Disease relevance of styrene

• Probing structure/function relationships of HIV-1 reverse transcriptase with styrene oxide N2-guanine adducts [1].
• There appear to be many similarities between the toxicity and metabolism of styrene in rodents and humans [2].
• 2. Styrene oxide was carcinogenic to the forestomach of both sexes of rats and mice after gavage exposure and was associated with an increase in liver neoplasms in male mice in one study [3].
• Copolymers of vinyl bases with acrylic acid and styrene or 1-vinyluracil with maleic acid were found to stimulate in vitro polyphenylalanine synthesis using a system extracted from Escherichia coli MRE600 [4].
• Kinetic mechanism of the enantioselective conversion of styrene oxide by epoxide hydrolase from Agrobacterium radiobacter AD1 [5].

Psychiatry related information on styrene

• Epidemiologists have suggested that neuropsychological deficits such as slowing of reaction time, loss of color vision, and vestibulooculomotor dysfunction are reliably induced by styrene at levels near or below current exposure standards, which range from 20 to 50 ppm in most of the world [6].
• This study shows that despite the weakening of hepatocyte defense mechanisms by hypoxia, styrene is not acutely toxic to these cells [7].
• Those with higher styrene exposure showed a significant impairment of short-term memory only [8].
• Finally, when a 7-day recovery period for noise-induced hearing loss was interposed before audiometric testing, the combined exposure to styrene and noise was not more potent than noise alone in elevating auditory thresholds [9].
• A group of 98 male workers occupationally exposed to styrene was interviewed for information on the amount and frequency of alcohol consumption and changes in consumption frequency and tolerance [10].

High impact information on styrene

• Early data showed that styrene oxide hydrolase activity was associate with the microsomal subcellular fraction [11].
• Antibodies against homogeneous epoxide hydratase provide evidence for a single enzyme hydrating styrene oxide and benz(a)pyrene 4,5-oxide [12].
• Composed of a glycidylmethacrylate (GMA) and styrene copolymer core with a GMA polymer surface, the beads minimize nonspecific protein binding and maximize purification efficiency [13].
• Biochemistry, genetics and physiology of microbial styrene degradation [14].
• The compound is of major importance in the petrochemical and polymer-processing industries, which can contribute to the pollution of natural resources via the release of styrene-contaminated effluents and off-gases [14].

Chemical compound and disease context of styrene

• The toxicity of vinyltoluene to cultured lymphocytes was similar to that of styrene while 4-methoxy-beta-chlorostyrene was about 10 times and beta nitrostyrene about 100 times more toxic than styrene [15].
• The P450 forms responsible for transforming styrene to styrene glycol were determined by analyzing cDNA-expressed individual P450 forms produced in cultured hepatoma G2 cells by recombinant vaccinia viruses [16].
• Towards a biocatalyst for (S)-styrene oxide production: characterization of the styrene degradation pathway of Pseudomonas sp. strain VLB120 [17].
• Naphthalene dioxygenase (NDO) from Pseudomonas sp. strain NCIB 9816-4 adds both atoms of the dioxygen molecule to styrene to form (R)-l-phenyl-1,2-ethanediol [18].
• Purification and characterization of phenylacetaldehyde reductase from a styrene-assimilating Corynebacterium strain, ST-10 [19].

Biological context of styrene

• After accounting for the disparate exposures to the two chemicals, a typical worker received 71% of the systemic dose of SO via inhalation; nonetheless, 5 of the 20 subjects received the majority of the SO dose from styrene [20].
• Metabolic activation of styrene by erythrocytes detected as increased sister chromatid exchanges in cultured human lymphocytes [21].
• Among individual subjects, albumin and DNA adducts as well as sister chromatid exchanges were significantly correlated with styrene exposure [20].
• Ten reactive metabolites of five polycyclic aromatic hydrocarbons and styrene were investigated to determine the generality of ester adduct formation with human hemoglobin in the form of RBC and hydrolysis to the corresponding tetrahydrotetrols or dihydrodiols [22].
• The question addressed was whether stimulation of cell proliferation could be responsible for tumor induction in the forestomach by styrene 7,8-oxide (SO) [23].

Anatomical context of styrene

• This level of induction correlates well with the 5-fold induction in catalytic activity of epoxide hydrolase (using styrene 7,8-oxide as substrate) in microsomes isolated from phenobarbital-treated rats [24].
• The results show that erythrocytes are essential for the activation of styrene in the lymphocyte test system [21].
• Addition of 1 mM styrene oxide caused 75-100% and 4-8-fold increase in AFB1-DNA binding in control and treated hepatocytes, respectively, with corresponding decreases in thiol conjugation [25].
• There is preliminary evidence for the presence of DNA adducts and for adducts in hemoglobin and albumin in blood cells of styrene-exposed workers [26].
• Styrene oxide, like many intermediate metabolites of foodstuffs, is genotoxic and, if introduced directly into the stomachs of rodents in high doses/concentrations, gives rise to cancers of the forestomach [27].

Associations of styrene with other chemical compounds

• Also, the addition of styrene 7,8-oxide and glutathione to ram seminal vesicle microsomes did not yield styrene glutathione adducts [28].
• The roles of His-64, Tyr-103, Tyr-146, and Tyr-151 in the epoxidation of styrene and beta-methylstyrene by recombinant sperm whale myoglobin [29].
• The xenobiotic epoxide hydrolase inhibitor, 3,3,3-trichloropropene 1,2-oxide, potently inhibited microsomal hydrolysis of delta 16-ANDO 16,17-epoxides as well as of benzo[a]pyrene 4,5-epoxide and styrene 7,8-epoxide [30].
• The metabolism of styrene by prostaglandin hydroperoxidase and horseradish peroxidase was examined [28].
• CcP thus has a sufficiently open active site to form a phenyl-iron complex, to oxidize thioanisole to the sulfoxide, and to epoxidize styrene and beta-methylstyrene [31].

Gene context of styrene

• PHEMAs cannot be recommended as biomarkers of exposure to styrene, unless the GSTM1 genotype is considered in data interpretation [32].
• These data indicate that several human hepatic and/or pulmonary P450 forms are capable of metabolizing styrene, albeit at different rates [16].
• Multifactorial regression analysis indicated that SSB in DNA were significantly associated with styrene exposure and with heterozygosity in CYP2E1 (5'-flanking region and intron 6; r(2)=0.614) [33].
• The field survey confirms that styrene exposure is associated with increased DNA damage and indicates a modulating role for GSTM1 and GSTT1 genotypes [34].
• When the combined influence of the CYP2B6 genotype and the predicted activity of EPHX1 were examined, urinary metabolites in subjects with low enzyme activity were lower than in those with medium or high activity after high styrene exposure (>or=50 ppm) [35].

Analytical, diagnostic and therapeutic context of styrene

• Rat and mouse forestomach tumors induced by chronic oral administration of styrene oxide [36].
• Second, interruption of the submucosal collateral plexus by the intra-arterial injection of styrene microspheres (27-, 50-, or 90-microns diameter) produced acute intestinal mucosal damage [37].
• The specific activity of glutathione-S-epoxide transferase with styrene oxide and 3-methylcholanthrene-11, 12-oxide was determined in rat liver and lung during development from the fetal to the adult stage and after partial hepatectomy [38].
• Epidemiological studies of styrene-exposed populations [39].
• Several cohort studies have suggested that workers exposed to styrene in the chemical industry have increased mortality from lymphatic and hematopoietic cancer [39].

References