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PubMed1999

Biomonitoring of exposure to ethylene oxide and propylene oxide by determination of hemoglobin adducts: correlations between airborne exposure and adduct levels.

OBJECTIVES: Ethylene oxide (EO) and propylene oxide (PO) are important industrial chemicals. Exposure to these directly acting mutagens may be monitored by determination of their adducts to hemoglobin (Hb). This study establishes correlations between airborne concentrations of EO and PO and their Hb adducts in petrochemical workers. METHODS: In three different studies conducted during maintenance shutdown of petrochemical plants the external occupational exposure to EO and PO was assessed by personal air monitoring (PAM). The internal exposure to EO and PO was concomitantly assessed by determination of N-(2-hydroxyethyl)valine (HOEtVal) and N-(3-hydroxypropyl)valine (HOPrVal) in blood samples of the operators using the N-alkyl-Edman degradation method. RESULTS: In the first study, PAM was applied once a month at random over a period of 4 months. Blood samples for Hb-adduct determination were collected at the end of this period. No significant correlation was found between PAM and Hb-adduct data. In the next two studies, PAM was applied to the operators during the entire shift on every working day during the shutdown. Blood samples were collected before and immediately after the shutdown period. Highly significant correlations were found between the increment in the concentration of HOEtVal and HOPrVal over this period and the total exposure to EO and PO, respectively. CONCLUSIONS: Time-integrated exposure to EO or PO can be readily and reliably assessed by measurement of the concentration of HOEtVal or HOPrVal in a small blood sample. In workers occupationally exposed to low concentrations of EO or PO, good correlations were found between these Hb adducts and the airborne concentrations of EO and PO. These correlations allow the calculation of tentative biological exposure limits (BELs) for EO and PO. At the current Dutch occupational exposure limit (OEL) for EO (0.84 mg m(-3), 8-h TWA) the BEL is 3.2 nmol HOEtVal/g globin. At the value of 10 mg m(-3) (8-h TWA), which is currently being investigated as the new Dutch OEL for PO, the corresponding BEL is 5.3 nmol HOPrVal/g globin.

Air Pollutants, Occupational↗

PubMed2005

Mixed-effects variance components models for biometric family analyses.

Recent substantive research on biometric analyses of twin and family data has used both a biometric path analysis model (PAM) and a biometric variance components model (VCM). Methodological research on these same topics have suggested benefits of using linear structural equation model algorithms (SEMA) as well as mixed effect multilevel algorithms (MEMA). To better understand the potential similarities and differences among these approaches we first highlight the algebraic equivalence between the standard biometric PAM and the corresponding biometric VCM models for family data. Second, we demonstrate how several SEMA programs based on either the PAM or VCM approach produce equivalent estimates for all phenotypic and biometric parameters. Third, we show how the biometric VCM approach (but not the PAM approach) can be easily programmed using current MEMA programs (e.g., SAS PROC MIXED). We then expand the scope of these different approaches to include measured covariates, observed variable interactions and multiple relatives within each family. MEMA software is compared to SEMA software for programming complex models, including the flexibility of data input, treatment of missing data, inclusion of covariates, and ease of accommodating varying numbers of observations (per family or individual).

Algorithms↗

PubMed1991

A colorimetric assay for measuring peptidylglycine alpha-amidating monooxygenase using high-performance liquid chromatography.

In many peptide hormones and neuropeptides, the carboxy-terminal alpha-amide structure is essential in eliciting biological activity. In the present study, a rapid and sensitive assay method for the determination of peptidylglycine alpha-amidating monooxygenase (PAM) activity has been reported. This method is based on the monitoring of the absorption at 460 nm of 4-dimethylaminoazobenzene-4'-sulfonyl-Gly-L-Phe-NH2 (Dabsyl-Gly-Phe-NH2), enzymatically formed from the substrate 4-dimethylaminoazobenzene-4'-sulfonyl-Gly-L-Phe-Gly, after separation by high-performance liquid chromatography (HPLC) using a C-18 reversed-phase column by isocratic elution. This method is sensitive enough to measure Dabsyl-Gly-Phe-NH2 at concentrations as low as 1 pmol and yield highly reproducible results and requires less than 5 min per sample for separation and quantitation. The concentrations of copper and ascorbic acid required for maximal enzyme activity were 1 microM and 2 mM, respectively. The pH optimum for PAM activity was 5.0 to 5.5. The Km and Vmax values were respectively 3.5 microM and 100 pmol/micrograms/h with the use of enzyme extract obtained from bovine pituitary. By using this method, PAM activity could be readily detected in a single rat saliva. The sensitivity of this assay method will also aid in the effort to examine the regulation of in vivo PAM activity.

Amino Acid Sequence↗

PubMed1992

Alkylation of cysteine with acrylamide for protein sequence analysis.

Alkylation of cysteine in proteins with acrylamide under mildly alkaline conditions yields a thioether derivative, Cys-S-beta-propionamide (Cys-S-Pam), which is stable during automated Edman degradation. Its phenylthiohydantoin derivative, PTH-Cys-S-Pam, is easily separated from other PTH-amino acids by HPLC and is thus useful for cysteine identification during protein sequencing. PTH-Cys-S-Pam was first noticed during sequencing polypeptides blotted onto polyvinylidene difluoride membranes from polyacrylamide gels, in which cysteine had reacted with residual unpolymerized acrylamide. Cysteine in proteins is easily alkylated by reaction of proteins in aqueous solution with acrylamide. Methods are also presented for alkylation of cysteine in proteins adsorbed on fiberglass disks in the reaction cartridge of a protein sequencer. Finally, PTH-Cys-S-Pam was synthesized chemically. The synthetic compound is unstable in neutral solution, but can be stabilized by acidification. It has the same HPLC retention time as the product formed from cysteine when sequencing proteins alkylated with acrylamide.

Acrylamide↗

PubMed1986

Cigarette smoke-induced alterations in the release of arachidonate metabolites by pulmonary alveolar macrophage from selenium-fed and selenium-deficient rats.

Male weanling F-344 rats were maintained on selenium-supplemented or -deficient diets and were exposed to fresh cigarette smoke daily for 28 weeks. The deficient status of animals was demonstrated by a significant reduction in the pulmonary and hepatic glutathione peroxidase (GSH-Px) activity of rats on selenium-deficient diet. Sham and smoke treatment did not influence the GSH-Px activity in either diet group. Elevated levels of blood carboxyhemoglobin and pulmonary aryl hydrocarbon hydroxylase activity in the smoke-exposed rats of both diet groups indicated effective inhalation of cigarette smoke by animals. Studies of the extracellular release of arachidonate metabolites by pulmonary alveolar macrophages (PAMs) indicated that resting cells released small amounts of prostaglandin E2 (PGE2), thromboxane B2 (TXB2) and leukotriene B4 (LTB4). Upon phagocytic challenge by opsonized zymosan particles, the release of the three metabolites was substantially increased in all diet and treatment groups. While the release of cyclooxygenase products, PGE2 and TXB2, remained unaffected by cigarette smoke, an inhibition of approximately 50% in the release of lipoxygenase product, LTB4, was observed in cells from selenium-fed animals. In selenium-deficient animals, cigarette smoke almost completely inhibited (greater than 80%) the zymosan-stimulated release of LTB4 by PAMs and additionally caused about 50% reduction in TXB2 release. These results suggest a specific inhibition of lipoxygenase pathway by cigarette smoke in PAMs of selenium-fed rats and suggest that cigarette smoke may additionally impair enzymes of the cyclooxygenase pathway in PAMs of selenium-deficient animals.

Administration, Oral↗

PubMed1987

Oxime-induced decarbamylation and atropine/oxime therapy of guinea pigs intoxicated with pyridostigmine.

The generally accepted explanation for the effects of oximes in countering organophosphorus (OP) anticholinesterase is reactivation of the inhibited acetylcholinesterase (AChE). With soman, the inhibited AChE rapidly becomes resistant to oxime reactivation due to a phenomenon called aging. Thus, pretreatment with pyridostigmine (Py) or physostigmine (Ph) followed by atropine sulfate therapy is required to achieve significant protection against soman; the effectiveness of a pretreatment/therapy (P/T) regimen can be further increased against certain OPs (e.g. sarin and VX) by including an oxime in the therapy regimen. The P/T regimen is clouded by a controversy concerning the use of oximes in the treatment of carbamate intoxication, because 2-PAM has been reported to exacerbate intoxication by some carbamates and to have no effect on decarbamylation rates. To better understand the role of oxime therapy in the theory of pretreatment of OP intoxication we examined the effects of 2-PAM and HI-6 on the rate of decarbamylation of Py-inhibited erythrocyte AChE in vitro and in vivo, and studied the effects of atropine plus 2-PAM or HI-6 on Py toxicity. In decarbamylation experiments, Py-inhibited guinea pig erythrocytes were washed free of excess Py and incubated with vehicle or oxime (2 X 10(-4) M, pH 7.3 and 37 degrees C). Aliquots were assayed for AChE activity at various times during a 60 min incubation period. Rate constants were calculated and compared to determine whether the presence of oxime affected decarbamylation. The data from in vitro and in vivo experiments revealed that oximes accelerated the decarbamylation (p less than 0.05) of inhibited AChE. Lethality data for Py-treated guinea pigs showed that treatment with atropine (23 mumoles/kg, im) plus 2-PAM or HI-6 (145 mumoles/kg, im) at one min after injection of Py increased the protective ratio from 4.2 (atropine only) to 5.1 and 12.2, respectively. It is suggested that the enhanced therapeutic efficacy of atropine by oximes against Py intoxication is related to oxime-induced reactivation.

Acetylcholinesterase↗

PubMed1987

Cell and species differences in metabolic activation of chemical carcinogens.

Metabolic activation and DNA binding of aflatoxin B1 (AFB1), N-nitrosodimethylamine (DMN) and benzo[a]pyrene (B[a]P) were compared in human, rat and mouse hepatocytes and human pulmonary alveolar macrophages (PAM). The degree of carcinogen activation by hepatocytes and PAM was measured by cell-mediated mutagenesis assays in which co-cultivated Chinese hamster V79 cells were used to monitor mutagenic metabolites. Hepatocytes from human, mouse and rat metabolized DMN and released the active metabolites to induce either ouabain- or 6-thioguanine-resistant mutation. The mutation frequencies mediated by hepatocytes of the 3 animal species were approximately 3-9 mutants/10(5) survivors at a concentration of 0.2 mM DMN. The variations of radioactivity bound to liver cell DNA were relatively small in cultured mouse, rat, and human hepatocytes exposed to 14C label DMN (0.5 mM) and the binding values were in a range of 6-12 X 10(3) pmoles/mg DNA. However, rat hepatocytes were at least 10-fold more effective than either human or mouse hepatocytes in generating mutagenic metabolites of AFB1 and also had a much higher AFB1 metabolite DNA-binding value. The AFB1 DNA-binding levels were 4.1, 12-27 (range), 120 pmoles/mg DNA respectively in mouse, human, and rat liver cells following AFB1 (3.3 microM) exposure for 20 h. Hepatocytes from the 3 animal species were unable to mediate mutation in the presence of 4 microM B[a]P; PAM activated B[a]P and effectively mediated mutation in the co-cultivated V79 cells. In contrast to results with hepatocytes, PAM failed to generate enough mutagenic metabolites of AFB1 (3.3 microM) and the mediation of mutations was seen only at very high concentration of DMN (80 mM). The genotoxic effects of the 3 carcinogens on hepatocytes from different species in vitro were in agreement with the in vivo animal experiments in that mice are relatively resistant to AFB1 carcinogenesis whereas rats are sensitive; B[a]P is not effective as a complete liver carcinogen in adult rat and mouse whereas DMN induces liver cancer.

Aflatoxin B1↗

PubMed1991

Human ovarian cancer cell lines resistant to cisplatin, doxorubicin, and L-phenylalanine mustard are sensitive to delta 7-prostaglandin A1 and delta 12-prostaglandin J2.

The antitumor activity of delta 7-prostaglandin A1 (delta 7-PGA1) or delta 12-prostaglandin J2 (delta 12-PGJ2) on human ovarian cancer cell lines resistant to cisplatin (CDDP), doxorubicin (ADR), and L-phenylalanine mustard (l-PAM) was studied in vitro. A2780AD, A2780 (parent cells of A2780AD), 2008DDP, and 2008 cells (parent cells of 2008DDP) were used. The antitumor activities of the drugs were defined with 50% inhibitory concentration (IC50) estimated from growth inhibition curves, which were obtained by an indirect colorimetric method. Drug-resistance ratios obtained from IC50 values, by comparing A2780AD and A2780 cells, were 62.5 for ADR, 4.6 for CDDP, 4.9 for l-PAM, 1.5 for delta 7-PGA1, and 1.8 for delta 12-PGJ2. Those obtained by comparing 2008DDP and 2008 cells were 1.1 for ADR, 16.0 for CDDP, 2.9 for l-PAM, 2.3 for delta 7-PGA1, and 3.2 for delta 12-PGJ2. Thus some human ovarian cancer cells resistant to ADR, CDDP, and l-PAM remain sensitive to antitumor PGs.

Antineoplastic Agents↗

PubMed1988

Ontogenesis of peptidylglycyl alpha-amidation activity in the mouse hypothalamus in vivo and in serum-free medium cultures. Relation with thyroliberin (TRH) accumulation and release in vitro.

The influence of peptidylglycine alpha-amidating monooxygenase (PAM) and of its co-factor, ascorbate, were studied in relation to thyroliberin (TRH) activity during mouse hypothalamus development. In vivo, PAM activity developed slowly at fetal stages, and exhibited a sharp rise around the 5th-8th postnatal day, the adult level being reached around day 15. The same developmental pattern was observed when studied in serum-free cultures initiated from fetal mouse hypothalamus. Using this in vitro model, we investigated the effects of ascorbate, a necessary co-factor of PAM, on TRH. Upon ascorbate supplementation of the culture medium, the TRH accumulation normally occurring in our cultures was further enhanced. The half maximum effect was attained with 20 microM, and the amplitude of the response to ascorbate was maximum around 9-13 days in vitro. Moreover, ascorbate increased to an even larger extent the amounts of TRH released upon chemical depolarization. These results are consistent with a direct role of ascorbate on PAM activity, but other more general effects on the maturation of the neuronal response to physiological stimuli cannot be excluded.

Age Factors↗

PubMed1984

Theophylline reversal of alkylator-induced replicon initiation inhibition: no correlation with DDP-induced cytotoxicity.

The synergistic cytotoxic activity exhibited by bifunctional alkylating agents in the presence of methylxanthines has been associated with methylxanthine-induced reversal of alkylator-induced DNA replicon initiation inhibition. This has also been seen with methylxanthines and ionizing irradiation. Methylxanthines do not appear exacerbate drug or ionizing radiation-induced damage. We report here a situation in which methylxanthine-induced reversal of DNA replicon initiation inhibition is not associated with increased cytotoxicity of the alkylator. Murine L1210 leukemia cells were assayed for cytotoxicity following treatment with either L-PAM or cis-DDP in the presence or absence of theophylline. Theophylline increased the cytotoxicity seen after L-PAM treatment but failed to increase the cis-DDP induced cytotoxicity. Analysis of pulse-labeled DNA on alkaline sucrose gradients revealed the expected decrease in DNA replicon initiation in L1210 cells treated with either L-PAM or cis-DDP. Theophylline had no effect on replicon initiation in untreated cells. Theophylline reversed the replicon initiation inhibition in cells treated with either L-PAM or cis-DDP. The reason for the apparent lack of added toxicity of the replicon initiation inhibition reversal in L1210 cells treated with theophylline and DDP is unknown.

Animals↗

PubMed1990

Comparison of sister-chromatid exchange frequencies in mouse T- and B-lymphocytes after exposure to 4-hydroxycyclophosphamide or phosphoramide mustard.

The present study was designed to investigate the genotoxicity of 4-hydroxycyclophosphamide (4-OHCP) and phosphoramide mustard (PAM), both reactive metabolites of cyclophosphamide (CP), for possible differences in SCE-inducing activity in mouse T- and B-lymphocytes. Mouse peripheral blood lymphocytes were isolated and stimulated to divide with either phytohemagglutinin (T-cell mitogen) or lipopolysaccharide (a polyclonal B-cell activator). Significant concentration-dependent increases in SCE frequencies were observed for both 4-OHCP and PAM with both mitogens, with 4-OHCP being almost twice as potent as PAM. There was no difference in SCE response between T- and B-lymphocytes after exposure to either PAM or 4-OHCP. These data do not support the idea that the difference in SCE response in T- and B-lymphocytes by CP in vivo is due to differential responses to either of the proposed putative metabolites of CP.

Animals↗

PubMed1994

Rate constants of carbamylation and decarbamylation of acetylcholinesterase for physostigmine and carbaryl in the presence of an oxime.

Membrane-bound bovine erythrocyte acetylcholinesterase was inhibited with physostigmine or carbaryl, and the rate constants of carbamylation and decarbamylation were determined from the proportion of inhibited acetylcholinesterase in the steady state, and the rate of approach to the steady state. The oximes 2-PAM, HI-6, HS-6, TMB-4 and toxogonin, at 0.1 mM, all decreased the rate of carbamylation by physostigmine, but increased the rate of carbamylation by carbaryl. TMB-4 and toxogonin were the most effective oximes in potentiating carbamylation by carbaryl, with an enhancement of the second-order rate constant of 54- and 17-fold respectively. The greatest reduction in the rate constant for carbamylation by physostigmine (3.7-fold) was caused by HI-6. HS-6 and HI-6 increased the rate of decarbamylation, while 2-PAM reduced the rate of decarbamylation if physostigmine was the carbamate. 2-PAM and HI-6 were also studied with soluble bovine erythrocyte acetylcholinesterase, and similar results were obtained. The results extend those in a recent report by other authors who studied the half-life of carbamylation for acetylcholinesterase and butyrylcholinesterase in an attempt to understand the mechanism by which oximes increase the toxicity of carbaryl in vivo. These authors proposed binding of the oximes to an allosteric site on the enzyme. While not discounting this possibility, the present results, taken with other reports in the literature, suggest that binding of the oximes to the anionic subsite of the active site of the enzyme is also feasible. The present results also offer an explanation for another recent report, in which anomalous results were presented for decarbamylation of physostigmine-inhibited and carbaryl-inhibited erythrocyte acetylcholinesterase in the presence of 2-PAM or HI-6.

Acetylcholinesterase↗

PubMed1985

Alterations of alveolar macrophage function and level of bronchopulmonary protease inhibitors in O,O,S-trimethyl phosphorothioate-induced lung injury.

O,O,S-Trimethyl phosphorothioate (OOS-TMP), an impurity present in widely used organophosphorus insecticides, has been shown to induce pneumotoxicity after oral administration. To date very little is known about the pathogenesis of the injury. Protease-anti-protease imbalance has been proposed as a mechanism of various lung injuries; thus, the effect of OOS-TMP on alpha 1-protease inhibitor capacity, pulmonary alveolar macrophage (PAM) esterases, cytotoxic activity and on specific esterase inhibitors in the bronchopulmonary lavage fluid and serum were measured. OOS-TMP (20 mg/kg) administered orally to rats produced a 27% increase in PAM esterase activity 6 h after treatment. The activity then declined to 63% of control value on day 3 and had not recovered to any significant extent on day 7. The cytotoxic activity of PAM was significantly increased at 6 h and 24 h following treatment. Chymotrypsin inhibitory capacity (CIC) of the lavage fluid was decreased by 45% at 6 h but recovered rapidly and reached control levels by 24 h. Trypsin inhibitory capacity (TIC) of serum was affected to a lesser extent such that no change was detected after 6, 12 or 24 h. These data, early elevation of PAM esterase levels with a concomitant increase in cytotoxic activity and decreased TIC and CIC in bronchopulmonary lavage fluid, support the view that pathogenesis of OOS-TMP produced lung injury could be due to increased protease levels.

Administration, Oral↗

PubMed1984

The effect of timing on chemosensitization by clinical levels of SR-2508.

The nitroimidazole SR-2508 is currently being tested clinically as a radiosensitizer. Its relatively low toxicity allows it to be used at higher doses than misonidazole so that its potential as a chemosensitizer is also of considerable interest. Multiple injections of SR-2508 were given to SCC VII/St tumor-bearing mice to achieve a clinically realistic plasma concentration of approximately 300 micrograms/ml over 8 hrs. Single doses of melphalan (L-PAM) or cyclophosphamide (CY) were given at different times after the first SR 2508 injection. With L-PAM, a delay of at least 2 hr was necessary before enhancement of L-PAM cytotoxicity was observed. A similar result was obtained when a simulation was carried out with SCC VII/St tumor cells in vitro. Results with CY were less clear, although the most consistent enhancement was observed when a 4 to 8 hr interval elapsed between the beginning of SR 2508 exposure and the CY injection. In general, although precise timing was not essential for enhancement, an interval of at least 4 hr is recommended between the administration of SR 2508 and either alkylating agent. This is particularly important for L-PAM where no enhancement would be expected if the drugs were given simultaneously.

Animals↗

PubMed1995

Enhanced host cell reactivation capacity and expression of DNA repair genes in human breast cancer cells resistant to bi-functional alkylating agents.

Human breast carcinoma (MCF7-MLNr) cells resistant to the bifunctional drugs L-phenylalanine mustard (L-PAM, 5-fold resistance), mechlorethamine (9-fold), cisplatin (3-fold), and BCNU (3-fold) were used to investigate the role of DNA repair in the development of resistance to alkylating agents. We have previously shown that neither L-PAM transport and metabolism nor glutathione-associated enzymes were altered in MCF7-MLNr cells, compared to the sensitive cells MCF7-WT. This study shows that treatment of pRSV-CAT plasmid with L-PAM at concentrations up to 1 microM proportionally inhibit the expression of chloramphenicol acetyl transferase (CAT) activity, while higher concentrations abolished CAT activity. pRSV-CAT reactivation was significantly increased when plasmid was transfected into MCF7-MLNr cells, compared to MCF7-WT cells. This indicates that resistant cells have more efficient capacity to recognize and repair L-PAM induced DNA damage. The mRNA expression of DNA nucleotide excision repair genes ERCC1, XPD (ERCC2), XPB (ERCC3), and polymerase beta was found to be similar in both the MCF7-WT and MCF7-MLNr cells. Western blot analysis also reveals no difference in the expression of ERCC1, AP endonuclease, poly (ADP-ribose) polymerase, and alkyl-N-purine-DNA glycosylase proteins. The lack of correlation between enhanced host cell reactivation capacity in resistant cells, and the expression of these specific DNA repair genes suggests that proteins encoded by these genes are not rate limiting steps for resistance to bi-functional alkylating drugs in human breast cancer cells.

Adenocarcinoma↗

PubMed2005

Mitochondrial presequence translocase: switching between TOM tethering and motor recruitment involves Tim21 and Tim17.

The presequence translocase of the inner mitochondrial membrane (TIM23 complex) operates at a central junction of protein import. It accepts preproteins from the outer membrane TOM complex and directs them to inner membrane insertion or, in cooperation with the presequence translocase-associated motor (PAM), to the matrix. Little is known of how the TIM23 complex coordinates these tasks. We have identified Tim21 (YGR033c) that interacts with the TOM complex. Tim21 is specific for a TIM23 form that cooperates with TOM and promotes inner membrane insertion. Protein translocation into the matrix requires a switch to a Tim21-free, PAM bound presequence translocase. Tim17 is crucial for the switch by performing two separable functions: promotion of inner membrane insertion and binding of Pam18 to form the functional TIM-PAM complex. Thus, the presequence translocase is not a static complex but switches between TOM tethering and PAM binding in a reaction cycle involving Tim21 and Tim17.

Amino Acid Sequence↗

PubMed2006

Development and validation of a new fluorescence-based bioassay for aquatic macrophyte species.

Bioassays with unicellular algae are frequently used as ecotoxicological test systems to evaluate the toxicity of contaminated environmental samples or chemicals. In contrast, aquatic macrophyte test systems are still rarely used as they are laborious to handle because species exhibit distinct ecological requirements. The aim of this study was to establish a fast and reproducible measuring system for aquatic macrophyte species to overcome those limitations for use. Thus, a newly developed pulse-amplitude modulated chlorophyll fluorometer (Imaging-PAM) was applied as an effect detection in short-term bioassays with aquatic macrophyte species. This multiwell-plate-based measuring device enables the incubation and measurement of up to 24 samples in parallel. The Imaging-PAM was used (i) to establish and validate the sensitivity of the test systems to three Photosystem II (PSII) inhibitors (atrazine, prometryn, isoproturon), (ii) to compare the test systems with established biotests for macrophytes and (iii) to define necessary time scales in aquatic macrophyte testing. The results showed that fluorescence-based measurements with the Imaging-PAM allow rapid and parallel analysis of large amounts of aquatic macrophyte samples and of toxicants effects of the PSII inhibitors tested on aquatic macrophytes. Measurements revealed a good correlation between obtained median effective concentrations (EC50s) for the new and the established biotest systems. Hence, the Imaging-PAM measuring device is a promising tool to allow fast chemical effect screening for high amounts of samples with little time and material and thus offers scope for high-throughput biotesting using aquatic macrophyte species.

Atrazine↗

PubMed2006

Relative curing degree of polyacid-modified and conventional resin composites determined by surface Knoop hardness.

OBJECTIVES: The aim of the present study was to investigate the relative curing degree at a depth of 2 mm of several polyacid-modified composites (PAM-Cs) as a function of shade. METHODS: The Knoop hardness of the irradiated top and non-irradiated bottom surfaces of 2 mm thick samples of the PAM-Cs Hytac, F2000, Glasiosite, Dyract, Dyract AP, and Compoglass F and of the resin composites Z100, Herculite Enamel XRV, and Durafill VS, were determined for shades A2 and A4. RESULTS: The top and bottom hardness of F2000 and Glasiosite ranged between that of the two composites Herculite and Z100. Compoglass, Dyract and Dyract AP had a lower top and bottom hardness than the hybrid composites, but higher than that of the microfilled composite Durafill. The top hardness of Hytac compared with that of the first group, whereas the bottom hardness compared with the second group. The bottom-to-top KHN ratio reflecting the relative curing degree at a depth of 2 mm was less than 80% for the two shades of Hytac and Compoglass as well as for the A4 shade of Dyract AP and Herculite. SIGNIFICANCE: A hard top surface of a PAM-C is not an indication of adequate in depth polymerization. Shade A2 results in significantly greater values for the curing degree compared to shade A4, the effect depending quantitatively on the formulation of the material. Some formulations of PAM-C do not reach an adequate curing degree at a depth of 2 mm so that it is recommended to apply the incremental technique even in box-only cavities with layers of maximum 2 mm.

Color↗