidacloprid against Nilaparvata lugens.

Interactions between the entomopathogenic fungus, Beauveria bassiana SG8702, and imidacloprid on Nilaparvata lugens (Homoptera: Delphacidae) were studied in laboratory bioassays by spraying suspensions of unformulated conidia (assay 1) and aqueous dilutions of emulsifiable conidia formulation alone (assay 2) or together with imidacloprid at the sub-lethal rates of 0.5, 1.0 and 2.0 microg ml(-1) (assays 3-5). Each assay consisted of five conidia concentrations plus an appropriate control and three replicates, each including 30-40 third-instar nymphs, so as to generate time-concentration-mortality data for modeling analysis. A mineral oil-based emulsion used to formulate B bassiana slightly enhanced fungal activity but had no significant impact on the background mortality of N lugens. On the basis of LC50 estimates and associated variances on days 4-12 after spraying, synergistic interactions of both agents or formulations were determined by estimating relative potencies of assay 2 over assay 1 (1.2-9.0), assay 3 over assay 2 (1.3-1.7), assay 4 over assay 2 (7.5-9.6), assay 5 over assay 2 (22.7-101), assay 4 over assay 3 (3.8-5.8), assay 5 over assay 3 (16.1-61.0), and assay 5 over assay 4 (3.0-10.5). The time-concentration-mortality modeling method was not only mathematically but also biologically robust to evaluate the interactions of B bassiana and imidacloprid on N lugens. Compared with their counterparts, enhanced fungal formulations displayed consistently earlier or greater activities against the pest species based on LC50 and LT50 estimates determined from their time-concentration-mortality relationships. The results highlight a potential for pest control by combined formulation or application of B bassiana and imidacloprid.

Animals↗
PubMed2005

Analysis of residues of imidacloprid in tobacco by high-performance liquid chromatography with liquid-liquid partition cleanup.

A practical method for analysis of residues of imidacloprid in baked tobacco leaves has been developed using HPLC with liquid-liquid partition clean-up. Imidacloprid was extracted with ethyl acetate under ultrasound, and cleaned up by liquid-liquid partition with 50 g litre(-1) aqueous sodium chloride followed by dichloromethane. The water-soluble and fat-soluble components in tobacco, which interfere with imidacloprid in HPLC, were removed. The separation was performed on a Supelco LC-18 column (250 mm x 4.6 mm ID) with a mobile phase of acetonitrile + 5 mM ammonium acetate (20 + 80 by volume) at a flow-rate of 1 ml min(-1). The baseline separation between imidacloprid and the tobacco blank was achieved within 10 min. With a detection wavelength at 270 nm, the limit of quantitation was 0.04 mg kg(-1). The recovery ranged from 89.8 to 95.4% and the RSDs were less than 2.3%. The proposed method was successfully employed for the determination of imidacloprid residues in 300 samples of flue-cured tobacco leaves.

Chromatography, High Pressure Liquid↗
PubMed1997

A comparison of acute mortality and population growth rate as endpoints of toxicological effect.

The objective of this study was to determine how closely acute (72-hr) lethal concentration estimates developed from probit analysis compared to the demographic toxicological endpoints, net reproductive rate (Ro), the intrinsic rate of increase (rm), and realized fecundity (Ux), in terms of predicting effects of pesticides on populations. Lethal and sublethal effects of the insecticide imidacloprid on the arthropod Acyrthosiphon pisum Harris (pea aphid) were determined for populations exposed to foliar-sprayed broad bean Vicia faba L. (variety Banner). An examination of Ro indicated that sublethal effects were occurring that reduced reproduction. However, by looking at the mean number of offspring produced per surviving female and Ux, it was determined that the reduction in Ro was entirely due to acute mortality and a reduction in life span. Also, exposure to increasing concentrations of imidacloprid did not cause a shift in either the day of initial reproduction or the day of peak reproduction. Therefore, this pesticide caused no sublethal effects on reproduction and, as such, a lethal concentration estimate should have been a good predictor of effect at the population level. However, the 72-hr lethal concentration estimate was not a good predictor of effect of this pesticide on population growth. Populations exposed to the 72-hr LC60 were able to maintain rates of population increase (rm = 0.224) similar to those of the control (rm = 0.295). The data indicate that the reason for the discrepancy between acute lethal concentration estimates and population growth was that surviving individuals were able to sustain heightened rates of reproduction following acute exposure to imidacloprid. The ability of surviving individuals to maintain these high reproductive rates allowed them to compensate for losses and act as reservoirs for future reproduction. It is not possible, using acute mortality estimates alone, to predict this "reservoir effect," and therefore not possible to predict how a population's growth rate will respond or change based on this endpoint. Thus this would suggest that the assessment of a xenobiotic based solely on acute mortality estimates will lead to flawed conclusions about a population's exposure response.

Animals↗
PubMed2005

Evaluation of genotoxicity of combined soil pollution by cadmium and imidacloprid.

Cadmium (Cd) is one of the important pollutants of soil and the genotoxicity of Cd-contaminated soil was studied in combination with imidacloprid. The single cell gel electrophoresis or comet assay was used to quantify DNA strand breaks as a measure of DNA damage induced by Cd and imidacloprid contamination in soil. The soil was artificially contaminated by Cd (0.0, 0.2, 0.5, 1.0, 2.0 mg x kg(-1) dry soil) or Cd (0.0, 0.2, 0.5, 1.0, 2.0 mg x kg(-1) dry soil) and imidacloprid (0.5 mg x kg(-1) dry soil). Roots of Vicia faba were exposed to the contaminated soil for 2 h at 25 degrees C and were used in the comet assay. DNA damage was measured as the values of percentage of nuclei with tails, tail length, tail DNA, tail moment (TM), and Olive tail moment (OTM). DNA damages of root tips of Vicia faba increased after Cd treatment and there were dose-related increases in DNA damage measured as these parameters. However, the addition of imidacloprid further increased the DNA damage. These data confirmed the genotoxic effect of Cd to plants, and that the combined pollution with imidacloprid can enhance the genotoxicity of Cd.

Cadmium↗
PubMed2001

Comparative study on the effects of three insecticides (fipronil, imidacloprid, selamectin) on developmental stages of the cat flea (Ctenocephalides felis Bouché 1835): a light and electron microscopic analysis of in vivo and in vitro experiments.

The effects of three insecticides (fipronil, imidacloprid and selamectin) on developmental stages of cat fleas (Ctenocephalides felis) were studied in vivo, in vitro and by means of light and electron microscopy. The results were documented by video. Adult fleas were attached to the skin of dogs that had been treated 7 days before with one of the three compounds. Furthermore, adult fleas were exposed exclusively to the hair and skin debris of such treated dogs or were placed on filter papers that had been impregnated with one of these three compounds or with the blood of treated dogs. Larval fleas were exposed to hair of treated dogs, to debris obtained by combing treated dogs, to dried blood samples of treated dogs or were placed onto filter papers impregnated with one of the three compounds. In these experiments with adult and larval fleas, it was noted that none of the three insecticides had a repellent effect on adult or larval fleas. Imidacloprid was the only compound that acted exclusively by body contact, and was apparently taken up by adult and larval fleas via the thin, non-sclerotized intersegmental membranes of the flea's body, shown when flea stages were exposed to hairs taken from dogs treated with one of the compounds or placed onto drug-impregnated filter papers. Imidacloprid killed larvae and adult fleas within 1 h, while it took at least 24 h until all adult fleas had died on fipronil- or selamectin-treated dogs, thus allowing longer feeding periods, increasing the risk of transmission of flea-derived diseases. Flea larvae covered with debris from dogs topically treated 7 days before with fipronil, imidacloprid or selamectin died, like the untreated control, within 16-28 h after exposure. This was, however, probably mainly due to a drying effect. Adult and larval fleas exposed to filter papers impregnated with the blood of treated dogs survived longer than 7 days, as did the untreated controls. All three drugs apparently acted on nerves and muscles and thus stopped motility.

Animals↗
PubMed2001

In vivo and in vitro effects of imidacloprid on sheep keds (Melophagus ovinus): a light and electron microscopic study.

The effects of imidacloprid (Advantage) on sheep keds (Melophagus ovinus Linne 1758) were studied in vivo and in vitro by means of direct observation (monitored on video tape) and by light and electron microscopy. It was found that: 1. Imidacloprid acted rapidly on all motile stages of the sheep keds. Within 3-4 min after exposure they became immobile and their legs and the abdomen started tetanic trembling movements for 15-30 min, leading to death. 2. The compound is apparently taken up by the body, since it also acted on those sheep keds that had been exclusively exposed to imidacloprid-contaminated filter papers. 3. The compound is available and active for more than 1 month in the wool of sheep; even rainfall does not reduce its efficacy. Body contact between treated mother sheep and their lambs protects them from infestation with these ectoparasites. 4. The compound initiates an ultimately lethal destruction of the ganglia, nerve chords and related muscle fibers, as can be seen in electron micrographs.

Administration, Topical↗