Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Styrenes”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1978

Cytogenetic effects of styrene and styrene oxide on human lymphocytes and Allium cepa.

Styrene and styrene oxide induce cytogenetic effects already at very low concentrations (0.01% v/v or even less); the effects are similar in both in vitro human lymphocytes and in vivo onion root tip cells (Allium cepa L.). It is characteristic that styrene treatment is more potent in causing chromosome breakage in both systems. In Allium styrene induced inhibition of mitotic spindle action as revealed by a strong c-mitotic effect. Also the number of micronuclei and nuclear bridges increased in both test systems, especially after styrene oxide treatment. Furthermore, the metaphase chromosome morphology in the cells treated with styrene oxide was strongly affected. In both systems, chromosome destruction was observed, or else the chromosome material was decondensed and resulted in a characteristic fuzzy appearance of Allium chromosomes or a banded appearance of human lymphocyte chromosomes. A specific effect of styrene oxide on the chromosomal proteins is thus suggested. The data obtained from the autoradiographic studies with Allium support the idea that [7--3H] styrene oxide binds irreversibly to the cytoplasmic and nuclear macromolecules.

Autoradiography↗
PubMed1994

Styrene-7,8-oxide in blood of workers exposed to styrene.

A field study was carried out on 13 workers exposed to styrene vapors at time-weighted average concentrations between 10 and 73 ppm. The reactive intermediate styrene-7,8-oxide was determined in blood samples using a direct gas chromatographic method. Styrene-7,8-oxide concentrations were in the range between 0.9 and 4.1 micrograms/l blood. Linear correlations were found between styrene-7,8-oxide in blood and styrene in ambient air and blood. For an exposure concentration of 20 ppm styrene (German MAK value) a steady-state level of about 1 microgram styrene-7,8-oxide/l blood was calculated.

Adult↗
PubMed1983

Bone marrow cell chromosomal aberrations and styrene biotransformation in mice given styrene on a repeated oral schedule.

Styrene's capacity to induce chromosomal aberrations was studied in bone marrow cells of CD1 male mice. No mutagenic effect could be detected after either a 4-day treatment course with daily oral doses of 500 mg/kg or a 70-day course with daily oral doses of 200 mg/kg. Urinary elimination of styrene metabolites related to styrene-7,8-oxide formation (i.e. phenylethylene glycol, mandelic acid, benzoic acid, phenylglyoxylic acid and total mercapturic acids) was quantitatively evaluated in the group of mice given the 200 mg/kg dose. In parallel, kinetic studies were made on styrene and styrene-7,8-oxide blood concentrations in the same group of animals. These determinations were carried out on days 1 and 70 of treatment by spectrophotometric, gas chromatographic and mass fragmentographic procedures. Not even nanograms of styrene-7,8-oxide were found in the blood of styrene-treated mice. This suggests that the metabolite does not migrate from the cellular compartment where it is formed being immediately metabolized or irreversibly bound to cellular structures. This observation could well explain the lack of mutagenic effects observed.

Administration, Oral↗
PubMed1986

Effect of in vitro exposure to styrene, styrene oxide, and other structurally related compounds on murine cell-mediated immunity.

Spleen cells from C57BL/6 mice were exposed to nontoxic doses of styrene, styrene oxide, styrene glycol, allylbenzene, ethylbenzene and toluene. None of these compounds except allylbenzene showed any great suppression or stimulation of the cytotoxic-T lymphocyte response. Allylbenzene was a strong suppressor of the cytotoxic-T lymphocyte response but, like the other compounds, had no effect on natural cytotoxicity. Styrene glycol, ethylbenzene and toluene also did not suppress natural killer cell activity. In contrast, styrene, styrene oxide and allylbenzene were strong suppressors of natural killer cell activity. The natural killer cell inhibition caused by styrene oxide did not occur if treatment was performed at 0 degree C instead of 37 degrees C, and was reversed by the addition of 5 mM glutathione or a 30 min recovery period at 37 degrees C. The natural killer cell suppression caused by allylbenzene was not reversed by these methods. These compounds may be causing natural killer cell suppression by different mechanisms, depending on the compound under study, and on whether these compounds contain a double bond or an epoxide moiety.

Animals↗
PubMed1981

Interactions of styrene and styrene oxide with partially purified cytochrome P-450 and P-448 from rat liver microsomes.

Styrene and styrene 7,8-oxide were able to bind both to partially purified cytochrome P-450 isolated from phenobarbital (PB)-treated rat liver and to cytochrome P-448 from liver microsomes of 3-methylcholanthrene (3-MC)-treated rats. In the presence of either purified preparation or "fresh" microsomes from PB- or 3-MC-treated animals, styrene produced a characteristic Type I difference spectrum as did styrene 7,8-oxide with "fresh" microsomes from PB rats. In other experiments, the addition of styrene oxide produced spectra which resembled Type I spectra but were somewhat shifted to longer wavelengths. A comparison of the binding parameters for the interaction of styrene or styrene 7,8-oxide with partially purified preparations and "fresh" microsomes indicated that the binding is catalyzed by more than one type of P-450 hemoprotein and that the binding affinity is slightly reduced by the purification procedure. The addition of phosphatidylcholine was unable to restore the binding parameters.

Animals↗
PubMed1993

Styrene and styrene oxide: results of studies on carcinogenicity in experimental animals.

Fourteen long-term toxicity studies were reviewed in an effort to evaluate the potential carcinogenic activity of styrene and styrene oxide in animals. Each study was reviewed and evaluated for detail and adequacy of design, adequacy of reported data and interpretation. The results of the review are: 1. There is no convincing evidence for a carcinogenic action of styrene in animals, even though it has been studied in several species and by several routes of exposure: inhalation, gavage, in the drinking-water and by intraperitoneal and subcutaneous injection. Most of the studies of styrene, however, have deficiencies in design and/or conduct. 2. Styrene oxide was carcinogenic to the forestomach of rats and mice of each sex after exposure by gavage at all doses tested, including one as low as 50 mg/kg per day. An increase in the incidence of liver neoplasms was observed in male mice in one study. No carcinogenic activity was observed in mice exposed by skin painting. The relevance to humans of the studies in which exposure was by gavage is limited because: (i) the route is less than ideal for extrapolating to human risk from exposure by inhalation or dermally; (ii) xenobiotics often cause neoplasms at this site when given at high concentrations; and (iii) neoplasms at sites distant from the site of exposure were found in only one sex of one species. 3. None of the studies of styrene or styrene oxide reported here is well suited for extrapolating to potential carcinogenic activity in humans, because all have deficiencies in design, conduct and/or interpretation. An up-to-date chronic inhalation study would have to be conducted in order to evaluate this aspect of hazard assessment.

Animals↗
PubMed1977

Organ distribution and nervous system binding of styrene and styrene oxide.

Ten adult male rats were injected intraperitoneally with 460 mumol of styrene oxide with radioactive label. Fifteen similar rats were injected similarly with 577 mumol of styrene. The distribution of styrene in central nervous system, blood, liver, lungs, kidneys and duodenum was studied 3, 6 and 24 h after the injection while the same studies were done with styrene oxide 3 and 6 h after the injection. The liver, brain, kidney and duodenal contents of styrene and styrene oxide were higher than that in blood, lungs and spinal cord while the macromolecule-associated styrene oxide in the central nervous system was small. The removal of injected compounds was slow between 3 and 6 h after the injection in the organ systems although lipid-soluble compounds tended to diminish in brain more rapidly than the total radioactivity.

Animals↗
PubMed2005

Ring-oxidized metabolites of styrene contribute to styrene-induced Clara-cell toxicity in mice.

Styrene produced cytotoxicity in the terminal bronchioles of mice, but not rats, due to metabolites produced in situ by CYP2F2 metabolism. It has generally been presumed that styrene toxicity is mediated by styrene 7,8-oxide, but styrene oxide is not much more toxic than styrene. In contrast, ring-oxidized metabolites (4-vinylphenol or its metabolites) induce much greater toxicity. Administration of 4-vinylphenol results in pneumotoxicity, based on analysis of bronchoalveolar lavage fluid (BALF) at a 5- to 10 fold lower dose than does styrene oxide. In the current research, studies demonstrated that ip administration of 4-vinylphenol for 14 consecutive days at dosages of 6, 20, or 60 mg/kg/d (split into 3 doses) produced cytotoxicity in the terminal bronchioles of mice, but not rats. While higher doses of 4-vinylphenol produced adverse effects in both liver and lung, no liver toxicity was seen in mice exposed to 60 mg/kg/d for 14 d. Approximately 4 d was required for BALF parameters to return to normal following a single administration of 4-vinylphenol. These studies add further support for the role of ring-oxidized metabolites in the pneumotoxicity induced by styrene in mice and the lack thereof in rats.

Animals↗
PubMedDate not supplied

Analysis of styrene and its metabolites in blood and urine of workers exposed to both styrene and acetone.

A purge-and-trap gas chromatographic (PT-GC) method for determining styrene concentrations in urine and blood samples has been used in the biological monitoring of workers exposed to styrene and acetone. Blood and urine samples were collected from 34 individuals exposed to both solvents at the end of a 4-h shift and measured for styrene in urine (Su), blood (Sb), and the two major urinary metabolites, mandelic acid (MA) and phenylglyoxylic acid (PGA). A second urine sample was taken at the beginning of the next shift. Environmental exposure was measured using passive personal monitoring and GC. Urinary excretion of MA and PGA was measured by high-performance liquid chromatography. The average exposures to styrene and acetone were 70.5 mg/m3 and 370.5 mg/m3, respectively. In end-of-shift samples there was a significant correlation between concentrations of Su and Sb and the metabolites PGA, MA (r = 0.714 and 0.788, p < 0.001 for Su and r = 0.644 and 0.566, p < 0.005 for Sb). A high correlation between Sb and Su (r = 0.732, p < 0.001) also existed. Poor correlations were found between Su and metabolites in samples collected at the beginning of the next shift (r = 0.491 and 0.474 for PGA and MA, respectively, p < 0.05). There was a better correlation between the biological parameters at the end of the shift and the environmental styrene (r = 0.841 for PGA, r = 0.834 for MA, r = 0.788 for Su, and r = 0.698 for Sb; p < 0.001) compared with those at the start of the shift (r = 0.81 for PGA, 0.675 for MA, and 0.650 for Su; p < 0.001). We found that the concentration of excreted metabolites decreased significantly when environmental concentrations of acetone increased (p < 0.05), particularly at the end of the shift. Although the best correlation with environmental styrene was obtained with the sum of PGA and MA at the end of the shift (r = 0.862, p < 0.001), urine and blood styrene were shown to be more useful biological monitoring indicators because their concentrations were not affected by acetone co-exposure.

Acetone↗
PubMed1978

Blood styrene and urinary metabolites in styrene polymerisation.

The results of the analysis of blood and urine samples for styrene and its metabolites in 491 workers in a styrene polymerisation plant in the United States are reported. The levels of exposure to styrene were estimated to be less than 10 ppm, but nevertheless styrene and metabolites were detectable in more than 50% of workers in polymerisation jobs, within 4 h of exposure. Workers involved in the manufacture and purification of styrene from ethyl benzene also had detectable blood styrene and urinary metabolites in 83% of recently exposed subjects. The relationship between styrene in blood and in subcutaneous fat and urinary metabolites as pharmacokinetic variables is discussed.

Chemical Industry↗
PubMed1979

Styrene and styrene oxide concentrations in the air during the lamination process in the reinforced plastics industry.

Styrene and styrene oxide concentrations were measured during the lamination process in the reinforced plastics industry. The mean concentration of styrene in the personal samples was 130 ppm, the highest value measured being 350 ppm. The average concentration for styrene oxide alone was 0.1 ppm, whereas the corresponding measurement for styrene oxide and its decomposition products combined was 0.7 ppm. In comparison then, the concentrations of styrene oxide and its derivatives were much lower (about 0.5% of the total) than those of styrene.

Air↗
PubMed1989

Metabolism of Styrene Oxide and 2-Phenylethanol in the Styrene-Degrading Xanthobacter Strain 124X.

Styrene oxide and 2-phenylethanol metabolism in the styrene-degrading Xanthobacter sp. strain 124X was shown to proceed via phenylacetaldehyde and phenylacetic acid. In cell extracts 2-phenylethanol was oxidized by a phenazine methosulfate-dependent enzyme, probably a pyrroloquinoline quinone enzyme. Xanthobacter sp. strain 124X also contains a novel enzymatic activity designated as styrene oxide isomerase. Styrene oxide isomerase catalyzes the isomerization of styrene oxide to phenylacetaldehyde. The enzyme was partially purified and shown to have a very high substrate specificity. Of the epoxides tested, styrene oxide was the only substrate transformed. The initial step in styrene metabolism in Xanthobacter sp. strain 124X is oxygen dependent and probably involves oxidation of the aromatic nucleus.

Journal Article↗
PubMed1985

Perinatal development of cytochrome P-450, cytochrome C reductase, aryl hydrocarbon hydroxylase, styrene monooxygenase, and styrene epoxide hydrolase in rabbit liver microsomes and nuclei.

The development of cytochrome P-450, cytochrome C reductase, aryl hydrocarbon hydroxylase, styrene monooxygenase, and styrene epoxide hydrolase was studied in fresh rabbit liver nuclear and microsomal preparations. Enzymatic activities were determined in rabbit fetus at 21 and 30 days of gestation and in rabbits at 1, 5, 11, 22, 44, and 60 days of age. In extrauterine life, nuclear cytochrome P-450, aryl hydrocarbon hydroxylase, and styrene epoxide hydrolase were found to develop later than their microsomal counterparts, whereas nuclear cytochrome C reductase developed earlier than its microsomal counterpart. The behavior of styrene monooxygenase was more complex. The only activities detectable before birth were styrene epoxide hydrolase, styrene monooxygenase, and cytochrome C reductase in both nuclei and microsomes. The microsomes-to-nuclei epoxide hydrolase activity ratio was almost ten times the microsomes-to-nuclei styrene monooxygenase ratio, indicating a dissociation in the development of the two enzymes in rabbits. Nuclear metabolic activity was high at all ages, suggesting possible toxicological relevance.

Animals↗
PubMed1984

Activation of styrene to styrene oxide in hepatocytes and subcellular fractions of rat liver.

The oxidation of styrene to styrene oxide and the hydration of this metabolite to styrene glycol was investigated in hepatocytes, 9000 x g supernatant (S9) and the microsomal fraction from rat liver. Similar amounts of free styrene oxide were found in microsomes, hepatocytes and S9. However, on the basis of the formation of styrene glycol and the depletion of glutathione (GSH), it appeared that hepatocytes were the most active system in the metabolism of styrene, followed by S9 and microsomes.

Animals↗
PubMed1997

Effects of inducers and inhibitors on the microsomal metabolism of styrene to styrene oxide in mice.

Styrene is both hepatotoxic and pneumotoxic in mice, with non-Swiss albino (NSA) mice being more sensitive than Swiss (CD-1) mice. The toxicity of styrene is potentiated by treatment with phenobarbital, beta-naphthoflavone, or pyridine. Since the toxicity of styrene is generally associated with its metabolism to styrene oxide (SO), the formation of SO by hepatic and pulmonary microsomes of NSA and CD-1 mice was measured to examine correlations with toxicity. Both enantiomers of SO were quantified since the R-SO enantiomer is more toxic than the S-SO enantiomer. No strain differences in rates of styrene metabolism or enantiomeric ratio were observed in control mice or mice treated with inducers. Pyridine, an inducer of CYP2E1, increased S-SO but not R-SO formation in liver. Phenobarbital, an inducer of CYP2B, increased the production of both enantiomers. beta-Naphthoflavone, an inducer of CYP1A, had no effect. None of the inducers had any effect in lung. Addition of the CYP2E1 inhibitor diethyldithiocarbamate decreased the formation of both enantiomers in both tissues from control mice, whereas 5-phenyl-1-pentyne (an inhibitor of CYP2F2) inhibited metabolism primarily in lung. In both control and phenobarbital-treated mice, SKF525A inhibited both R-SO and S-SO in liver but only S-SO in lung. Thus there are tissue differences in metabolism and susceptibility to induction and inhibition but no strain differences in metabolism to explain differences in susceptibility to styrene-induced toxicity.

Animals↗
PubMed1996

Styrene metabolism in Exophiala jeanselmei and involvement of a cytochrome P-450-dependent styrene monooxygenase.

The yeast-like fungus Exophiala jeanselmei degrades styrene via initial oxidation of the vinyl side chain to phenylacetic acid, which is subsequently hydroxylated to homogentisic acid. The initial reactions are catalyzed by a NADPH- and flavin adenine dinucleotide-dependent styrene monooxygenase, a styrene oxide isomerase, and a NAD(+)-dependent phenylacetaldehyde dehydrogenase. The reduced CO-difference spectrum of microsomal preparations of styrene-grown cells shows a characteristic absorption maximum at 450 nm, which strongly suggests the involvement of a cytochrome P-450-dependent styrene monooxygenase. Inhibition of styrene monooxygenase activity in cell extracts by cytochrome P-450 inhibitors SKF-525-A, metyrapone, and CO confirms this assumption.

Air Pollutants↗
PubMedDate not supplied

Inhibitory characteristics of styrene & styrene oxide on Na+,K+ activated adenosine triphosphatase.

Styrene, an important ingredient of plastic, is reported to cause it neurotoxic effects through its important metabolite styrene oxide. Na+, K+ -ATPase (NKA), an important enzyme in the neurotransmission processes, is found to be inhibited by styrene (200 mg/kg) and styrene oxide (55 mg/Kg) by 15 and 45% respectively. Kinetic evaluations show that Km values, number of interaction sites and rate of reaction, with respect to K+ ions, decreased in styrene oxide treated NKA samples. However, high Km values of Na+ sites suggest for low affinity with respect to Na+ ions. Na+ and K+ ion activation, ATP hydrolysis and ouabain titration patterns indicate for a conformational change in NKA mainly due to styrene oxide.

Administration, Oral↗
PubMed1981

Styrene oxidation to styrene oxide in human blood erythrocytes and lymphocytes.

Human erythrocytes and lymphocytes catalyzed styrene oxidation to styrene oxide. The erythrocyte catalyzed reaction was inhibited by CO, occurred in the absence of NADPH and NADH and was undetectable in the absence of O2 and with erythrocyte membranes. Lymphocyte catalyzed styrene oxide formation required the addition of cofactors and these cells showed 6 times the activity of erythrocytes with a 4 times lower styrene concentration. Although lymphocytes appear to be more active than red blood cells in styrene oxidation, their contribution to styrene metabolism in whole blood seems extremely small.

Epoxy Compounds↗