Potential Risk to Pollinators from Nanotechnology-Based Pesticides.

The decline in populations of insect pollinators is a global concern. While multiple factors are implicated, there is uncertainty surrounding the contribution of certain groups of pesticides to losses in wild and managed bees. Nanotechnology-based pesticides (NBPs) are formulations based on multiple particle sizes and types.

Effect of pH and ionic strength on exposure and toxicity of encapsulated lambda-cyhalothrin to Daphnia magna.

Encapsulation of pesticide active ingredients in polymers has been widely employed to control the release of poorly water-soluble active ingredients. Given the high dispersibility of these encapsulated pesticides in water, they are expected to behave differently compared to their active ingredients; however, our current understanding of the fate and effects of encapsulated pesticides is still limited. In this study, we employed a central composite design (CCD) to investigate how pH and ionic strength (IS) affect the hydrodynamic diameter (HDD) and zeta potential of encapsulated λ-cyhalothrin and how those changes affect the exposure and toxicity to Daphnia magna.

Circadian clock regulates response to pesticides in Drosophila via conserved Pdp1 pathway.

Daily rhythms generated by the circadian clock regulate many life functions, including responses to xenobiotic compounds. In Drosophila melanogaster, the circadian clock consists of positive elements encoded by cycle (cyc) and Clock (Clk) and negative elements encoded by period (per) and timeless (tim) genes. The epsilon-isoform of the PAR-domain protein 1 (Pdp1epsilon) transcription factor is controlled by positive clock elements and regulates daily locomotor activity rhythms.

Does the clock make the poison? Circadian variation in response to pesticides.

Background: Circadian clocks govern daily physiological and molecular rhythms, and putative rhythms in expression of xenobiotic metabolizing (XM) genes have been described in both insects and mammals. Such rhythms could have important consequences for outcomes of chemical exposures at different times of day. To determine whether reported XM gene expression rhythms result in functional rhythms, we examined daily profiles of enzyme activity and dose responses to the pesticides propoxur, deltamethrin, fipronil, and malathion.

Proteomic analysis of MCF-7 cells treated with benzo[a]pyrene, dibenzo[a,l]pyrene, coal tar extract, and diesel exhaust extract.

Polycyclic aromatic hydrocarbon (PAH) DNA adducts have been associated with carcinogenesis, which is accompanied by multiple alterations in gene expression. We used two-dimensional electrophoresis to distinguish protein expression changes induced in MCF-7 cells by individual PAH (B[a]P and DB[a,l]P) and PAH mixtures (coal tar extract [SRM 1597] and diesel exhaust extract [SRM 1975]). Spots of interest were identified by MALDI-TOF-TOF.

Effects of suberoylanilide hydroxamic acid and trichostatin A on induction of cytochrome P450 enzymes and benzo[a]pyrene DNA adduct formation in human cells.

In this study, we investigated the effects of histone deacetylase (HDAC) inhibitors suberoylanilide hydroxamic acid (SAHA) and trichostatin A (TSA) on the metabolism of polycyclic aromatic hydrocarbons (PAH) in human mammary carcinoma derived MCF-7 cells in culture. Benzo[a]pyrene (B[a]P) induces cytochrome P450 (CYP) 1A1, CYP1B1 and other xenobiotic metabolizing enzymes. Results from our study indicated a significant increase in CYP activity in comparison to vehicle control in cells treated with SAHA or TSA as measured by ethoxyresorufin-O-deethylase assay.

Carcinogenic polycyclic aromatic hydrocarbon-DNA adducts and mechanism of action.

Polycyclic aromatic hydrocarbons (PAHs) are a class of widespread environmental carcinogens. Most of our knowledge of their mechanisms of metabolic activation to DNA-binding "ultimate carcinogenic" metabolites has come from analysis of the DNA interaction products formed by these highly reactive intermediates. Studies of their role in forming DNA-binding intermediates identical to those formed in vivo from the PAH itself have also allowed identification of the particular cytochrome P450 enzymes involved in activating various structural classes of carcinogenic PAHs.