Impact of Acrylamide on Calcium Signaling and Cytoskeletal Filaments in Testes From F344 Rat.

Acrylamide (AA) at high exposure levels is neurotoxic, induces testicular toxicity, and increases dominant lethal mutations in rats. RNA-sequencing in testes was used to identify differentially expressed genes (DEG), explore AA-induced pathway perturbations that could contribute to AA-induced testicular toxicity and then used to derive a benchmark dose (BMD). Male F344/DuCrl rats were administered 0.

Integrating Bar-Code Medication Administration Competencies in the Curriculum: Implications for Nursing Education and Interprofessional Collaboration.

This article describes an innovative project involving the integration of bar-code medication administration technology competencies in the nursing curriculum through interprofessional collaboration among nursing, pharmacy, and computer science disciplines. A description of the bar-code medication administration technology project and lessons learned are presented.

Differential genotoxicity of acrylamide in the micronucleus and Pig-a gene mutation assays in F344 rats and B6C3F1 mice.

Acrylamide is used in many industrial processes and is present in a variety of fried and baked foods. In rodent carcinogenicity assays, acrylamide exposure leads to tumour formation at doses lower than those demonstrated to induce genotoxic damage. We evaluated the potential of acrylamide to induce structural DNA damage and gene mutations in rodents using highly sensitive flow cytometric analysis of micronucleus and Pig-a mutant frequencies, respectively.

Transcriptomics analysis and hormonal changes of male and female neonatal rats treated chronically with a low dose of acrylamide in their drinking water.

Acrylamide is known to produce follicular cell tumors of the thyroid in rats. RccHan Wistar rats were exposed to a carcinogenic dose of acrylamide (3 mg/Kg bw/day) from gestation day 6 to delivery and then through their drinking water to postnatal day 35. In order to identify potential mechanisms of carcinogenesis in the thyroid glands, we used a transcriptomics approach.

Dosimetry of Acrylamide and Glycidamide Over the Lifespan in a 2-Year Bioassay of Acrylamide in Wistar Han Rats.

Acrylamide is an industrial chemical used to manufacture polymers, and is produced in foods during cooking at high heat. Hemoglobin adducts provide a long-lived dosimeter for acrylamide and glycidamide. This study determined acrylamide and glycidamide hemoglobin adducts (AAVal and GAVal) during a lifetime carcinogenesis bioassay.

Very low-activity stress/high-activity rest, single-day myocardial perfusion SPECT with a conventional sodium iodide camera and wide beam reconstruction processing.

Background: A stress (S)/rest (R) 1-day Tc-99m sestamibi protocol is logistically advantageous and facilitates stress-only imaging. However, with conventional 370 MBq (10 mCi) S activity and subsequent 1,110-1,295 MBq (30-35 mCi) R activity there is a risk of S-to-R "shine-through" and underestimation of defect reversibility. New software methods cope with lower counting statistics and should allow for both a reduced S activity and also less likelihood of S-to-R "shine-through.

A comparison of the image quality of full-time myocardial perfusion SPECT vs wide beam reconstruction half-time and half-dose SPECT.

Objectives: Wide Beam Reconstruction (WBR) (UltraSPECT, Ltd) uses resolution recovery and noise modeling to cope with decreased SPECT count statistics. Because WBR processing reconstructs half the usual SPECT count statistics, we postulate that image quality equivalent to a full-time acquisition can be achieved in either half the time or with half the radiopharmaceutical activity.

Methods: In 156 consecutive patients (pts) rest and 8-frame gated post-stress myocardial perfusion SPECT was performed following 333-444 and 1184-1480 MBq (9-12 and 32-40 mCi) Tc-99m sestamibi injections, respectively, with full-time (rest = 14 min; stress = 12.

Investigation of the low-dose response in the in vivo induction of micronuclei and adducts by acrylamide.

Acrylamide is an industrial chemical used in polymer manufacture. It is also formed in foods processed at high temperatures. It induces chromosome aberrations and micronuclei (MN) in somatic cells of mice, but not rats, and mutations in transgenic mice.

Inhibition of rat testicular nuclear kinesins (krp2; KIFC5A) by acrylamide as a basis for establishing a genotoxicity threshold.

Acrylamide is a toxic substance that induces a variety of cellular responses including neurotoxicity, male reproductive toxicity, tumorigenicity, clastogenicity, and DNA alkylation. Evidence is provided that inhibition of the microtubule motor protein kinesin is responsible for acrylamide-induced clastogenicity and aneuploidy. Two kinesin motors, KIFC5A and KRP2, which are responsible for spindle assembly and disassembly of kinetochore MT, respectively, are inhibited by acrylamide.

Acrylamide does not induce tumorigenesis or major defects in mice in vivo.

Chronic administration of acrylamide has been shown to induce thyroid tumors in rat. In vitro acrylamide also causes DNA damage, as demonstrated by the comet assay, in various types of cells including human thyroid cells and lymphocytes, as well as rat thyroid cell lines. In this work, mice were administered acrylamide in their drinking water in doses comparable with those used in rats, i.

Acrylamide effects on kinesin-related proteins of the mitotic/meiotic spindle.

The microtubule (MT) motor protein kinesin is a vital component of cells and organs expressing acrylamide (ACR) toxicity. As a mechanism of its potential carcinogenicity, we determined whether kinesins involved in cell division are inhibited by ACR similar to neuronal kinesin [Sickles, D.W.

Kinetics of elimination of urinary metabolites of acrylamide in humans.

Acrylamide (AM), used in the manufacture of polyacrylamide and grouting agents, is produced during the cooking of foods. Workplace exposure to AM can occur through the dermal and inhalation routes. The objective of this study was to define the kinetics of elimination of AM and its metabolites following oral and dermal administration.

Comparison of acrylamide metabolism in humans and rodents.

Acrylamide is metabolized by direct conjugation with glutathione or oxidation to glycidamide, which undergo further metabolism and are excreted in urine. In rats administered 3 mg/kg 1,2,3-13C3 acrylamide, 59% of the metabolites excreted in urine was from acrylamide-glutathione conjugation, whereas 25% and 16% were from two glycidamide-derived mercapturic acids. Glycidamide and dihydroxypropionamide were not detected at this dose level.

Gene expression profiling of intrinsic thermotolerance in Escherichia coli.

DNA microarrays were employed to compare gene expression in a thermotolerant, nalidixic acid-resistant mutant of Escherichia coli with that of the parental strain. When grown at 37 degrees C, up-regulated genes in the mutant included those coding for multiple antibiotic resistance proteins and enzymes for the degradation of small molecules, whereas among the down-regulated genes were those coding for fimbrial, flagellar, and outer membrane proteins as well as sigma 38. When the mutant grown at 42 degrees C was compared to the mutant grown at 37 degrees C, enhanced expression of several genes coding for flagellar proteins was detected.

Effects of acrylamide on primary neonatal rat astrocyte functions.

The present study assessed biochemical endpoints indicative of acrylamide toxicity in astrocyte cultures derived from neonatal rat pups. Given earlier reports on the possible ability of acrylamide to induce astrocytomas in the Fischer 344 rat, we performed studies in neonatal rat astrocyte cultures from the Fischer 344 to assess the ability of acrylamide to induce astrocytic proliferation. Measurements on astrocytic proliferation included [3H]-leucine incorporation, [3H]-thymidine incorporation, and changes in proliferating cell nuclear antigen (PCNA).

Dose-response modeling of in vivo genotoxicity data for use in risk assessment: some approaches illustrated by an analysis of acrylamide.

Methods for dose-response modeling of in vivo genotoxicity data are introduced and applied to a case study of acrylamide. Genetic toxicity results are typically summarized as being either positive or negative, with no further consideration of the dose-response patterns that can be estimated from such studies. This analysis explores the use of three modeling approaches: Poisson regression of counts of genetic effects per cell; dynamic modeling of the time-course of micronucleus production and loss as a function of exposure; and categorical regression of sets of genetic toxicity experiments, the results of which are recoded in terms of severities of response.

Metabolism and hemoglobin adduct formation of acrylamide in humans.

Acrylamide (AM), used in the manufacture of polyacrylamide and grouting agents, is produced during the cooking of foods. Workplace exposure to AM can occur through the dermal and inhalation routes. The objectives of this study were to evaluate the metabolism of AM in humans following oral administration, to compare hemoglobin adduct formation on oral and dermal administration, and to measure hormone levels.

Epidemiologic evidence for assessing the carcinogenicity of acrylamide.

Acrylamide (ACM) has recently been found in fried and baked foods, suggesting widespread public exposure. ACM is an industrial chemical that causes neurotoxicity in humans and an increase in benign tumors of the endocrine system of laboratory rats. The U.

The acute effects of acrylamide on astrocyte functions.

We assessed biochemical endpoints indicative of acute toxicity in neonatal rat primary astrocyte cultures exposed to acrylamide. Metallothionein (MT), glutamine synthetase (GS), glutamate/aspartate transporter (GLAST), and taurine transporter (tau-T) mRNA expression levels as well as cell volume were determined in astrocytes acutely treated with 0.1 and 1.

Effects of acrylamide on rodent reproductive performance.

Acrylamide monomer causes peripheral neurotoxicity, mutagenicity, clastogenicity, male reproductive toxicity, prenatal lethality, and endocrine-related tumors in rodents. Acrylamide (and/or its metabolite glycidamide) binds to dopamine receptors and spermatid protamines and inhibits activity of kinesin and dyneine, resulting in interference with neuronal intracellular transport and sperm motility. Glycidamide binds to various proteins and DNA.

Interactive software automates personalized radiation safety plans for Na131I therapy.

NRC regulations have liberalized the criteria for release from control of patients administered radioactive materials but require written radiation safety instruction if another individual is expected to receive more than 1 mSv. This necessitates calculation of expected doses, even when the calculated maximum likely dose is well below the 5 mSv release criterion. NRC interpretations of the regulation provide the biokinetic model to be used to evaluate the release criterion for patients administered Na131I, but do not provide guidance as to either the specifics of minimizing the dose of others or the length of time restrictions should remain in effect.

Fast axonal transport: a site of acrylamide neurotoxicity?

The cellular and molecular site and mode of action of acrylamide (ACR) leading to neurotoxicity has been investigated for four decades, without resolution. Although fast axonal transport compromise has been the central theme for several hypotheses, the results of many studies appear contradictory. Our analysis of the literature suggests that differing experimental designs and parameters of measurement are responsible for these discrepancies.

Acrylamide-induced cellular transformation.

Acrylamide is a monomer of polyacrylamide, whose products are used in biochemistry, the manufacture of paper, water treatment, and as a soil stabilizer. While polymeric acrylamide is nontoxic, the monomer can cause several toxic effects and has the potential for human occupational exposure. While acrylamide is not mutagenic in prokaryotic mutagenesis assays, chronic acrylamide treatment in rodents has been shown to produce tumors in both rats and mice.