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PubMedDate not supplied

Styrene oxide as a stereochemical probe for the mechanism of aralkylation at different sites on guanosine.

The stereochemistry at the alpha-carbon atom of the styrene moiety in styrene oxide-guanosine products was established, and the stereochemical consequences of reaction of optically active styrene oxide with guanosine were investigated. Inversion of stereochemistry in products at the alpha-carbon of styrene oxide decreased in the sequence 7- much greater than N2- greater than O6-substituted guanosines. These findings show that an extensively ionized substrate is needed for reaction at the exocyclic N2 and O6 sites on guanosine but that the reactive intermediate is not an ideal planar trigonal carbonium ion. This follows because inversion exceeds retention in both of the exocyclic substituted products.

Alkylation↗
PubMed1998

Styrene oxide adducts in an oligodeoxynucleotide containing the human N-ras codon 12: minor groove structures of the R(12,1)- and S(12,1)-alpha-(N2-guanyl) stereoisomers determined by 1H nuclear magnetic resonance.

The R- and S-alpha-(N2-guanyl)styrene oxide (SO) adducts at X5 in d(G1G2C3A4X5G6T7G8G9T10G11).d(C12A13C14C15A16C17C18T19G20C21C22 ), encompassing codon 12 of the human N-ras protooncogene (underlined), were examined using 1H NMR spectroscopy. These were the R(12,1) and S(12,1) adducts, indicating the location of the R or S adduct at the first position of codon 12. These differed from the R- and S(12, 2)-alpha-SO adducts [Zegar, I. S., Setayesh, F. R., DeCorte, B. L., Harris, C. M., Harris, T. M., and Stone, M. P. (1996) Biochemistry 35, 4334-4348] in that the base pair 5' to the lesion was changed from G.C to A.T, while the base pair 3' to the lesion was changed from T.A to G.C. Comparison of the R- and S(12,1) adducts with the R- and S(12,2) adducts allowed the effects of flanking bases on the conformations of the alpha-SO adducts to be examined. This change in flanking base affected the R-SO lesion. The R(12,1) adduct structure was disordered at the adduct site, and a refined structure could not be obtained. NOE and chemical shift data suggested that the styrenyl moiety was oriented in the minor groove and in the 3'-direction from the site of adduction. In contrast, this change in flanking base did not affect the S-SO lesion. The S(12,1) adduct yielded a refined structure, with the styrenyl moiety edgewise in the minor groove and oriented in the 5'-direction relative to the site of adduction. A total of 232 interproton distances, including 13 styrene-DNA distances, were obtained. A total of 12 NOE-restrained molecular dynamics calculations converged with pairwise root-mean-square deviation of 1.10 A. The sixth-root residual index between calculated and experimental NOE intensities was 8.0 x 10(-)2 A. The styrene aromatic protons appeared as three resonances, suggesting rapid rotation. The possibility of a hydrogen bond between the styrene hydroxyl and C18 O2 in the S(12,1) adduct could not be confirmed. This work illustrates the dual roles of stereochemistry and sequence in modulating the properties of guanine N2 alpha-SO adducts.

Codon↗
PubMed2000

Reduction of stilbene oxide and styrene oxide to the corresponding alkenes by intestinal bacteria.

1. This study provides the first evidence that stilbene oxide and styrene oxide are reductively metabolized to the corresponding alkenes by intestinal bacteria in animals. 2. When trans- or cis-stilbene oxide were incubated with the caecal contents of rat under anaerobic conditions, both trans- and cis-stilbene were isolated from the incubation mixture. Styrene oxide was also reduced to styrene by rat caecal contents. 3. Caecal contents of mouse, hamster and guinea pig also exhibited alkene oxide reductase activities toward cis- and trans-stilbene oxides, and styrene oxide. In contrast, liver microsomes or cytosol exhibited no epoxide reductase activities toward these substrates. 4. Seven pure strains of intestinal bacteria exhibited alkene oxide reductase activities of varying degrees under anaerobic conditions, with the highest activity being observed in Clostridium sporogenes. 5. Cell-free extracts of either the intestinal bacteria in rat caecal contents or C. sporogenes exhibited reductase activity when supplemented with both NAD(P)H and FMN under anaerobic conditions. Reductase activity was also observed on addition of the photochemically reduced form of FMN instead of both NAD(P)H and FMN.

Animals↗
PubMed1995

Styrene oxide-induced HPRT mutations, DNA adducts and DNA strand breaks in cultured human lymphocytes.

Styrene-7,8-oxide (SO) is the major in vivo metabolite of styrene, a widely used plastic monomer. SO has been classified as probably carcinogenic to humans. We studied the genotoxic effects of SO in human peripheral blood lymphocytes (PBL) in vitro. SO-treatment in the range of 0.05-0.6 mM for 24 h resulted in a dose-dependent decrease of cell survival and increase of HPRT mutation, O6-guanine DNA adducts and DNA strand breaks, whereas higher concentrations caused pronounced cell death. SO was a weak mutagen, inducing at most 10-20 mutants per 10(6) clonable cells (approximately 4-fold over the background) after treatment with 0.2-0.4 mM for 24 h or 6 days. The levels of DNA adducts in treated cells correlated with SO-concentrations, but only four adducts per 10(8) nucleotides were detected at the highest treatment concentrations. Yet, adducts were still detectable in cells that had been cultured for 6-8 days after treatment. SO-induced DNA strand breaks, measured with the Comet assay, were detectable after 1 h exposure to 0.05-0.1 mM. Post-treatment incubation for 24 h decreased the level of DNA strand breaks to the control level. There was no correlation between the levels of DNA adducts and frequency of HPRT mutation. The present results indicate that SO is relatively inefficient in inducing HPRT mutation and O6-guanine DNA adducts in human lymphocytes in vitro, which may be related to its pronounced cytotoxicity at concentrations above 0.4 mM. A comparison with previous in vivo data obtained by the same assays in T-lymphocytes of styrene-exposed workers suggests that chronic, low dose exposure to styrene in the work environment may be more efficient in inducing persistent DNA adducts and HPRT mutation than acute, short-term exposure.

Animals↗
PubMed2001

Effects of styrene-7,8-oxide over p53, p21, bcl-2 and bax expression in human lymphocyte cultures.

Styrene is one of the most important organic chemicals in use today. The highest human exposures to styrene take place by inhalation during the production of fibreglass-reinforced plastics. Styrene is oxidized by hepatic cytochrome P450 to styrene-7,8-oxide (SO), an epoxide that has been shown to induce chromosome aberrations, sister chromatid exchanges and micronuclei in many cell systems. In this work, the effect of SO on the expression of some genes involved in the cell cycle and apoptosis regulation in human white blood cells was studied. Lymphocyte cultures from four donors were exposed to 50 and 200 microM SO, 1% DMSO being the control. Aliquots of the cultures were taken at six different time points (30, 36, 42, 48, 60 and 72 h), total mRNA was extracted in each one of them and RT-PCR was carried out to analyze the expression of the genes p53, p21, bcl-2 and bax. Moreover, a cytokinesis block assay was performed to estimate cell proliferation kinetics by calculating the cytokinesis block proliferation index (CBPI), and to evaluate the number of cells undergoing apoptosis. Furthermore, apoptotic events were detected by the DNA fragmentation assay. In our results, a high interindividual variation in the expression of the studied genes was observed. Expression curves obtained for the four genes, together with the data from the CBPI and apoptotic cells scored, suggest that exposure to high levels of SO may induce a delay in the cell cycle, probably directed to allowing repair systems to act on the genotoxic damage produced, more than driving cells towards programmed cell death.

Adult↗
PubMed1983

Effect of methyl substitution on microbial degradation of linear styrene dimers by two soil bacteria.

The microbial degradation of 10 linear unsaturated dimers (I to IV) prepared from styrene and o-, m-, or p-methylstyrene was investigated with two soil bacteria, Alcaligenes sp. strain 559 and Pseudomonas sp. strain 419. The two strains decomposed styrene dimer I and all styrene-methylstyrene codimers II and III, but methylstyrene homodimers IV remained intact. The degradation rates of codimers II and III of o- and m-methylstyrenes were found to depend on both their structure and the strain used; i.e., Alcaligenes sp. strain 559 decomposed III faster than II, whereas the reverse order (II > III) was obtained with Pseudomonas sp. strain 419. In biodegradation by the former strain, the codimers were degraded faster in the presence of styrene dimer I than in its absence, but no such effect of dimer I was observed with the latter.

Journal Article↗
PubMed1984

Subcellular distribution of styrene oxide in rat liver.

The subcellular distribution of (3H )-styrene-7,8-oxide was studied in the rat liver. The compound was added to liver homogenate to give a final concentration of 2 X 10(-5); 2 X 10(-4) and 2 X 10(-3) M. Subcellular fractions were obtained by differential centrifugation. Most of styrene oxide (59-88%) was associated with the cytosolic fraction. Less than 15 percent of the compound was retrieved in each of the nuclear, mitochondrial and microsomal fractions. A considerable percentage of radioactivity was found unextractable with the organic solvents, suggesting that styrene oxide reacted with the endogenous compounds. The intracellular distribution of this epoxide was also studied in the perfused rat liver. Comparable results with those previously described were obtained. The binding of styrene oxide to the cytosolic protein was investigated by equilibrium dialysis and ultrafiltration. Only a small percentage of the compound was bound to protein.

Animals↗
PubMed1979

Bioassay of a solution of b-nitrostyrene and styrene for possible carcinogenicity.

A bioassay of a solution of 30 percent b-nitrostyrene and 70 percent styrene for possible carcinogenicity was conducted using Fischer 344 rats and B6C3F1 mice. The solution of the two test materials in corn oil was administered by gavage, at either of two dosages, to groups of 50 male and 50 female animals of each species. The high and low dosages utilized in the study were, respectively, 300 and 150 mg/kg for male rats; 150 and 75 mg/kg for female rats; and 175 and 87.5 mg/kg for mice of both sexes. These dosages are expressed in terms of the b-nitrostyrene contained in the styrene solution. Twenty animals of each species and sex were placed on test as controls, and were gavaged with corn oil on the same schedule as dosed animals. A 79-week period of chemical administration was followed by an additional observation period of 29 weeks for rats, and a 78-week period of chemical administration was followed by an additional 14-week observation period for mice. There was no significant difference between the survival of rats dosed with the test solution and that of their controls, and there was no significant association between dosage and mortality among female mice. There was a significant positive association between dosage and mortality among male mice; however, adequate numbers of animals in all groups survived sufficiently long to be at risk from late-developing tumors. There was distinct mean body weight depression when high dose female mice or male rats were compared to their controls, indicating that the dosage administered to these animals may have approximated the maximum tolerated dosage. Since no distinct mean body weight depression, no significantly accelerated mortality, and no other toxic effects were associated with the administration of b-nitrostyrene and styrene to female rats or male mice, it is possible that these animals may have been able to tolerate a higher dosage. There were no significant positive associations between administration of the solution and increased tumor incidence in rats of either sex. When those male mice having either alveolar/bronchiolar carcinomas or alveolar/bronchiolar adenoma were combined and the resulting tumor incidences for each group were statistically analyzed, the low dose to control Fisher exact comparison was significant. The Cochran-Armitage test and the high dose to control comparison, however, were not. No other tests for tumors of any site in either male or female mice were significant. Under the conditions of this bioassay, there was no convincing evidence for the carcinogenicity of a solution of b-nitrostyrene and styrene in Fischer 344 rats or in B6C3F1 mice.

Journal Article↗
PubMed2003

Isolation and application of a styrene-degrading strain of Pseudomonas putida to biofiltration.

A bacterial strain ST201 capable of degrading styrene was isolated from soil and identified as Pseudomonas putida. This strain had high tolerance to styrene and could degrade it completely in 48 h at concentrations up to 600 mg/l. P. putida ST201 was also demonstrated to degrade a mixture of benzene, toluene, ethylbenzene and p-xylene. A packed tower biofilter inoculated with P. putida ST201 was constructed which removed styrene vapor with a styrene elimination capacity of 90 g/m3.h.

Journal Article↗
PubMed1996

Study of urinary mandelic acid concentration and peripheral nerve conduction among styrene workers.

The relationship between exposure to styrene and nerve conduction velocities was investigated in 32 workers occupationally exposed to styrene. There was a dose-dependent relationship between urinary mandelic acid and ulnar and peroneal motor distal latencies (MDLs). The ulnar and peroneal MDLs of subgroup B (urinary mandelic acid > or = 250 mg/l) were significantly longer than those of subgroup A (urinary mandelic acid < 250 mg/l)(p < 0.05), and the referent group (p < 0.03). After adjusting confounding factors, urinary mandelic acid had a significant positive relationship with ulnar and peroneal MDL. Our study suggests that a low level of styrene, below the 50 ppm exposure limit of the American Conference of Governmental Industrial Hygienists (ACGIH), involves the risk of inducing adverse effects on the peripheral nervous system. The study also indicated that motor distal latency is a sensitive parameter of toxic peripheral neuropathy.

Action Potentials↗
PubMed1998

Associations between several sites of cancer and occupational exposure to benzene, toluene, xylene, and styrene: results of a case-control study in Montreal.

BACKGROUND: Except for the leukemogenic effects of benzene, there is inadequate or sparse evidence on the carcinogenicity of the most common monocyclic aromatic hydrocarbons. The purpose of this study was to generate hypotheses on associations between exposure to benzene, toluene, xylene, and styrene and various common types of cancer. METHODS: In the context of a population-based case-control study carried out in Montreal, 3,730 cancer patients (15 types of cancers, not including leukemia) and 533 population controls were interviewed, and their job histories were translated by a team of experts into occupational exposures, including benzene, toluene, xylene, and styrene. In the present analysis, exposure to these substances was compared between each case series and a control group pooling selected cancer patients and population controls, using logistic regression analysis. RESULTS: Exposure levels were low for most exposed subjects, and there was a high correlation between exposure to benzene, toluene and xylene. For most sites of cancer there was no evidence of excess risk due to these substances. However, limited evidence of increased risk was found for the following associations: esophagus-toluene, colon-xylene, rectum-toluene, rectum-xylene and rectum-styrene. CONCLUSIONS: These latter observations warrant further investigation.

Adult↗
PubMed1997

Styrene toxicity: an ecotoxicological assessment.

Although other aromatic compounds (e.g., benzene, toluene, polycyclic aromatic hydrocarbons (PAH), etc.) have been thoroughly studied over the years, styrene has been given little attention probably due to its lower rate of industrial use. In addition, it is less toxic than benzene and PAH, proven carcinogens. However, it is classified as a mutagen and thus potentially carcinogenic. Its main use is in the production of the polymer polystyrene and in the production of plastics, rubber, resins, and insulators. Entry into the environment is mainly through industrial and municipal discharges. In this review, the toxicological effects of styrene on humans, animals, and plants are discussed. Its mode of entry and methods of monitoring its presence are examined. Although its effects on humans and aquatic life have been studied, the data on short- or long-term exposures to plants, birds, and land animals are insufficient to be conclusive. Since exposure to workers can result in memory loss, difficulties in concentration and learning, brain and liver damage, and cancer, development of accurate methods to monitor its exposure is essential. In addition, the review outlines the present state of styrene in the environment and suggests ways to deal with its presence. It might appear that the quantities are not sufficient to harm humans, but more data are necessary to evaluate its effect, especially on workers who are regularly exposed to it.

Animals↗
PubMed1993

Nervous system effects of occupational exposure to styrene: a clinical and neurophysiological study.

Quantitative EEG of 99 workers occupationally exposed to styrene was analyzed and compared to exposure parameters. All of the workers came from reinforced plastics industry. The workplaces and factories were previously evaluated, and the exposure levels were known rather accurately. The exposure information form workplaces and the individual exposure data were combined to form an Exposure Index, which reliably reflected long-term exposure to styrene in various occupational settings. All of the subjects underwent careful medical, neurological, and neurophysiological examinations. Quantitative EEG was recorded from 19 channels and analyzed for absolute and relative power, asymmetry, coherence, frequency distribution, and statistical normative database comparisons (Neurometrics). The EEG data showed a significant increase of abnormal EEG classifications in workers with higher exposure. When the workers were divided into two groups, based on the exposure data, those with higher exposure had higher absolute EEG power in alpha and beta bands in the frontotemporal regions of the brain. The findings indicate that abnormalities in cerebral function can be demonstrated even with relatively low mean exposure levels. It is concluded that the efforts to lower the administrative hygienic levels of styrene have been in the right direction.

Adult↗
PubMed1985

Styrene metabolism and striatal dopamine depletion in rabbits.

The striatal concentration of dopamine (DA), norepinephrine (NE), and homovanillic acid (HVA) was assessed in adult male rabbits exposed to styrene vapours or dosed with mandelic acid (MA), phenylglyoxylic acid (PGA) and phenylglycine (PG). Styrene exposure produced a marked and dose-dependent decrease in striatal DA, concomitant with a consistent increase in HVA. The same effects were caused by i.p. administration of PGA and PG, but not of MA. The increased catabolism of DA was concomitant with a normal turnover time after inhibition of tyrosine hydroxylase by the administration of methyl-p-tyrosine. The amination of PGA to PG with a subsequent competition of the latter with DA for the vesicular storage capacity is suggested as the possible mechanism for styrene-induced brain dysfunction.

Animals↗
PubMed1992

Chromosome aberrations and micronuclei in lymphocytes of workers exposed to low and medium levels of styrene.

In the present study we analysed 19 workers exposed to styrene in two factories where polyester resins were used. Because of the different sizes of the pieces undergoing resin processing, the environmental styrene concentrations and urinary mandelic acid (MA) levels of the analysed subjects were quite different in the two plants examined. Cytogenetic monitoring was performed by analysis of chromosome aberrations (CAs) and micronuclei (Mn) in peripheral blood lymphocytes. Cytogenetic analysis revealed a significant increase in the percentage of aberrant cells and total aberrations in the group with higher styrene exposure (group 2) and no increase in the group with lower exposure (group 1), as compared with matched controls. Mn frequencies were not significantly increased in the two exposed populations. No correlations between length of exposure and CA or Mn frequency were found, and a weak correlation was found between exposure levels, measured as urinary MA, and Mn frequencies. Only 5 of the 12 exposed workers examined in group 2 had urinary MA levels higher than the limit recommended by the ACGIH in 1990-91 [1]. Significant increases in DNA damage are therefore already found at urinary MA levels lower than the internationally suggested exposure limits.

Adult↗
PubMed1994

Determination of the urinary metabolites of styrene: estimation of the method evaluation function and evaluation of reference values in Danish subjects.

A European study on styrene exposure was initiated in 1989 to evaluate the health effects of environmental and occupational exposure. A part of this study included the development of an analytical method for use in a biological monitoring program. The urinary metabolites of styrene, mandelic acid (MA) and phenylglyoxylic acid (PGA) were quantitated by a direct and convenient high-performance liquid chromatography method. Urine samples were diluted with eluent and analysed by HPLC with a C8 reversed-phase column and a buffer to acetonitrile (9:1) eluent with a counterion added. The detector used was a variable UV detector and the wavelength was lambda = 210 nm. The method was statistically evaluated by a method evaluation demonstrating no systematic error. The uncertainty was 23.8 mumol/l and 11.5 mumol/l for MA and PGA, respectively. The limit of detection (LOD) of MA is 71.4 mumol/l and the LOD of PGA is 34.5 mumol/l, sufficiently low for the measurement of styrene exposure at a low exposure level. The present study indicates that reference values for MA and PGA are low. The fraction of reference values below LOD was 0.80 for MA and 0.66 for PGA; consequently, the reference values were described by a non-parametric one-sided tolerance interval. The 95% one-sided upper tolerance limits calculated for MA and PGA were 31.0 mumol/mmol creatinine and 20.1 mumol/mmol creatinine, respectively, with the coverage 0.95 +/- 0.045 for both metabolites. The method has been used for biological monitoring in several studies of environmentally and occupationally exposed subjects in concentrations up to 200 mumol/mmol creatinine for MA and 150 mumol/mmol creatinine for PGA.

Air Pollutants, Occupational↗
PubMed1996

Application of a single-compartment model for estimation of styrene uptake from measurements of urinary excretion of mandelic and phenylglyoxylic acids after occupational exposure.

In biological monitoring of styrene, the exposure is usually related to the urinary concentration of mandelic (MA) and/or phenylglyoxylic (PGA) acids in a urine sample taken after the workshift or on following morning. To study this relationship further, a single-compartment mathematical model was developed by which measured occupational repetitive uptake of styrene during a working day was related to measured excretion rates of the urinary metabolites. The model was used in practice to calculate the unknown uptake (dose) from MA and PGA excretion analyzed in urine samples. For comparison, a styrene limit dose was calculated from the exposure limit. Analytical results of samples from plastic boat builders were compared with the limit values.

Chemical Industry↗
PubMed1995

Partial conversion of cinnamic acid into styrene by growing cultures and cell-free extracts of the yeast Cryptococcus elinovii.

Cultures of Cryptococcus elinovii CBS 7051 grown at the expense of cinnamic acid as the sole source of carbon and energy partially converted this substrate into styrene. The latter is toxic and eventually kills the culture. Cell-free extracts of cultures grown on cinnamic acid produced styrene from cinnamate. Other basidiomycetous yeasts tested did not produce styrene from cinnamic acid.

Cell Death↗