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PubMed1995

Sodium arsenite induces chromosome endoreduplication and inhibits protein phosphatase activity in human fibroblasts.

Arsenic, strongly associated with increased risks of human cancers, is a potent clastogen in a variety of mammalian cell systems. The effect of sodium arsenite (a trivalent arsenic compound) on chromatid separation was studied in human skin fibroblasts (HFW). Human fibroblasts were arrested in S phase by the aid of serum starvation and aphidicolin blocking and then these cells were allowed to synchronously progress into G2 phase. Treatment of the G2-enriched HFW cells with sodium arsenite (0-200 microM) resulted in arrest of cells in the G2 phase, interference with mitotic division, inhibition of spindle assembly, and induction of chromosome endoreduplication in their second mitosis. Sodium arsenite treatment also inhibited the activities of serine/threonine protein phosphatases and enhanced phosphorylation levels of a small heat shock protein (HSP27). These results suggest that sodium arsenite may mimic okadaic acid to induce chromosome endoreduplication through its inhibitory effect on protein phosphatase activity.

Arsenites↗

PubMed2006

Precursor ion scanning for the non-targeted detection of individual arsenosugars in extracts of marine organisms.

Arsenosugars are a group of arsenic compounds reported to be present in a wide variety of marine organisms. Numerous such compounds have been identified and characterized in marine organisms; however, unknown arsenosugar species may also be present. This indicates the need for an analytical technique suitable for their non-targeted detection. One such technique is tandem mass spectrometry operated in the precursor ion scanning mode. This technique is based on scanning for precursor ions that give specific product ions, characteristic of the compounds under investigation. In the present study two subgroups of arsenosugar species were examined, the oxo- and the thioarsenosugars, the CID behavior of which is well known from previous studies. In the case of the oxoarsenosugars characteristic product ions were observed at m/z 237 and 97, and for the thioarsenosugars at m/z 253 and 97. Validation of this approach was carried out by analyzing extracts of two commercial kelp powders with known contents of arsenosugar species. All arsenosugars reported to exist in these materials were detected successfully using the precursor ion scanning approach. The limits of detection for the oxo- and the thioarsenosugar species, and the selectivity and sensitivity of the method, strongly indicate the suitability of this approach for the non-targeted detection of arsenosugars in extracts of marine origin.

Animals↗

PubMed2003

Assessment of effects of chromated copper arsenate (CCA)-treated timber on nontarget epibiota by investigation of fouling community development at seven European sites.

To assess the effect of the anti-marine-borer timber preservative CCA (a pressure-impregnated solution of copper, chromium, and arsenic compounds) on nontarget epibiota, fouling community development was investigated. Panels of Scots pine treated to target retentions of 12, 24, and 48 kg CCA per m3 of wood (covering the range of retentions recommended for marine use) plus untreated controls were submerged at seven coastal sites (Portsmouth, UK; La Tremblade [two sites], France; Ria Formosa, Portugal; Sagres, Portugal; Kristineberg, Sweden; Athens, Greece). The fouling community on the surfaces of the panels was assessed both qualitatively and quantitatively after 6, 12, and 18 months of exposure. Multivariate statistical methods were used to compare community structure between panel treatments. Panels treated to the three CCA loadings supported very similar fouling assemblages, which in most cases had higher numbers of taxa and individuals than assemblages on untreated panels. No detrimental effects on epibiota due to CCA preservatives were detected at any of the treatment levels at all seven exposure sites, suggesting that the range of environmental conditions at the sites had no bearing on preservative impact on fouling biota. Differences in community structure between CCA-treated and untreated panels may be due to enhanced larval settlement on CCA-treated timber by some species as a result of modifications to the surface properties of the timber by the preservative. Possible reasons for the higher numbers of certain species on the surface of CCA-treated panels are discussed.

Animals↗

PubMed2003

Arsenicals (melarsoprol), pentamidine and suramin in the treatment of human African trypanosomiasis.

Human African trypanosomiasis (HAT), otherwise known as sleeping sickness, has remained a disease with no effective treatment. Recent progress in HAT research suggests that a vaccine against the disease is far from being successful. Also the emergence of drug-resistant trypanosomes makes further work in this area imperative. So far the treatment for the early stage of HAT involves the drugs pentamidine and suramin which have been very successful. In the second stage of the disease, during which the trypanosomes reside in the cerebrospinal fluid (CSF), treatment is dependent exclusively on the arsenical compound melarsoprol. This is largely due to the inability to find compounds that can cross the blood brain barrier and kill the CSF-residing trypanosomes. This review summarises our current understanding on the treatment of HAT.

Animals↗

PubMed2004

Comparison of the cytotoxicity induced by different exposure to sodium arsenite in two fish cell lines.

Arsenic, a common environmental pollutant, is toxic to many mammalian cells. However, the arsenic-induced toxicity to aquatic animal species is unclear. This study attempted to compare the arsenic-induced cytotoxicity in various fish cells. Two fish cell lines, JF (fin cells of Therapon jarbua) and TO-2 cells (ovary cells of Tilapia), were treated with sodium arsenite in two ways to mimic acute and subacute exposure. The distinguishable alterations of cell morphology and microtubule network were observed in the cells treated by two arsenite exposure protocols. By the colony-forming assay, we demonstrated that the survival of both cell lines, treated with the high concentrations of arsenite (20-160 microM) for 2 h or with the low concentrations (0.125-10 microM) for 24 h, was decreased in a dose-dependent manner. The difference between the susceptibility of JF and TO-2 cells to arsenite was revealed by the factorial ANOVA to compare the survival rates of the arsenite-treated cells; JF cells were more sensitive than TO-2 cells (P = 0.008 and 0.013 for the high-concentration and the low-concentration treatment, respectively). The possible mechanisms to provoke the cytotoxicity of arsenite in two cell lines were also addressed. Antioxidants, N-acetyl-cysteine and dithiothreitol, significantly prevented JF cells, but not TO-2 cells, from the arsenite-induced inhibition of survival. Additionally, apparent apoptosis of JF cells and a mitotic arrest of TO-2 cells in response to the treatment of arsenite were also demonstrated by the DNA-fragmentation analysis and the flow cytometric analysis of cell-cycle progression. The results indicate that sodium arsenite induces apoptosis in JF cells probably by causing oxidative stress and disturbs the cell cycle of TO-2 cells. These two fish cell lines can serve as the potential tools to in detail study the toxicity and the hazards of arsenic compounds to aquatic animals at molecular level in the future.

Acetylcysteine↗

PubMed2006

Arsenite interactions with phospholipid bilayers as molecular models for the human erythrocyte membrane.

There are scanty reports concerning the effects of arsenic compounds on the structure and functions of cell membranes. With the aim to better understand the molecular mechanisms of the interaction of arsenite with cell membranes we have utilized bilayers of dimyristoylphosphatidylcholine (DMPC) and dimyristoylphosphatidylethanolamine (DMPE), representative of phospholipid classes located in the outer and inner monolayers of the human erythrocyte membrane, respectively. The capacity of arsenite to perturb the bilayer structures was determined by X-ray diffraction and fluorescence spectroscopy, whilst the modification of their thermotropic behaviour was followed by differential scanning calorimetry (DSC). The experiments carried out by X-ray diffraction and calorimetry clearly indicated that NaAsO(2) interacted with DMPE and modified its thermotropic behaviour. No such information has been so far reported in the literature.

Arsenites↗

PubMed2004

Sensitive method for the determination of roxarsone using solid-phase microextraction with multi-detector gas chromatography.

We describe the development, optimization, and application of a novel method for the unequivocal identification and quantification of roxarsone (3-nitro-4-hydroxyphenylarsonic acid, 3-NHPAA) at low microg L(-1) levels. The method is based on capillary gas-liquid chromatography with parallel quadrupole ion-trap mass spectrometric (QIT-MS) and pulsed flame photometric detection (PFPD). The sensitive method couples the arsenic specificity of PFPD with the high selectivity of molecular MS for the determination of roxarsone, dimethylarsenic acid (DMAA), and monomethylarsonic acid (MMAA) in complex matrices. Analytes were derivatized based on the approach we previously reported [B. Szostek, J.H. Aldstadt, J. Chromatogr. A 807 (1998) 253 and D.R. Killelea, J.H. Aldstadt, J. Chromatogr. A 918 (2001) 169] for the reaction of organoarsenicals with 1,3-propanedithiol (PDT). The cyclic dithiaarsenolines formed were extracted from the sample matrix in the liquid phase by solid-phase microextraction (SPME). The optimized SPME conditions employed a 65 microm polydimethlysiloxane-divinylbenzene (PDMS-DVB) fiber, extraction temperature of 70 degrees C and fiber equilibration time of 15.0 min. The mass spectrum of the dithiaarsenoline of roxarsone showed a base peak that corresponded to the predicted structure at m/z 319 and the tell-tale peak of an arsenic compound derivatized with PDT at m/z 181. Further peaks at m/z 149 and 228 were observed and found to be unique to roxarsone, formed by an interesting internal rearrangement of the ONOH functionality. A linear calibration model was prepared for roxarsone over an environmentally relevant range (0.0-100 microg L(-1)) and a detection limit of 2.69 microg L(-1) (3sigma) was observed. The method was applied to several fortified environmental surface water samples (50 microg L(-1)) where the average recovery for roxarsone was 103+/-10.9%.

Calibration↗

PubMed2001

Toxicity of chromated copper arsenate (CCA)-treated wood to non-target marine fouling communities in Langstone Harbour, Portsmouth, UK.

The effect of the anti-marine-borer timber preservative chromated copper arsenate (CCA) (a pressure impregnated solution of copper, chromium and arsenic compounds) on non-target marine fouling animals was investigated during a subtidal exposure trial. Panels of Scots pine treated to target retentions of 12, 24 and 48 kg CCA per m-3 of wood, plus untreated controls were submerged at a coastal site on the south coast of the UK for 6, 12 and 18 months. After each exposure period the fouling communities that formed on the surface of panels were assessed both qualitatively and quantitatively. Community structure was similar on panels treated to the three CCA loadings, but was significantly different from community structure on untreated panels. The total number of species (species richness) was similar on all panels, although the number of individual organisms attached to the surface of panels was significantly higher on CCA-treated panels than on untreated panels. k-dominance curves revealed that the difference in numbers of individuals between CCA-treated and untreated panels was caused by higher numbers of the dominant species (Elminius modestus, Hydroides ezoensis, and Electra pilosa) on CCA-treated panels. Other species were present in similar numbers on panels of all treatments. Results indicate that there are no detrimental toxic effects to epibiota caused by the presence of CCA preservative within the matrix of the wood at any of the treatment levels. Differences in community structure between CCA-treated and untreated panels may be due to enhanced larval settlement on CCA-treated timber by some species as a result of modifications to the surface properties of the timber by the CCA preservative.

Animals↗

PubMed2001

Effects of chromated copper arsenate (CCA) wood preservative on early fouling community formation.

The effects of the anti-marine-borer timber preservative CCA (a pressure impregnated solution of copper, chromium and arsenic compounds) on early fouling community formation were investigated during a number of field trials. The formation of a biofilm on the surface of CCA-treated and untreated timber panels of Scots pine was examined by scanning electron microscopy following submersion in Langstone Harbour, Portsmouth, UK for periods of 2, 7, 14 and 28 days. Results indicated a slightly faster rate of biofilm formation after 2 and 7 days of exposure on untreated timber compared to CCA-treated timber, although no differences were visible between panels after 14 and 28 days exposure, or between panels treated to different CCA loadings after all exposure periods. Settlement of the serpulid Ficopomatus enigmaticus and two species of barnacles (Elminius modestus and Balanus crenatus) onto the surface of untreated and CCA-treated panels of Scots pine was examined following 4 weeks exposure in a brackish water millpond at Emsworth, West Sussex. Numbers of individuals were higher on CCA-treated panels than on untreated panels, and in the case of F. enigmaticus abundance of individuals increased with increasing preservative loadings. Early colonization by macroalgal species on the surface of CCA-treated and untreated panels of Scots pine was examined following submersion of panels in Langstone Harbour for a period of 4 weeks. Percentage cover of most species of algae was similar on the surface of CCA-treated and untreated panels, with the exception of Hincksia granulosa and Ceramium nodulosum which had significantly higher percentage cover on untreated panels. Possible explanations for the recruitment patterns are discussed.

Animals↗

PubMed2003

Experimental studies of electroosmotic flow dynamics during sample stacking for capillary electrophoresis.

Electroosmotic flow dynamics during a field-amplified sample stacking experiment have been studied experimentally using the periodic photobleaching of a dilute, neutral fluorophore added to the separation buffer. The effects of hydrodynamically injecting different sample plug lengths containing a mixture of arsenic compounds dissolved in 0.125 mM (120, 240, and 600 s) and 41.7 microM (27, 45, and 74 s) phosphate buffer with a separation buffer concentration of 12.5 mM phosphate buffer were examined. Changes in electroosmotic flow during sample stacking and separation were monitored at a rate of 1 Hz. The observed effects of increasing the sample plug length on electroosmotic flow and electrophoretic current agreed qualitatively with predictions by theoretical models presented in the literature. Electroosmotic flow changes on the order of 100% (1.6-3.3 mm/s) were observed. Broadening of the flow monitoring peaks has been used to examine parabolic flow due to the discontinuous buffer systems used for sample stacking.

Journal Article↗

PubMed2002

Understanding soluble arsenate removal kinetics by zerovalent iron media.

Zerovalent iron filings have been proposed as a filter medium for removing arsenic compounds from potable water supplies. This research investigated the kinetics of arsenate removal from aqueous solutions by zerovalent iron media. Batch experiments were performed to determine the effect of the iron corrosion rate on the rate of As(V) removal. Tafel analyses were used to determine the effect of the As(V) concentration on the rate of iron corrosion in anaerobic solutions. As(V) removal in column reactors packed with iron filings was measured over a 1-year period of continuous operation. Comparison of As(V) removal by freely corroding and cathodically protected iron showed that rates of arsenate removal were dependent on the continuous generation of iron oxide adsorption sites. In addition to adsorption site availability, rates of arsenate removal were also limited by mass transfer associated with As(V) diffusion through iron corrosion products. Steady-state removal rates in the column reactor were up to 10 times faster between the inlet-end and the first sampling port than between the first sampling port and the effluent-end of the column. Faster removal near the influent-end of the column was due to a faster rate of iron oxidation in that region. The presence of 100 microg/L As(V) decreased the iron corrosion rate by up to a factor of 5 compared to a blank electrolyte solution. However, increasing the As(V) concentration from 100 to 20,000 microg/L resulted in no further decrease in the iron corrosion rate. The kinetics of arsenate removal ranged between zeroth- and first-order with respect to the aqueous As(V) concentration. The apparent reaction order was dependent on the availability of adsorption sites and on the aqueous As(V) concentration. X-ray absorption spectroscopy analyses showed the presence of iron metal, magnetite (Fe3O4), an Fe(III) oxide phase, and possibly an Fe(II,III) hydroxide phase in the reacted iron filings. These mixed valent oxide phases are not passivating and permit sustained iron corrosion and continuous generation of new sites for As(V) adsorption.

Adsorption↗

PubMed2001

Arsenite inhibits Ras-dependent activation of ERK but activates ERK in the presence of oncogenic Ras in baboon vascular smooth muscle cells.

Exposure to arsenical compounds enhances the risk of atherosclerosis. The reason is unknown but it might be because an effect of arsenite (As3+) on plaque smooth muscle cells (SMCs) activation of extracellular signal-regulated kinase (ERK), a crucial mediator of SMC function. We found that arsenite inhibits the activation of ERK by platelet-derived growth factor-BB (PDGF-BB). This inhibitory effect depends on the time of arsenite exposure, is reversible, and is attenuated by preincubation of SMCs with the antioxidant N-acetyl-cysteine. These observations are consistent with the assumption that oxidative stress is involved. The blockade of ERK by arsenite may be mediated by an inhibition of Ras as arsenite prevents GTP-loading of Ras in response to PDGF-BB. Moreover, the Ras blockade by arsenite is not specific for PDGF-BB because it was also observed following stimulation of SMCs with EGF. To address the role of Ras, we expressed constitutively active, GTP-bound Ha-Ras (V12Ras). Unexpectedly, in V12Ras expressing-SMCs, arsenite stimulates ERK, but still decreases ERK activity in the presence of PDGF-BB. Our data suggest that arsenite inhibits the Ras/ERK pathway in SMCs, and that arsenite may activate ERK in Ras-transformed cells by mechanisms different from those employed by growth factors.

Animals↗

PubMed2000

Field cryofocussing hydride generation applied to the simultaneous multi-elemental determination of alkyl-metal(loid) species in natural waters using ICP-MS detection.

Two hydride generation manifold systems, utilizing flow injection and cryotrapping techniques for alkyl-metal(loid) speciation analysis in natural waters, are described in this paper. They provide shipboard capacity for simultaneous derivatization of analytes with NaBH4 and cryotrapping of the generated products in a field packed column at -196 degrees C. The first system is a large-volume hydride generator, using a reagent-injection flow technique as a flow batch type, that has been fully optimized and applied to the simultaneous detection of alkylated species in estuarine waters. The technique permits the analysis of a large volume sample (0.5-11) at a sampling rate of 3 h-1. The second is an online continuous flow hydride generator. A sampling rate of 3-12 h-1 can be achieved with samples of 0.1-0.51. In addition, shipboard operation eliminates major problems related to sample pretreatment, transport and storage. Ultra-trace multi-element determination is finally performed in the laboratory by cryogenic GC hyphenated with ICP-MS. Routine detection limits of 0.5-10 pg (as metal) for 0.51 water samples were achieved for the selected alkyl-metal(loid) species of arsenic, germanium, mercury and tin. Concentrations of various species, obtained from water samples taken from the Rhine estuary, are also presented. These species include alkylated arsenic compounds, other than methyl derivatives, that have been tentatively identified and are reported here for the first time.

Chemistry Techniques, Analytical↗

PubMed1984

The mechanism of pyrophosphorolysis of RNA by RNA polymerase. Endowment of RNA polymerase with artificial exonuclease activity.

DNA-directed RNA polymerase from Escherichia coli can break down RNA by catalysing the reverse of the reaction: NTP + (RNA)n = (RNA)n+1 + PPi where n indicates the number of nucleotide residues in the RNA molecule, to yield nucleoside triphosphates. This reaction requires the ternary complex of the polymerase with template DNA and the RNA that it has synthesized. It is now shown that methylenebis(arsonic acid) [CH2(AsO3H2)2], arsonomethylphosphonic acid (H2O3As-CH2-PO3H2) and arsonoacetic acid (H2O3As-CH2-CO2H) can replace pyrophosphate in this reaction. When they do so, the low-Mr products of the reaction prove to be nucleoside 5'-phosphates, so that the arsenical compounds endow the polymerase with an artificial exonuclease activity, an effect previously found by Rozovskaya, Chenchik, Tarusova, Bibilashvili & Khomutov [(1981) Mol. Biol. (Moscow) 15, 636-652] for phosphonoacetic acid (H2O3P-CH2-CO2H). This is explained by instability of the analogues of nucleoside triphosphates believed to be the initial products. Specificity of recognition of pyrophosphate is discussed in terms of the sites, beta and gamma, for the -PO3H2 groups of pyrophosphate that will yield P-beta and P-gamma of the nascent nucleoside triphosphate. Site gamma can accept -AsO3H2 in place of -PO3H2, but less well; site beta can accept both, and also -CO2H. We suggest that partial transfer of an Mg2+ ion from the attacking pyrophosphate to the phosphate of the internucleotide bond of the RNA may increase the nucleophilic reactivity of the pyrophosphate and the electrophilicity of the diester, so that the reaction is assisted.

Binding Sites↗

PubMed1999

Dogmas and misunderstandings in East Coast fever.

East Coast fever (ECF) is the most important tick-borne disease in eastern, central and southern Africa and caused an estimated loss of US $186 million in 1989 in the 11 countries where it occurs. It was brought to southern Africa with cattle from Tanzania in 1901 and, over the next 3 years, devastated the cattle that had survived the rinderpest pandemic of the 1890s. Chemical control of ticks using arsenical compounds was introduced in the early 1900s and became the main control measure for both ticks and the diseases they transmit. This method of control has become less reliable over the last 30 years for many reasons, including reduced government spending on livestock and extension, the cost of acaricides, acaricide resistance, poor management of dips and spray races, and poor application of cattle movement control and quarantine. Significant advances in immunization and treatment have been made in the last 30 years, and more robust integrated strategies combining immunization, reduced frequency of chemical control and treatment are being adopted or considered. Throughout its history, ECF has been a source of great anxiety and cost to farmers, and of intense interest to research workers. Many dogmas and misconceptions have become established, some of which still flourish while others took years to demolish. This paper briefly reviews these as well as the history of the disease and explores recent epidemiological findings and their relevance to applying effective control.

Africa↗

PubMed2001

Induction of oxyradicals by arsenic: implication for mechanism of genotoxicity.

Although arsenic is a well-established human carcinogen, the mechanisms by which it induces cancer remain poorly understood. We previously showed arsenite to be a potent mutagen in human-hamster hybrid (A(L)) cells, and that it induces predominantly multilocus deletions. We show here by confocal scanning microscopy with the fluorescent probe 5',6'-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate that arsenite induces, within 5 min after treatment, a dose-dependent increase of up to 3-fold in intracellular oxyradical production. Concurrent treatment of cells with arsenite and the radical scavenger DMSO reduced the fluorescent intensity to control levels. ESR spectroscopy with 4-hydroxy-2,2,6,6-tetramethyl-1-hydroxypiperidine (TEMPOL-H) as a probe in conjunction with superoxide dismutase and catalase to quench superoxide anions and hydrogen peroxide, respectively, indicates that arsenite increases the levels of superoxide-driven hydroxyl radicals in these cells. Furthermore, reducing the intracellular levels of nonprotein sulfhydryls (mainly glutathione) in A(L) cells with buthionine S-R-sulfoximine increases the mutagenic potential of arsenite by more than 5-fold. The data are consistent with our previous results with the radical scavenger DMSO, which reduced the mutagenicity of arsenic in these cells, and provide convincing evidence that reactive oxygen species, particularly hydroxyl radicals, play an important causal role in the genotoxicity of arsenical compounds in mammalian cells.

Animals↗

PubMedDate not supplied

Mortality in a cohort of orchard workers exposed to lead arsenate pesticide spray.

During the period from 1890 to 1940, lead arsenate was the major pesticide used in apple orchards to control the coddling moth. In the Wenatchee area of Washington State, lead arsenate spray was used for longer periods and in larger quantities than in other areas of the United States. In 1938, a cohort of 1,231 people who lived in this area was selected for a study to determine the effects of exposure to lead arsenate spray and residue. This same cohort was re-examined to determine whether there was excess mortality that could be attributed to the lead arsenate exposure. Three levels of exposure (i.e., orchardist, intermediate, consumer) were defined, based upon the use of lead arsenate pesticide spray before and during the 1938 apple growing season. Age-adjusted hazard ratios for all causes of mortality were elevated for both male orchardists and male intermediates. The only significantly increased age-adjusted hazard ratio (1.94) was heart disease in male intermediates. No significantly elevated age-adjusted hazard ratios were observed for women in any exposure group. The lack of evidence that supported an increase in mortality from respiratory cancer in this cohort may have resulted from the lower cumulative concentration of arsenic exposure, the type of arsenical compound, and the small number of study subjects.

Adolescent↗

PubMed1997

DNA-protein cross-links produced by various chemicals in cultured human lymphoma cells.

Chemicals such as cis-platinum, formaldehyde, chromate, copper, and certain arsenic compounds have been shown to produce DNA-protein cross-links in human in vitro cell systems at high doses, such as those in the cytotoxic range. Thus far there have only been a limited number of other chemicals evaluated for their ability to produce cross-links. The purpose of the work described here was to evaluate whether select industrial chemicals can form DNA-protein cross-links in human cells in vitro. We evaluated acetaldehyde, acrolein, diepoxybutane, paraformaldehyde, 2-furaldehyde, propionaldehyde, chloroacetaldehyde, sodium arsenite, and a deodorant tablet [Mega Blue; hazardous component listed as tris(hydroxymethyl)nitromethane]. Short- and long-term cytotoxicity was evaluated and used to select appropriate doses for in vitro testing. DNA-protein cross-linking was evaluated at no fewer than three doses and two cell lysate washing temperatures (45 and 65 degrees C) in Epstein-Barr virus (EBV) human Burkitt's lymphoma cells. The two washing temperatures were used to assess the heat stability of the DNA-protein cross-link, 2-Furaldehyde, acetaldehyde, and propionaldehyde produced statistically significant increases in DNA-protein cross-links at washing temperatures of 45 degrees C, but not 65 degrees C, and at or above concentrations of 5, 17.5, and 75 mM, respectively. Acrolein, diepoxybutane, paraformaldehyde, and Mega Blue produced statistically significant increases in DNA-protein cross-links washed at 45 and 65 degrees C at or above concentrations of 0.15 mM, 12.5 mM, 0.003%, and 0.1%, respectively. Sodium arsenite and chloroacetaldehyde did not produce significantly increased DNA-protein cross-links at either temperature nor at any dose tested. Excluding paraformaldehyde and 2-furaldehyde treatments, significant increases in DNA-protein cross-links were observed only at doses that resulted in complete cell death within 4 d following dosing. This work demonstrates that DNA-protein cross-links can be formed in vitro following exposure to a variety of industrial compounds and that most cross-links are formed at cytotoxic concentrations.

Acetaldehyde↗