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At least 19 recordsLinked to original sources
PubMed2004

Scandium half-metallocene-catalyzed syndiospecific styrene polymerization and styrene-ethylene copolymerization: unprecedented incorporation of syndiotactic styrene-styrene sequences in styrene-ethylene copolymers.

On treatment with 1 equiv of [Ph3C][B(C6F5)4], the scandium half-sandwich bis(alkyl) complex (C5Me4SiMe3)Sc(CH2SiMe3)2(THF) showed extremely high activity (up to 1.36 x 104 kg of sPS/(mol Sc.h)) and syndiospecificity (rrrr > 99%) for the polymerization of styrene at room temperature in toluene. More remarkably, this catalyst system could also effect the syndiospecific copolymerization of styrene with ethylene to yield styrene-ethylene copolymers having syndiotactic styrene-styrene sequences. The styrene content in the copolymers could be easily controlled by changing the styrene feed and could reach higher than 80 mol %. This is the first example of formation of such types of styrene-ethylene copolymers, which are expected to show novel properties.

Journal Article↗
PubMed1984

Occurrence of styrene-7,8-oxide and styrene glycol in mouse after the administration of styrene.

Styrene-7,8-oxide and its hydrated product styrene glycol were determined in mouse tissues at different times (0.5-5 h) after the intraperitoneal administration of 7-[14C]-styrene (3.8 mmol/kg). In a study of the influence of dose on the metabolite pattern of styrene, mice were killed 2 h after a dose of 1.1, 2.3, 3.4, and 5.1 mmol/kg, respectively. The mouse tissues studied (blood, liver, kidney, lung, brain, subcutaneous adipose tissue) were isolated and extracted first with hexane to remove styrene and styrene-7,8-oxide and then with ethyl acetate to remove styrene glycol. beta-Glucuronidase was used to liberate conjugated styrene glycol. A gas-liquid chromatographic method based on the use of an electron capture detector (GLC-EC) was used to quantify styrene glycol, as well as styrene-7,8-oxide, after hydrolysis. In addition all homogenates and extracts were assayed by radioactivity counting. Styrene-7,8-oxide and styrene glycol reached maximum concentrations within 2 h. The highest levels of styrene-7,8-oxide were detected in the kidneys and subcutaneous adipose tissue, while the lungs showed the lowest levels. Styrene glycol was found in the highest concentrations in the kidneys, liver, blood, and lungs. The concentration of unmetabolized styrene increased exponentially at higher doses. There seemed to be a linear increase with the dose of styrene-7,8-oxide and styrene glycol in all the tissues studied. The more polar metabolites occurred at relatively lower levels in the liver and kidneys at higher doses. In a complementary study the epoxide hydratase inhibitor trichloropropene oxide was added to the removed tissues, and the hexane extracts were analyzed for styrene-7,8-oxide both by GLC-EC and mass spectrometry (GLC-MS).

Animals↗
PubMed1995

Dosimetry of styrene 7,8-oxide in styrene- and styrene oxide-exposed mice and rats by quantification of haemoglobin adducts.

Rats (Sprague Dawley) and mice (NMRI) were administered nonlabelled or labelled styrene and styrene oxide by i.p. injection. Blood samples were collected 6 and 24 h after treatment for studies of dose-response and 6 h to 32 days after treatment for studies of adduct stability. Haemoglobin (Hb) and plasma protein adduct levels were determined by radioactivity measurements or, in the case of adducts to N-terminal valine in Hb, by the so-called N-alkyl Edman procedure. Adducts to N-terminal valine were found to be chemically stable during the life-span of the erythrocytes, whereas adducts to carboxylic acid residues showed a reduced stability. The Hb-adduct levels found after styrene oxide treatment were compatible with a linear dose-response at low doses (< or = 0.4 mmol/kg body weight). At higher doses the detoxification of styrene oxide was overloaded resulting in a higher than proportional increase in adduct levels. Saturation of detoxification of styrene oxide could also explain the non-linear dose-response relationship observed in the mouse following treatment with styrene. Styrene oxide gave 4-7 times higher adduct levels than styrene when administered to the animals at equimolar low concentration. For both compounds, the levels of adducts to N-terminal valine were 2-3 times higher in the mouse than in the rat. A comparison of Hb-adduct levels in the styrene-exposed animals with adduct levels in styrene-exposed reinforced plastics workers (Christakopoulos et al., Scand. J. Work Environ. Health, 19(4) (1993) 255-263) suggests that styrene is less effective in humans than in mice and rats.

Animals↗
PubMed1995

Assessment of the neurotoxicity of styrene, styrene oxide, and styrene glycol in primary cultures of motor and sensory neurons.

The neurotoxicity of styrene and its major metabolites, styrene oxide and styrene glycol, was investigated in dissociated primary cultures of murine spinal cord-dorsal root ganglia (DRG)-skeletal muscle using morphological and electrophysiological endpoints. Styrene and styrene oxide (but not styrene glycol) were acutely cytotoxic to both neuronal and non-neuronal cells in the cultures; concentrations in excess of 2 and 0.2 mM, respectively, induced blebbing, vacuolation, detachment from the substratum and cell death in neuronal and non-neuronal cells within 4 days. No effects on neuronal morphology were observed in cultures treated with sublethal concentrations of styrene or styrene oxide for up to 3 weeks. The results suggest that oxidation of multiple cellular macromolecules that underlies the toxicity of styrene in other organ systems may also be responsible for damage to cells in the nervous system. No changes in action potential production indicative of a 'solvent effect' on membrane electrical properties was apparent in cultures treated with up to 8 mM styrene or 10 mM styrene glycol.

Animals↗
PubMed1983

Tissue distribution of styrene, styrene glycol and more polar styrene metabolites in the mouse.

A primary objective of the present investigation was to determine the tissue distribution of styrene, styrene glycol, and more polar metabolites in mice at different times (0.5-5 h) after the intraperitoneal administration of styrene (3.3 mmol/kg). Another aim was to determine the dose dependence of the metabolite pattern of styrene in the different tissues. The dose range chosen was 1.1-4.9 mmol of styrene/kg administered intraperitoneally, and the time delay 2 h after dosing. The highest initial concentrations of unchanged styrene were found in adipose tissue, pancreas, liver, and brain. Styrene glycol reached its maximum concentration within 1 h in most tissues. The levels in the kidneys, lungs, pancreas, and liver far exceeded those in subcutaneous adipose tissue. Only in the liver and kidneys was a notable amount of styrene glycol conjugated. Polar metabolites occurred to a considerable extent in the liver, kidneys, lungs, and plasma. The concentration of unmetabolized styrene seemed to increase exponentially with the dose in subcutaneous adipose tissue, liver, kidneys, lungs, and brain. No tendency towards a decreased relative occurrence of styrene glycol was observed at higher doses. However, when the dose was increased, the more polar metabolites occurred at relatively lower levels in all tissues except brain.

Animals↗
PubMed2002

Pilot-scale production of (S)-styrene oxide from styrene by recombinant Escherichia coli synthesizing styrene monooxygenase.

Recombinant Escherichia coli JM101(pSPZ10) cells produce the styrene monooxygenase of Pseudomonas sp. strain VLB120, which catalyzes the oxidation of styrene to (S)-styrene oxide at an enantiomeric excess larger than 99%. This biocatalyst was used to produce 388 g of styrene oxide in a two-liquid phase 30-L fed-batch bioconversion. The average overall volumetric activity was 170 U per liter over a period of more than 10 h, equivalent to mass transfer rates of 10.2 mmoles per liter per hour at a phase ratio of 0.5. At this transfer rate, the biotransformation system appeared to be substrate mass-transfer limited. The reactor had an estimated power input in the order of 5 W. L(-1), which is close to values typically obtained with commercially operating units. The product could be easily purified by fractional distillation to a purity in excess of 97%. The process illustrates the feasibility of recombinant whole cell biotransformations in two-liquid phase systems with toxic substrates and products.

Cell Line↗
PubMed1984

Toxicity of the components of styrene polymers: polystyrene, acrylonitrile-butadiene-styrene (ABS) and styrene-butadiene-rubber (SBR). Reactants and additives.

The toxicity of the components of styrene polymers, e.g., polystyrene, ABS and SBR, were reviewed with primary focus on the reactive monomers (except styrene) (e.g., acrylonitrile, butadiene) as well as on impurities and solvents such as benzene, hexane and methylethyl ketone, and additives such as phenyl-2-naphthylamine, di-n-butyl phthalate, and a number of peroxide initiators and flame retardants (e.g., 2,3-dibromopropanol, decadibromodiphenyl oxide and antimony trioxide). It is stressed that toxicity data are generally lacking for the majority of additives employed in the production of styrene polymers. Information is also lacking as to the numbers of individuals at potential risk and the extent of their exposure to the large number of additives employed.

1-Naphthylamine↗
PubMed1982

Investigation of styrene in the liver perfusion/cell culture system. No indication of styrene-7,8-oxide as the principal mutagenic metabolite produced by the intact rat liver.

Mutagenic effect of styrene and styrene-7,8-oxide was studied with the isolated perfused rat liver as metabolizing system and Chinese hamster V79 cells as genetic target cells. Styrene-7,8-oxide which is mutagenic per se was rapidly metabolized by the perfused rat liver. Thus no mutagenic effect was detected neither in the perfusion medium nor in the bile. However when styrene was added to the perfusion system, an increase in V79 mutants was observed regardless of where in the circulating perfusion medium the V79 cells were placed: the same effect was obtained with V79 cells close to the liver as well as at a distance from the liver. No mutagenic effect was observed in the bile. Simultaneous analysis of the styrene-7,8-oxide concentration in the perfusion medium, suggest that this metabolite is not the cause of the mutagenic effect observed during perfusion with styrene. The effect of the two test compounds on some liver functions was also studied. Both styrene and styrene-7,8-oxide changed the bile flow without affecting bile acid secretion: styrene caused a reduction in bile flow as compared to control perfusions and styrene-7,8-oxide increased the bile flow. Styrene, but not styrene-7,8-oxide, reduced gluconeogenesis from lactate. Styrene had no effect on the liver's capacity to incorporate amino acids into plasma proteins, whereas styrene-7,8-oxide reduced the amino acid incorporation. The microsomal cytochrome P-450 content was not affected by the two test compounds. No alteration in microsomal N- and C-oxygenation of N,N-dimethylaniline (DMA) was observed with styrene-7,8-oxide or the lower styrene dose used (240 mumol), whereas the higher styrene concentration (480 mumol) reduced N-oxygenation and thus also the total DNA metabolism. It is suggested that the results on styrene and styrene-7,8-oxide found here using the liver perfusion/cell culture system mimic the metabolism expected to be found in the intact animal, thus indicating that styrene-7,8-oxide is not the principal mutagenic metabolite of styrene in vivo.

Animals↗
PubMed1993

In vitro kinetics of styrene and styrene oxide metabolism in rat, mouse, and human.

Styrene oxide (SO), a labile metabolite of styrene, is generally accepted as being responsible for any genotoxicity associated with styrene. To better define the hazard associated with styrene, the activity of the enzymes involved in the formation (monooxygenase) and destruction of SO (epoxide hydrolase and glutathione-S-transferase) were measured in the liver and lungs from naive and styrene-exposed male Sprague-Dawley rats and B6C3F1 mice (three daily 6-h inhalation exposures at up to 600 ppm styrene) and Fischer 344 rats (four daily 6-h inhalation exposures at up to 1000 ppm styrene), and in samples of human liver tissue. Additionally, the time course of styrene and SO in the blood was measured following oral administration of 500 mg styrene/kg body weight to naive Fischer rats and rats previously exposed to 1000 ppm styrene. The affinity of hepatic monooxygenase for styrene, as measured by the Michaelis constant (Km), was similar in the rat, mouse, and human. Based on the Vmax for monooxygenase activity and the relative liver and body size, the mouse had the greatest capacity and humans the lowest capacity to form SO from styrene. In contrast, human epoxide hydrolase and a greater affinity (i.e., lower Km) for SO than epoxide hydrolase from rats or mice while the apparent Vmax for epoxide hydrolase was similar in the rat, mouse, and human liver. However, the activity of epoxide hydrolase relative to monooxygenase activity was much greater in the human than in the rodent liver. Hepatic glutathione-S-transferase activity, as indicated by the Vmax, was 6- to 33-fold higher than epoxide hydrolase activity. However, the significance of the high glutathione-S-transferase activity is unknown because hydrolysis, rather than conjugation, is the primary pathway for SO detoxification in vivo. Human hepatic glutathione-S-transferase activity was extremely variable between individual human livers and much lower than in rat or mouse liver. Prior exposure to styrene had no effect on monooxygenase activity or on blood styrene levels in rats given a large oral dose of styrene. In contrast, prior exposure to styrene increased hepatic epoxide hydrolase activity 1.6-fold and resulted in lower (0.1 > P > 0.05) blood SO levels in rats given a large oral dose of styrene. Qualitatively, these data indicate that the mouse has the greatest capacity and the human the lowest capacity to form SO. In addition, human liver should be more effective than rodent liver in hydrolyzing low levels of SO.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Inhalation↗
PubMed1995

Effects of indomethacin and arachidonic acid on sister chromatid exchange induction by styrene and styrene-7,8-oxide.

Styrene is converted into styrene-7,8-oxide in human lymphocyte cultures, in a reaction probably mediated by oxyhemoglobin. As a consequence, styrene induces sister-chromatid exchanges (SCEs) in whole-blood lymphocyte cultures without exogenous metabolic activation systems. Another metabolic pathway that could be involved in the metabolism of styrene is cooxidation by prostaglandin-endoperoxide synthase (PES). To study the role of PES in the metabolism of styrene, human whole-blood lymphocyte cultures were treated for the entire culture time of 72 h with styrene (0.5 and 1 mM) or styrene-7,8-oxide (50 and 100 microM), in the presence and absence of 75 or 150 microM indomethacin (an inhibitor of PES) and arachidonic acid (substrate of PES). Indomethacin potentiated SCE induction by both styrene and styrene-7,8-oxide; a slight but statistically significant enhancement (16-32%; p < 0.05-0p < 0.001) was observed in all treatments with styrene and at 150 microM indomethacin in the case of styrene-7,8-oxide. At 150 microM, arachidonic acid induced a 15-20% suppression (p < 0.01) in SCE induction by both styrene (1 mM only) and styrene-7,8-oxide (100 microM only). Indomethacin or arachidonic acid did not alone influence the frequency of SCEs. The results suggest that PES acts as an inactivation route for styrene and styrene-7,8-oxide in human whole-blood lymphocyte cultures, possibly through PES-mediated binding to glutathione.

Adult↗
PubMed1995

Effects of indomethacin and arachidonic acid on sister chromatid exchange induction by styrene and styrene-7,8-oxide.

Styrene is converted into styrene-7,8-oxide in human lymphocyte cultures, in a reaction probably mediated by oxyhemoglobin. As a consequence, styrene induces sister-chromatid exchanges (SCEs) in whole-blood lymphocyte cultures without exogenous metabolic activation systems. Another metabolic pathway that could be involved in the metabolism of styrene is cooxidation by prostaglandin-endoperoxide synthase (PES). To study the role of PES in the metabolism of styrene, human whole-blood lymphocyte cultures were treated for the entire culture time of 72-h with styrene (0.5 and 1 mM) or styrene-7,8-oxide (50 and 100 microM), in the presence and absence of 75 or 150 microM indomethacin (an inhibitor of PES) and arachidonic acid (substrate of PES). Indomethacin potentiated SCE induction by both styrene and styrene-7,8-oxide; a slight but statistically significant enhancement (16-32%; p < 0.05-p < 0.001) was observed in all treatments with styrene and at 150 microM indomethacin in the case of styrene-7,8-oxide. At 150 microM, arachidonic acid induced a 15-20% suppression (p < 0.01) in SCE induction by both styrene (1 mM only) and styrene-7,8-oxide (100 microM only). Indomethacin or arachidonic acid did not alone influence the frequency of SCEs. The results suggest that PES acts as an inactivation route for styrene and styrene-7,8-oxide in human whole-blood lymphocyte cultures, possibly through PES-mediated binding to glutathione.

Adult↗
PubMed2006

Effects of styrene and styrene oxide on glutathione-related antioxidant enzymes.

Styrene is both hepatotoxic and pneumotoxic in mice. Its mode of action is not clear, but it may be related to oxidative stress including a very large decrease in reduced glutathione (GSH). The current studies evaluated if: (1) the more toxic R-styrene oxide had a greater effect on reduced GSH levels than the less toxic S-styrene oxide, (2) the ratio of reduced to oxidized forms of glutathione was altered by styrene or styrene oxide, (3) other enzymes involved in the oxidant status of the cell, namely glutathione reductase, glutathione peroxidase and gamma-glutamylcysteine synthetase were altered, and (4) lipid peroxidation, as measured by the determination of malondialdehyde, increased. R-Styrene oxide (300mg/kg, ip) caused greater decreases in mouse liver and lung GSH than did S-styrene oxide (300mg/kg, ip). Styrene (600mg/kg, ip) caused decreases in both GSH and GSSG in both liver and lung. Styrene and styrene oxide did not cause significant increases in lipid peroxidation in either liver or lung. Styrene and styrene oxide had minimal effects on glutathione reductase and glutathione peroxidase in liver and lung. Styrene increased gamma-glutamylcysteine synthetase activity. The results suggest that while styrene and its metabolite styrene oxide cause significant decreases in GSH levels, they have little effect on the enzymes glutathione reductase and glutathione peroxidase and that in response to decreased glutathione levels there is an increase in its synthesis via induction of gamma-glutamylcysteine synthetase activity.

Animals↗
PubMed1999

Styrene and styrene oxide affect the transport of dopamine in purified rat striatal synaptic vesicles.

Animal and human studies suggest a dopamine-mediated effect of styrene neurotoxicity. To date, mechanisms of cerebral membrane transport of neurotransmitter amines in the presence of styrene in relation to its neurotoxicity have not been addressed properly. So, the present study has examined to test the hypothesis that dopaminergic malfunction in vesicular transport is a critical component in styrene-induced neurotoxicity in rats. Both styrene and its intermediate reactive metabolite, styrene oxide antagonized the in vitro striatal binding of [3H] tyramine, a putative marker of the vesicular transporter for dopamine. Both styrene and styrene oxide potently inhibited the uptake of [3H] dopamine in purified synaptic vesicles prepared from rat brain striata, in a dose-related manner, with inhibitory constants (Ki) 2.5 and 2.2 microM respectively. However, neither styrene nor styrene oxide significantly increased the basal efflux of [3H] dopamine that has been preloaded into striatal vesicles in vitro. On the other hand, both styrene and styrene oxide have failed to significantly inhibit the uptake of either [3H] norepinephrine, or [3H] serotonin into striatal synaptic vesicles. It is concluded that both styrene and styrene oxide are capable of producing impairments in dopaminergic transport in purified striatal synaptic vesicles, an effect which may be a critical component in styrene-induced neurotoxicity.

Animals↗
PubMed2004

Comparison of the susceptibility of wild-type and CYP2E1 knockout mice to the hepatotoxic and pneumotoxic effects of styrene and styrene oxide.

Styrene causes both liver and lung damage in non-Swiss albino, CD-1, and other strains of mice. This is considered to be due to the bioactivation of styrene to styrene oxide by cytochromes P450, principally CYP2E1 and CYP2F2. If so, one would expect CYP2E1 knockout mice to be less susceptible to styrene-induced toxicity than wild-type mice. However, previous in vitro and in vivo studies demonstrated little difference in the metabolism of styrene to styrene oxide between wild-type and CYP2E1 knockout mice. These findings would suggest that there should be no difference in the toxic responses to styrene between these two strains. To determine which of these possibilities was correct, styrene (600 mg/kg) or styrene oxide (300 mg/kg) was administered i.p. 24 h prior to measurement of serum sorbitol dehydrogenase as a biomarker of hepatotoxicity or lactate dehydrogenase activity, protein, and cells in bronchoalveolar lavage fluid as biomarkers for pneumotoxicity. Styrene was more hepatotoxic in the wild-type mice than in the knockout mice suggesting CYP2E1 activity is important. Strain differences were not observed with styrene oxide indicating no difference in intrinsic susceptibility. For lung, the response was similar in both strains to both styrene and styrene oxide supporting the idea that CYP2F2 is important in the bioactivation of styrene in this tissue and that there is no strain difference in susceptibility to the active metabolite.

Animals↗
PubMed2006

Predictors of occupational exposure to styrene and styrene-7,8-oxide in the reinforced plastics industry.

OBJECTIVE: To identify demographic and work related factors that predict blood levels of styrene and styrene-7,8-oxide (SO) in the fibreglass reinforced plastics (FRP) industry. METHODS: Personal breathing-zone air samples and whole blood samples were collected repeatedly from 328 reinforced plastics workers in the Unuted States between 1996 and 1999. Styrene and its major metabolite SO were measured in these samples. Multivariable linear regression analyses were applied to the subject-specific levels to explain the variation in exposure and biomarker levels. RESULTS: Exposure levels of styrene were approximately 500-fold higher than those of SO. Exposure levels of styrene and SO varied greatly among the types of products manufactured, with an 11-fold range of median air levels among categories for styrene and a 23-fold range for SO. Even after stratification by job title, median exposures of styrene and SO among laminators varied 14- and 31-fold across product categories. Furthermore, the relative proportions of exposures to styrene and SO varied among product categories. Multivariable regression analyses explained 70% and 63% of the variation in air levels of styrene and SO, respectively, and 72% and 34% of the variation in blood levels of styrene and SO, respectively. Overall, air levels of styrene and SO appear to have decreased substantially in this industry over the last 10-20 years in the US and were greatest among workers with the least seniority. CONCLUSIONS: As levels of styrene and SO in air and blood varied among product categories in the FRP industry, use of job title as a surrogate for exposure can introduce unpredictable measurement errors and can confound the relation between exposure and health outcomes in epidemiology studies. Also, inverse relations between the intensity of exposure to styrene and SO and years on the job suggest that younger workers with little seniority are typically exposed to higher levels of styrene and SO than their coworkers.

Adolescent↗
PubMed1996

Pneumotoxicity and hepatotoxicity of styrene and styrene oxide.

The purpose of this study was to investigate the toxicity of styrene and styrene oxide in the lung in comparison to the toxicity in the liver. Pneumotoxicity caused by styrene or styrene oxide was measured by elevations in the release of gamma-glutamyltranspeptidase (GGT) and lactate dehydrogenase (LDH) into bronchoalveolar lavage fluid (BALF), while hepatotoxicity was measured by increases in serum sorbitol dehydrogenase (SDH) in non-Swiss Albino (Hsd:NSA) mice. Intraperitoneal administration of styrene at doses of 500-1000 mg/kg caused consistent dose-dependent increases in both sets of biomarkers with the hepatic effect appearing earlier than the pulmonary effect. Pyridine, phenobarbital, and beta-naphthoflavone, inducers of CYP2E1, CYP2B, and CYP1A, respectively, increased the toxicity of styrene. Pyridine and phenobarbital treatments increased mortality due to styrene. Styrene oxide exists in two enantiomeric forms: (R)- and (S)-styrene oxide, and the differential toxicities of the two enantiomers and racemic styrene oxide were compared. In all studies, (R)-styrene oxide caused greater toxicity than the (S) enantiomer, especially in the liver. Trichloropropene oxide, an epoxide hydrolase inhibitor, was used to inhibit styrene oxide detoxification and increased its hepatotoxicity, while buthionine sulfoxamine, a glutathione depletor, did not. These results demonstrated the greater role of epoxide hydrolase in styrene oxide detoxification.

Animals↗