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PubMed1986

The developmental toxicity of xylene and xylene isomers in the Hydra assay.

Two laboratories tested multiple forms of xylene for their developmental toxicity hazard potential (A/D ratio) by means of the hydra assay. The three isomers, as well as a solution of mixed xylenes, all interfered with development (D) at or near to concentrations that also were toxic to adult (A) hydra. The A/D ratios ranged from 1 to 2 in hydra as they had in conventional tests made in pregnant laboratory animals. Each testing laboratory concluded that xylenes were not primary developmental hazards but coaffective agents capable of disrupting development only at or near to concentrations also toxic to adults. In each instance every xylene tested interfered with the same stage or developmental sequence and in a concentration-related manner. The hydra assay may be useful for establishing priorities to test agents in a more elaborate system, but substances less soluble than xylene may exceed the test's applicability.

Animals↗
PubMed1983

[Regulation of the enzyme activity of para-xylene catabolism in a spontaneous para-xylene-negative variant of Pseudomonas aeruginosa 2x79].

A spontaneous variant of Pseudomonas aeruginosa 2x unable to grow on p-xylene as the sole source of carbon and energy has been isolated. p-Xylenenegative variant of P. aeruginosa 2x79 differs from the wild type strain by the character of growth on the p-xylene oxidation intermediates p-toluate and protocatochuate. The cell of 2x79 variant inability to grow on p-xylene has been shown to be accompanied by the elimination of the activities of three enzymes - p-xylene methylhydroxylase, p-cresol methylhydroxylase and metapyrocatechase and by the considerable alteration in the regulation of orto-cleavage aromatic ring enzymes activity pyrocatechase and protocatechuate-3,4-dioxygenase. Possible reasons for appearing spontaneous variants 2x79 in the population of P. aeruginosa 2x growing on the p-xylene are being discussed.

Benzoates↗
PubMed1988

Oral toxicology studies with xylene isomers and mixed xylenes.

Xylene isomers and mixed xylenes were administered to male and female Sprague-Dawley rats to evaluate their effects on standard toxicological parameters which included body and organ weights, hematology, serum chemistries, urinalysis and histopathological examination. In the initial study, m, o- or p-xylene were administered in corn oil by gavage for 10 consecutive days at dose levels of 250, 1000 and 2000 mg/kg/day. The most noteworthy changes were increased liver weight in both sexes for all three isomers while decreases in spleen and thymus weights were seen less frequently. Rats were subsequently exposed to mixed xylenes by gavage in corn oil for 90 consecutive days at dose levels of 150, 750 and 1500 mg/kg/day. The most significant findings of the subchronic study were enlarged livers and kidneys. Histopathological evaluation of liver and kidney tissues revealed an increased incidence of minimal chronic renal disease in only female rats, while treatment related hepatic histopathological changes were not detected in either sex.

Administration, Oral↗
PubMed2002

Preparation and crystallographic characterization of a new endohedral, Lu3N@C80.5 (o-xylene), and comparison with Sc3N@C80.5 (o-xylene).

The trimetallic nitride template (TNT) approach has been successfully utilized to prepare the new endohedral Lu(3)N@C(80). Well-ordered crystals of Lu(3)N@C(80).5 (o-xylene) and Sc(3)N@C(80).5 (o-xylene) form upon cooling of o-xylene solutions of these endohedrals and they are isomorphous. Although the positions of the fullerene cage (which is fully ordered and located at a crystallographic center of symmetry) and the o-xylene molecules are nearly identical in these two structures, the positioning of the metal ions in the two crystals differ in significant ways. However, the expected difference in sizes of lutetium and scandium does not affect the dimensions of the C(80) cage. Nevertheless, the positions of the metal atoms do produce a slight outward dislocation of the immediately adjacent carbon atoms.

Journal Article↗
PubMed2002

Toluene, xylenes and xylene isomers in urine as biological indicators of low-level exposure to each solvent; a comparative study.

OBJECTIVE: To examine if xylenes and xylene isomers in end-of-shift urine are good biological indicators of low-level exposure to each solvent, similarly to toluene in urine. METHODS: The study was conducted in the latter half of a working week. Furniture makers, 86 subjects in total (76 men and ten women), participated in the study in combination with 11 non-exposed subjects. Time-weighted average (8-h TWA) exposures to mixtures of toluene (TOL-A), xylenes (XYLs-A), ethylbenzene (EB-A), acetone (ACE-A) etc. were monitored with diffusive samplers for lipophilic and hydrophilic solvents, respectively. Urine samples (i.e., TOL-U, XYLs-U, EB-U, ACE-U, etc.) were collected at the end of the shift and subjected to head-space gas chromatography analysis for each solvent. The exposure-excretion relationship was examined by simple as well as multiple regression analysis. RESULTS: The exposures to TOL and XYLs were around or below current occupational exposure limit levels. The exposures to other solvents [i.e., ACE, EB, methyl ethyl ketone (MEK), methyl isobutyl ketone (MIBK), etc.] were at substantially lower levels. The correlation of the TWA solvent exposure concentration with the concentration of the corresponding solvent in the end-of-shift urine sample was close for TOL, and also almost equally close in the case of XYLs and each of the three XYL isomers. Whereas the slope of the regression line for XYLs was significantly less steep than that for TOL when compared on an equi-molar basis, there was no difference among the three XYL isomers. No confounding effects of age, sex and co-exposure to other solvents were detected. The observation confirms previous reports that TOL-U is a good marker of TOL vapor exposure, indicates that XYL-U is also a reliable marker of exposure to vapors of XYLs or any of the three XYL isomers, and suggests that estimation of exposure to vapors of XYLs (i.e., three isomers in combination) is possible by the determination of one of the XYL isomers in urine, once the proportion of the isomers in air is known. Possible association of water solubility with solvent levels in urine is discussed. CONCLUSIONS: Biological monitoring of exposure by means of analysis of end-of-shift urine for mother solvent is possible, not only in the case of TOL as previously reported, but also in cases of XYLs, either for three isomers in combination or separately.

Adult↗
PubMed1996

The effect of ageing and in vitro exposure to xylene and KCl on [Ca2+]i in synaptosomes from rats exposed prenatally to xylene.

Female rats (Mol: WIST) were exposed prenatally to 500 p.p.m. of technical xylene on days 7-20. At the age of fourteen months the rats were sacrificed and the synaptosomal fraction prepared for in vitro studies. The cytosolic calcium concentration was measured using the FURA-2 technique. The cytosolic calcium was increased in synaptosomes from old rats compared to those from rats at the age of three months, but no effect of prenatal exposure was seen. When synaptosomes were incubated with xylene, potassium or both, the cytosolic calcium concentration was changed identically in all groups of rats. When synaptosomes were incubated simultaneously to xylene and potassium a dramatical leakage of FURA-2 was observed. The mechanisms behind the membrane leakage are discussed.

Aging↗
PubMed2003

Comparing differentiation of xylene isomers by electronic ionization, chemical ionization and self-ion/molecule reactions and the first observation of methyne addition ions for xylene isomers in self-ion/molecule reactions for non-nitrogenated compounds.

This study presents the self-ion/molecule reaction (SIMR) spectra of three xylene isomers, and proposes an approach to differentiating them based on observed differences in relative abundances of ions formed by SIMR in an internal source ion trap instrument. It also demonstrates the applicability of SIMR for isomer discrimination, which is better than electron ionization (EI) and dimethyl ether chemical ionization (DME CI) in an ion trap mass spectrometer (ITMS) since no CI reagent, metal ions or internal standards are required to perform SIMR. The merits of the new method for distinguishing isomers are that it is simple, rapid and economic. To date, methyne addition products ([M+13](+) ions) have been observed for several nitrogenated compounds including aza-crown ethers, aniline and dopamine from SIMR in the ITMS. The xylene isomers are, however, the first three non-nitrogenated compounds that have been shown to produce the methyne addition ions in SIMR.

Journal Article↗
PubMed1997

Induction of mouse cytochrome P450 2B enzymes by amine metabolites of musk xylene: contribution of microsomal enzyme induction to the hepatocarcinogenicity of musk xylene.

Musk xylene (MX) is a synthetic nitromusk perfume ingredient that, although uniformly negative in genotoxicity testing, causes liver tumors in B6C3F1 mice. MX is also capable of inducing cytochrome P450 enzymes in a manner similar to that of phenobarbital (PB), which suggests that epigenetic mechanisms may be involved in the carcinogenic response. At the same time, MX is metabolized in vivo by nitroreduction, a reaction catalyzed by intestinal flora that yields aromatic amine metabolites. These amine metabolites are also capable of inactivating CYP2B10, the major cytochrome P450 enzyme induced by MX treatment. In the study reported here, the monoamine metabolites of MX, o- and p-NH2-MX, were evaluated for their potential to induce CYP2B10 and CYP1A2 mRNAs. Northern blot analyses indicated that both amines markedly induced CYP2B10 mRNA, whereas CYP1A2 mRNA, the enzyme implicated in the bioactivation of aromatic amines and frequently induced by aromatic amines, was induced only slightly, a response that was not different from that seen with PB. Induction of CYP2B10 mRNA suggested that the amine metabolites may contribute to the enzyme induction profile seen with MX treatment. To test this hypothesis, mice were treated with broad-spectrum antibiotics (neomycin, tetracycline, and bacitracin) to eliminate the intestinal flora and prevent formation of o- and p-NH2-MX. In antibiotic-treated mice treated with MX (200 mg/kg) for 4 d, no evidence of microsomal enzyme induction was observed, including no increases in liver weight, total cytochrome P450 content, or CYP2B protein levels. These results indicate that the amine metabolites of MX are responsible for the enzyme induction seen after MX administration. Thus, the biochemical and molecular effects of amine metabolites of MX are markedly different from those of other aromatic amines but very similar to those of PB. Therefore, it appears that MX is a non-genotoxic chemical that may cause mouse liver tumors in a manner analogous to that of PB.

Amines↗
PubMed1997

The Effect of Sodium Dodecyl Sulfate and M-alpha-Cyclodextrin on the Solubility and Partitioning of Xylenes in Aqueous Solutions

The solubility and the partitioning of p- and o-xylene in aqueous solutions containing M-alpha-CD, a partially methylated alpha-cyclodextrin, and the anionic surfactant sodium dodecyl sulfate (SDS) were studied by extraction experiments to evaluate the applicability of liquid membrane permeation for the separation of xylene isomeres. Experiments were carried out with the pure xylenes and 1:1 mixtures of o- and p-xylene. The interactions of M-alpha-CD and SDS and their effects on the solubility and partitioning of xylenes were investigated. M-alpha-CD was found to form 1:1 complexes with p- and o-xylene. Formation constants were determined as 141 M-1 for p-xylene and 48 M-1 for o-xylene, respectively, which are higher than those reported with nonmethylated alpha-CD. This can be explained by additional hydrophobic interactions with the methyl groups of the cyclodextrin. In contrast to the solubility in CD solutions, o-xylene was found to be more soluble than p-xylene in aqueous solutions of SDS. At constant concentrations of M-alpha-CD the addition of SDS led to the displacement of p-xylene from the cyclodextrin cavity, which resulted in a decrease in its solubility. This decrease lasted until micelles were formed. Due to the solubilization of p-xylene in the micelles, further addition of SDS resulted in a linear increase in the solubility of p-xylene. However, at constant CD concentrations the solubility of o-xylene increased with the addition of SDS until about 5 mmol/liter SDS. This might be attributed to the formation of a ternary complex consisting of cyclodextrin, o-xylene, and SDS. At SDS concentrations greater than 5 mmol/liter, the solubility of o-xylene decreased, which was probably due to the formation of a more stable complex between SDS and M-alpha-CD. An addition of SDS beyond a critical concentration (CMC), where micelles are formed, resulted again in a linear increase of o-xylene solubility. The CMC was found to depend linearly on the concentration of M-alpha-CD in aqueous solution. Extraction experiments with a 1:1 mixture of o- and p-xylene showed that the two xylenes and SDS are in competition for M-alpha-CD. Since surfactants are always present when using emulsion liquid membranes and due to the complex interactions between SDS, the xylenes, and M-alpha-CD, no sufficient selectivity for the separation of the xylenes by liquid membrane permeation could be achieved.

Journal Article↗
PubMed2006

The role of toxicokinetics in xylene-induced ototoxicity in the rat and guinea pig.

In the rat, some aromatic solvents cause a high level of ototoxicity that is characterized by damage to outer hair cells in the cochlea, which results in irreversible hearing loss. However, there is a vast difference in their potency. Among the three isomers of xylene, only para-xylene has been shown to be ototoxic in the rat. Moreover, all the species do not show the same susceptibility to ototoxic solvents, the rat being the most susceptible and the guinea pig seeming resistant to this ototoxic effect. The objective of the study was to determine whether toxicokinetic factors could explain the differences in ototoxicity observed among the three isomers of xylene in the rat and the species-dependent ototoxicity in the rat and the guinea pig. Blood and brain concentrations of each isomer were monitored in Sprague-Dawley rats treated orally by gastric intubation with a single dose or a 10 day-repeated treatment of 8.47 mmol/kg (an ototoxic dosage for para-xylene) of each isomer. Moreover, histology of the cochlea was carried out and the toxicokinetics of meta-xylene was monitored in rats treated with a single dose or a 10 day-repeated treatment of 16.94 mmol/kg meta-xylene, a non-ototoxic isomer. Similarly, histology of the cochlea was carried out and the toxicokinetics of para-xylene was followed in guinea pigs treated by gavage with a single dose or a 10 day-repeated treatment of 8.47 mmol/kg para-xylene. Finally, the blood and brain concentrations of para-xylene were measured in both the rats and the guinea pigs after a 4-h exposure to 1800 ppm of para-xylene. Among the three isomers studied, para-xylene yielded the highest blood and brain concentrations in the acutely and repeatedly exposed rats. When given a high dosage of meta-xylene (16.94 mmol/kg), the rats showed blood and brain concentrations of meta-xylene in the same order as those obtained with 8.47 mmol/kg para-xylene, but no outer hair cell loss was observed. No outer hair cell loss was observed in the guinea pigs treated with para-xylene. Whatever the exposure pattern, the blood and brain concentrations of para-xylene in the rats were 3.1-9.5 times higher than those measured in the guinea pigs. These results indicate that toxicokinetic factors cannot explain the differences in ototoxicity observed with the three isomers in the rat. However, they suggest that the differences in susceptibility to para-xylene observed between the rats and the guinea pigs might be due to toxicokinetic factors.

Animals↗
PubMed1991

Metabolic interaction and disposition of methyl ethyl ketone and m-xylene in rats at single and repeated inhalation exposures.

1. Rats were exposed to m-xylene (300 ppm) and methyl ethyl ketone (MEK, 600 ppm) vapour, separately and in combination. 2. Repeated exposures to m-xylene enhanced liver drug-metabolizing capacity, whereas MEK showed no effects. After mixed exposure the cytochrome P-450-dependent monooxygenase activities were additively or synergistically induced. 3. In the presence of MEK the overall metabolism of xylene was strongly inhibited both after single and repeated exposures, an effect accompanied by elevation of xylene concentration in blood (18-29%) and fat (25-32%). 4. The 24-h excretion of the urine metabolites of m-xylene was decreased by 22-24% in mixed exposures: the excretion of methylhippuric acid was decreased (29%), but that of 2,4-dimethylphenol increased (9-35%). 5. After repeated inhalation exposures the excretion of xylene metabolites in urine was consistently higher, whereas the concentrations of xylene in fat (but not the concentration of MEK) were lower than after a single treatment, conceivably due to accelerated metabolic clearance of xylene. 6. Thioether excretion in urine was enhanced in xylene-treated rats (7-13-fold), but was not influenced by the induced changes in the metabolism of xylene. Xylene inhalation caused liver GSH to decrease slightly (10%), as did inhalation of MEK, but the latter did not enhance the excretion of thioethers. 7. MEK is a potent inhibitor of the side-chain oxidation of m-xylene producing methylhippuric acid, but not of its ring oxidation to 2,4-dimethylphenol, and exhibits a synergistic inducing effect on liver enzymes responsible for the oxidation of m-xylene. The increased ring oxidation of m-xylene was not associated with increased production of reactive metabolites indicated by GSH-depletion or thioether formation.

Administration, Inhalation↗
PubMed1985

An overview of environmental and toxicological aspects of aromatic hydrocarbons. III. Xylene.

The commercial product "mixed xylenes" (a technical product generally containing approximately 40% m-xylene and 20% each of o-xylene, p-xylene and ethylbenzene, as well as small quantities of toluene) analogously to toluene is an agent of major chemical and occupational significance. It is produced in very large quantities and is extensively employed in a broad spectrum of applications, primarily as a solvent for which its use is increasing as a "safe" replacement for benzene, and in gasoline as part of the BTX component (benzene-toluene-xylene); xylenes are also frequently used in the rubber industry with other solvents such as toluene and benzene. As individual isomers they are extensively employed in the synthesis of synthetic agents, for example phthalic acid, isophthalic acid, terephthalic acid and dimethylterephthalate, which have very broad applications in the further preparation of phthalate ester plasticizers and components of polyester fiber, film and fabricated items. There is a broad potential for exposure both to industrial workers in the production and use of the xylenes and to the general public (via vehicle exhausts, consumer products, etc). Compared with benzene and toluene, very much less is known of the human health hazards, particularly the chronic effects of xylenes, either as mixed xylenes, as individual isomers or in admixture with other alkylbenzenes. It is of importance to note that coal-based solvents (e.g., xylene) have been suggested to be possible potent lymphocytic leukemogens, such as benzene, in a limited study of the relationship between lymphocytic leukemia and exposures to benzene and other solvents in the rubber industry. Available animal data on the carcinogenicity of xylene(s) are inadequate to permit an evaluation. Mixed xylenes are currently being investigated in a chronic bioassay by the National Toxicology Program. In limited studies thus far, the individual isomers have not been found genotoxic when tested in a number of short-term tests.

Biological Transport↗
PubMed1986

Lung metabolism of benzo[a]pyrene in rats treated with p-xylene and/or ethanol.

The metabolism of benzo[a]pyrene (BaP) may be altered by xenobiotic compounds. The effects of p-xylene and ethanol on the lung metabolism of BaP were studied. p-Xylene was administered by ip injection at doses ranging from 0.1 to 1.0 g/kg (1:1 in soybean oil). Ethanol was administered po at 5 g/kg (40% w/v). Rats given p-xylene, ethanol, or p-xylene and ethanol were sacrificed 1 h after treatment. Additional time points of 15 min, 30 min, 4 h, and 24 h after p-xylene (1 g/kg) were examined. 3-Hydroxy-BaP (3-OH) formation was measured fluorometrically as aryl hydrocarbon hydroxylase activity (AHH) in lung microsomes. p-Xylene (1 g/kg) inhibited the formation of 3-OH BaP 40% at 15 min, 27% at 30 min, 43% at 1 h, and 39% at 4 h after treatment. Inhibition of AHH activity was still present 24 h after dosing (41%). AHH activity was inhibited 27% and 46% at 0.5 mg/kg and 1.0 mg/kg p-xylene (1 h), respectively, while the lowest dose (0.1 mg/kg) did not change activity. Analysis of the major metabolites of BaP by high-performance liquid chromatography (HPLC) demonstrated that the formation of 3-OH and 4,5-diol BaP were inhibited 32% and 50%, respectively, in lung microsomes prepared 24 h after a single injection of p-xylene (1 g/kg). None of the other metabolites analyzed were changed by p-xylene. Ethanol had no effect on 3-OH BaP formation during a 1-h treatment. A combined dose of ethanol and p-xylene moderately inhibited 3-OH BaP formation. These findings indicate that BaP detoxication (i.e., 3-OH formation) in rat lung is selectively inhibited by p-xylene but not ethanol. Ethanol appears to modify the inhibitory effect of p-xylene.

Animals↗