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PubMed1997

In vitro interference with hepatocellular uptake of bile acids by xylene.

Occupational exposure to a mixture of two widely used aromatic hydrocarbon solvents, xylene and toluene, has been associated with a significant rise in the concentrations of serum bile acids (SBA). We have recently shown that toluene interferes with the transport of bile acids by hepatocytes and this could explain elevated SBA after occupational exposure or following in vivo administration of this compound to experimental animals. However, it is not known if xylene, like its monomethylated homologue, toluene, could interfere with the processes of bile acid transport by hepatocytes. Therefore, the present studies were undertaken to examine this possibility. Direct addition of a non-cytotoxic dose (2.5 microliters/2.8 x 10(6) cells) of xylene (in vapour phase) to hepatocytes isolated from untreated rats significantly inhibited the initial rates (determined from slope of the lines in the linear range (20-80 s)) of uptake (V0) of 10 microM cholic acid (CA) and-taurocholic acid (TC) by 37 and 48%, respectively (P < 0.05). Similarly, accumulation of these substrates by hepatocytes over an extended incubation time up to 30 min was significantly inhibited to the same extent by xylene exposure. This inhibitory effect was found to be reversible when sufficient time was allowed for the cells to recover. In contrast, the initial rates (V0) of efflux (determined from slope of the lines in the linear range (1-5 min)) of these bile acids (25 microM) and their continuous efflux (up to 30 min) from preloaded cells incubated with a similar dose of xylene were not (except for the 1 min time point) significantly different from those of controls. In conclusion, xylene interferes with the transport of bile acids by hepatocytes in a manner largely similar to that of its monomethylated homologue, toluene. These findings extend our previous observations on aliphatic and aromatic hydrocarbon solvents and provide mechanistic data at a cellular level to support a causal role for xylene (as well as toluene) in raised SBA levels of exposed individuals.

Animals↗

PubMed1998

Sensitive determination of xylenes in whole blood by capillary gas chromatography with cryogenic trapping.

A new and sensitive method for measurement of o-, m- and p-xylenes in human whole blood by capillary gas chromatography (GC) with cryogenic trapping is presented. After heating 0.5 ml of whole blood and 0.5 ml of distilled water containing the xylenes and aniline (internal standard, I.S.) in a 4.0-ml vial at 100 degrees C for 30 min, 2 ml of the headspace vapor was drawn into a glass syringe. All vapor was introduced through the GC port into an AT-Wax middle-bore capillary column in the splitless mode at an oven temperature of 5 degrees C to trap the entire analytes, and the oven temperature was then programmed up to 180 degrees C. The present conditions gave sharp peaks for xylenes and aniline (I.S.), and low background noises for whole blood samples; the peaks of p- and m-xylenes showed about 90% separation with the AT-Wax column. As much as 41.0-46.3% of xylenes, which had been spiked to whole blood could be recovered. The calibration curves showed linearity in the range of 0.1-0.5 microg/0.5 ml of whole blood. The detection limit was estimated to be about 10 ng/0.5 ml. The coefficients of intra-day and inter-day variations for xylenes were not greater than 9.38%. The data for actual detection of xylenes in post-mortem blood of self-ignition suicide cases by the present method were also presented.

Aged↗

PubMed1999

Haemoglobin binding of a musk xylene metabolite in man.

1. Musk xylene (1-tert-butyl-3,5-dimethyl-2,4,6-trinitrobenzene) is used as a fragrance component in toiletries, detergents and skin care products. Musk xylene is widely distributed in the environment and has been identified as a persistent contaminant in fish and in mothers' milk. Experimental data in man indicate a slow elimination of musk xylene and a potential for accumulation. Nitroarenes may be biotransformed to the respective amines. Some aromatic amines are known to be tumorigenic in animals and in man. Quantitation of the binding of those aromatic amines to haemoglobin has been proposed as a biomarker of internal exposure. 2. To determine bioavailability, metabolic reduction and haemoglobin binding of musk xylene in man, we investigated the presence of musk xylene metabolites bound to haemoglobin in blood samples from rat and from 10 human volunteers not knowingly exposed to musk xylene. 3. Haemoglobin from the blood samples was isolated, and bound metabolites were liberated as amines by alkaline hydrolysis. In haemoglobin samples from all individuals, 1-tert-butyl-3,5-dimethyl-4-amino-2,6-dinitrobenzene and, after chemical derivatization, the corresponding N-perfluoropropyl amide were identified by GC/MS using electron-impact and electron-capture mass spectrometry. 4. The amounts of 1-tert-butyl-3,5-dimethyl-4-amino-2,6-dinitrobenzene bound to haemoglobin in the human blood samples ranged from 13 to 46 fmol/mg haemoglobin. 5. These data demonstrate that musk xylene is bioavailable in man. The use of haemoglobin binding as a biomarker for nitromusk exposure in the general population warrants further studies.

Adult↗

PubMed1999

Effect of low-level short-term o-xylene inhalation of benzo[a]pyrene (BaP) metabolism and BaP-DNA adduct formation in rat liver and lung microsomes.

o-Xylene is a commonly used solvent that alters mixed-function oxidase (MFO) activity in an organ- and isozyme-specific pattern following intraperitoneal (ip) administration. Similar MFO alterations have been observed after ip or inhalation exposure to other methyl benzenes. These MFO alterations shifted the metabolism of the carcinogen benzo[a]pyrene (BaP) toward formation of toxication metabolites in lung. The purpose of this study was to determine whether o-xylene inhalation caused similar MFO changes and whether these alterations were reflected in altered BaP metabolism and BaP-DNA adduct formation. o-Xylene (300 ppm, 6 h) decreased the activity of arylhydrocarbon hydroxylase (AHH) in lung. CYP2B1 activity (benzyloxyresorufin O-dealkylase; BROD), which is responsible for metabolism of BaP to relatively nontoxic metabolites, was decreased in lung, as was, to a lesser extent, CYP1A1 (ethoxyresorufin O-dealkylase; EROD), which is responsible for metabolism of BaP to reactive/toxic metabolites. The BROD/EROD ratio, an indirect indicator of the pattern of BaP toxication/detoxication, was decreased in lung, suggesting that BaP metabolism is shifted toward toxication. No MFO alterations were observed in liver. In lung microsomes, o-xylene increased formation of 7,8-BaP-diol, while 9,10-BaP-diol, 3-OH BaP, and 9-OH BaP were decreased. In liver, o-xylene increased 9-OH BaP formation, while 4,5- and 9,10-diols as well as total diols were decreased. The toxication/detoxication ratios for BaP individual and total metabolite groups were increased in lung microsomes and unaltered in liver. The major BaP-DNA adduct, BaP diol epoxide-N2-deoxyguanosine, was increased in lung but decreased in liver microsomes from o-xylene-exposed rats. Four minor BaP-DNA adducts were formed in lung and three in liver, only one of which (liver adduct 3) was decreased. The o-xylene-induced increase in BaP adduct formation in lung and decrease in liver indicate that coexposure to organic solvents such as the methyl benzenes may alter the carcinogenesis of BaP, or other PAHs, in an organ-specific fashion.

Administration, Inhalation↗

PubMed1999

Estimation of the dermal absorption of m-xylene vapor in humans using breath sampling and physiologically based pharmacokinetic analysis.

A physiologically-based pharmacokinetic model, containing a skin compartment, was derived and used to simulate experimentally determined exposure to m-xylene, using human volunteers exposed under controlled conditions. Biological monitoring was conducted by sampling, in exhaled alveolar air and blood, m-xylene and urinary methyl hippuric acid concentrations. The dermal absorption of m-xylene vapor was successfully and conveniently studied using a breath sampling technique, and the contribution to m-xylene body burden from the dermal route of exposure was estimated to be 1.8%. The model was used to investigate the protection afforded by an air-fed, half-face mask. By iteratively changing the dermal exposure concentration, it was possible to predict the ambient concentration that was required to deliver the observed urinary excretion of methylhippuric acid, during and following inhalation exposure to 50 ppm m-xylene vapor. This latter extrapolation demonstrates how physiologically-based pharmacokinetic modeling can be applied in a practical and occupationally relevant way, and permitted a further step not possible with biological monitoring alone. The ability of the model to extrapolate an ambient exposure concentration was dependent upon human metabolism data, thereby demonstrating the mechanistic toxicological basis of model output. The methyl hydroxylation of m-xylene is catalyzed by the hepatic mixed function oxidase enzyme, cytochrome P450 2E1 and is active in the occupationally relevant, (<100 ppm) exposure range of m-xylene. The use of a scaled-up in vitro maximum rate of metabolism (Vmaxc) in the model also demonstrates the increasingly valuable potential utility of biokinetic data determined using alternative, non-animal methods in human chemical-risk assessment.

Administration, Cutaneous↗

PubMed1978

The influence of two barrier creams on the percutaneous absorption of m-xylene in man.

Human volunteers were exposed to m-xylene by the percutaneous route (both hands immersed into the solvent for 20 minutes). The total amount of unchanged m-xylene eliminated through the respiratory tract during and after exposure and the total quantity of m-methylhippuric acid eliminated in urine during the subsequent 24 hours were measured. The majority of absorbed m-xylene (86 to 98%) is eliminated as m-methylhippuric acid in urine. The results obtained on eight subjects who repeated the test twice indicate that under similar experimental conditions the quantity of m-xylene absorbed percutaneously by an individual may vary with time by a factor of 2 or less. The interindividual variability in the total amount of m-xylene absorbed through the skin is greater than the intraindividual variability. Among 13 subjects, the ratio between the highest and the lowest value is 6.2; the mean percutaneous absorption rate of m-xylene amounts to 2.45 microgram/cm2 x min. The application of a barrier cream containing 10% silicone did not significantly influence the rate of percutaneous absorpiton of m-xylene by 11 subjects. Preliminary results obtained of five volunteers suggest that the application of a cream containing glycerol, stearates and oleostearates was not more effective.

Adult↗

PubMed1985

Conversely exposure-related effects between atmospheric m-xylene concentrations and human body sense of balance.

Effects of fixed and fluctuating concentrations of m-xylene in air were studied on human psychophysiological functions. Nine healthy male volunteers were exposed to m-xylene 4 hrs a day, 3 hrs in the morning and 1 hr in the afternoon, with a 40 min. break in between. The subjects were sedentary or exercised at 100 W for 10 min at the beginning of each session in the chamber. The m-xylene concentrations in the air were fixed (8.2 mumol/l; 870 mg/m3) or fluctuated with peaks (5.2-16.4 mumol/l; 550-1740 mg/m3) but the TWA (8 hrs) concentration of m-xylene was always 4.1 mumol/l (435 mg/m3). The two control days, with and without exercise, were similar to the exposure days, but without exposure. Reaction times were measured with a device in which subjects responded to visual and auditory stimuli. Body sway was measured with the subjects' eyes open and closed with a strain gauge transducer platform. Changes in reaction times did not correlate with m-xylene concentrations in the air. Changes of average and maximal body sway were, however, consistently negatively correlated with the intensity of the atmospheric exposure to m-xylene at the beginning of each session in the chamber. Physical exercise combined with exposure to m-xylene improved rather than impaired body sway.

Adult↗

PubMed2002

Substrate interactions during the biodegradation of benzene, toluene, ethylbenzene, and xylene (BTEX) hydrocarbons by the fungus Cladophialophora sp. strain T1.

The soil fungus Cladophialophora sp. strain T1 (= ATCC MYA-2335) was capable of growth on a model water-soluble fraction of gasoline that contained all six BTEX components (benzene, toluene, ethylbenzene, and the xylene isomers). Benzene was not metabolized, but the alkylated benzenes (toluene, ethylbenzene, and xylenes) were degraded by a combination of assimilation and cometabolism. Toluene and ethylbenzene were used as sources of carbon and energy, whereas the xylenes were cometabolized to different extents. o-Xylene and m-xylene were converted to phthalates as end metabolites; p-xylene was not degraded in complex BTEX mixtures but, in combination with toluene, appeared to be mineralized. The metabolic profiles and the inhibitory nature of the substrate interactions indicated that toluene, ethylbenzene, and xylene were degraded at the side chain by the same monooxygenase enzyme. Our findings suggest that soil fungi could contribute significantly to bioremediation of BTEX pollution.

Ascomycota↗

PubMed1974

Bacterial metabolism of para- and meta-xylene: oxidation of a methyl substituent.

Pseudomonas Pxy was isolated on p-xylene as sole source of carbon and energy. Substrates that supported growth were toluene, p-methylbenzyl alcohol, p-tolualdehyde, p-toluic acid, and the analogous m-methyl derivatives, including m-xylene. Cell extracts prepared from Pseudomonas Pxy after growth with either p-xylene or m-xylene oxidized the p- and m-isomers of tolualdehyde as well as p-methylbenzyl alcohol. The same cell extracts also catalyzed a "meta" fission of both 3- and 4-methylcatechol. Treatment of Pseudomonas Pxy with N-methyl-N'-nitro-N-nitrosoguanidine led to the isolation of two mutant strains. Pseudomonas Pxy-40, when grown on succinate in the presence of p-xylene, accumulated p-toluic acid in the culture medium. Under the same conditions Pseudomonas Pxy-82 accumulated p-toluic acid and also 4-methylcatechol. When Pseudomonas Pxy-82 was grown on succinate in the presence of m-xylene, 3-methylcatechol and 3-methylsalicylic acid were excreted into the culture medium. A pathway is proposed for the initial reactions utilized by Pseudomonas Pxy to oxidize p- and m-xylene.

Alcohol Oxidoreductases↗

PubMed1999

Initial reactions in anaerobic oxidation of m-xylene by the denitrifying bacterium Azoarcus sp. strain T.

The initial enzymatic steps in anaerobic m-xylene oxidation were studied in Azoarcus sp. strain T, a denitrifying bacterium capable of mineralizing m-xylene via 3-methylbenzoate. Permeabilized cells of m-xylene-grown Azoarcus sp. strain T catalyzed the addition of m-xylene to fumarate to form (3-methylbenzyl)succinate. In the presence of succinyl coenzyme A (CoA) and nitrate, (3-methylbenzyl)succinate was oxidized to E-(3-methylphenyl)itaconate (or a closely related isomer) and 3-methylbenzoate. Kinetic studies conducted with permeabilized cells and whole-cell suspensions of m-xylene-grown Azoarcus sp. strain T demonstrated that the specific rate of in vitro (3-methylbenzyl)succinate formation accounts for at least 15% of the specific rate of in vivo m-xylene consumption. Based on these findings, we propose that Azoarcus sp. strain T anaerobically oxidizes m-xylene to 3-methylbenzoate (or its CoA thioester) via (3-methylbenzyl)succinate and E-(3-methylphenyl)itaconate (or its CoA thioester) in a series of reactions that are analogous to those recently proposed for anaerobic toluene oxidation to benzoyl-CoA. A deuterium kinetic isotope effect was observed in the (3-methylbenzyl)succinate synthase reaction (and the benzylsuccinate synthase reaction), suggesting that a rate-determining step in this novel fumarate addition reaction involves breaking a C-H bond.

Anaerobiosis↗

PubMed1988

Interactions of m-xylene and aspirin metabolism in man.

In a series of experiments to investigate interactions between industrial solvents and common medications the interaction between m-xylene and aspirin was studied. As both these substances are metabolised and excreted as glycine conjugates there would possibly be competition for this conjugation pathway. Five male volunteers were exposed on separate occasions to m-xylene by inhalation (100 ppm), aspirin (1500 mg) by mouth, and m-xylene and aspirin together under controlled conditions in an exposure chamber. Urine and blood samples were collected and analysed for m-xylene, aspirin, and their metabolites. The amounts of the major glycine conjugates produced from m-xylene (m-methylhippuric acid) and aspirin (salicyluric acid) were significantly reduced by about 50% when m-xylene and aspirin were coadministered. There appears to be a mutual inhibition on the formation of the respective glycine conjugates. It is suggested that the inhibition is due to competition for either the enzymes, acyl-CoA synthetase, or glycine N-acylase. These findings have implications in the biological monitoring of workers exposed to m-xylene.

Adult↗

PubMed1982

Dose-related effects of m-xylene inhalation on the xenobiotic metabolism of the rat.

1. Male Wistar rats were exposed for two weeks (6 h/d, 5 d/week) to 0, 50, 400 or 750 p.p.m. of m-xylene vapour in the air. 2. Microsomal enzyme activities were significantly increased in the liver as follows: NADPH-cytochrome c reductase (less than or equal to 1.2-fold), O-deethylation reactions (less than or equal to 1.8-fold) and UDP-glucuronosyltransferase activity (less than or equal to 2.9-fold). Cytochrome P-450 concentrations also increased with dose. 3. Microsomal affinity to m-xylene increased with dose of m-xylene in vivo, similar to the increased affinity seen in type I spectra390-420nm formation with cytochrome P-450 in vitro. 4. Reduced glutathione concn. in liver declined significantly, while in the kidneys the glutathione remained unchanged. 5. In the kidneys, the concn. of cytochrome P-450 (less than or equal to 1.3-fold), O-deethylation activity (less than or equal to 5.3-fold) and the rate of glucuronidation (less than or equal to 1.8-fold) increased with the dose of xylene. 6. Microsomal protein contents in liver and kidneys increased with the two highest doses of xylene. 7. The hepatic and renal effects were dose-dependent and closely related to the accumulation of m-xylene in perirenal fat. 8. Despite stimulation of xenobiotic metabolism by m-xylene, inhalation did not alter the serum transaminase activity or cause morphological changes in the liver.

Adipose Tissue↗

PubMed1988

Coexposure of man to m-xylene and methyl ethyl ketone. Kinetics and metabolism.

In a study of the kinetics and metabolic interaction of xylene and methyl ethyl ketone (MEK) eight male volunteers were exposed to m-xylene (100 ppm) and MEK (200 ppm). The exposures to the two compounds were carried out both separately and in combination. Respiratory uptake and blood concentration, as well as urinary metabolites (methyl hippuric acid and 2,3-butanediol), were monitored. Coexposure to xylene and MEK resulted in inhibited xylene metabolism. The xylene concentration in blood increased significantly, and the urinary excretion of methyl hippuric acid decreased. The combined exposure did not cause any change in the concentration of MEK in the blood or the excretion of 2,3-butanediol in the urine. Exposure to MEK 20 h before the m-xylene exposure had no detectable effect on the kinetics of m-xylene.

Adult↗

PubMed1992

The toxic effects of combined exposure to toluene and m-xylene in animals. IV. Liver ultrastructure after subchronic inhalatory exposure.

The effects of combined inhalatory exposure to m-xylene and toluene on the rat hepatocytes were investigated. Limited proliferation of smooth endoplasmic reticulum and increase of the number of lysosomes were observed in hepatocytes after 3-months of single exposure to 1000 ppm of m-xylene and toluene. Moreover, mitochondria increased in most of hepatocytes. After combined exposure to mixture of m-xylene and toluene at concentrations of 500 + 500 ppm, respectively, the types of ultrastructural changes in hepatocytes followed the pattern observed after exposure of each of the single organic solvent. However, proliferation of the smooth endoplasmic reticulum was more eminent. The hepatocytes ultrastructure of rats exposed to 100 ppm of m-xylene and toluene for 6 months were similar to that observed in rats exposed to 1000 ppm of m-xylene for 3 months. In rats exposed to a mixture of m-xylene and toluene for 6 months, the ultrastructural changes in hepatocytes were a combination of those observed after a single exposure to each of the organic solvent. It may be concluded that changes in the hepatocytes ultrastructure were an adaptive rather than a toxic effect. Because in the case of combined exposures the doses were half of those used in single exposures, the additive effect on the proliferation of smooth endoplasmic reticulum was observed in the rat liver after combined exposure to toluene and m-xylene using electron microscopy.

Animals↗

PubMed1977

[Metabolism of m-xylene in rats after administration of chlorinated hydrocarbons (author's transl)].

Male albino rats of the Donryu strain were divided into 4 groups: the normal control group, tetrachloromethane (CCl4, TCM) group, tetrachloroethylene (CCl2 = CCl2, PCE) group and trichloroethylene (CHCl = CCl2, TCE) group. Each group was consisted of 6 animals. TCM, PCE and TCE were administered orally at a dosage of 13 mmoles/kg as a 50% v/v olive oil solution to rats 24 hours prior to an oral administration of m-xylene (8.2 mmoles/kg as a 50% v/v olive oil solution). The normal control group was administered only olive oil (2.5 ml/kg) 24 hours prior to m-xylene dose. Urine was collected 24, 48, 72 and 96 hours after administration of m-xylene. The urine was analysed for m-methylhippuric acid (m-MHA) by the paper chromatographic method of Ogata et al. The results obtained were as follows: 1) Total urinary excretion of m-MHA in the normal control group was equivalent on a molar basis to about 58% of m-xylene received, and the major portions of the metabolites were excreted on the 1st day. 2) In TCM group, total urinary excretion of m-MHA was about a half of that in the normal control group. It was equivalent on a molar basis to about 30% of m-xylene received (p less than 0.01), and the urinary excretion of m-MHA on the 1st day was significantly less than those of the normal control group (p less than 0.001) and TCE group (p less than 0.05). 3) In PCE group, urinary excretion of m-MHA on the 1st day was significantly less than that of the normal control group (p less than 0.01) and the excretion was delayed. 4) In TCE group, total urinary excretion of m-MHA was slightly but not significantly less than that of the normal control group (p less than 0.05). 5) In TCM-ip group of rats which were given TCM orally 24 hours prior to the administration of m-xylene by intraperitoneal injection, urinary excretion of m-MHA on the 1st day and in 4 days after administration of m-xylene was less than that of the control-ip group.

Administration, Oral↗

PubMedDate not supplied

[Peripheral metabolism of isomeric xylenes by Pseudomonas aeruginosa].

Microbiological oxidation of xylenes was studied with Pseudomonas aeruginosa, strain 7. The culture grows on m-xylene and, at a lower rate, on p-xylene, but does not grow on o-xylene though partly oxidizes it. Pathways of primary enzymatic oxidation of xylenes by the culture were established. Oxidation of m-xylene follows the pathway described earlier but methylsalicylic acid formed is not accumulated in the medium and is transformed into 3-methylcatechol. The aromatic ring is splitted according to the meta pathway. It has been demonstrated for the first time that o-xylene is oxidized to o-hydroxymethylbenzoic acid.

Benzoates↗

PubMed1996

Hematological alterations in rats from xylene and benzene.

Benzene and xylene are used by the chemical industry as raw materials for the manufacturing of paints, insecticides, gums, resins and other compounds. Through its myelotoxic actions, benzene produces hematologic changes ranging from pancytopenia to total bone marrow aplasia. The present investigation studied the possible effects of xylene on rat peripheral blood and compared these effects to those produced by benzene. Thirty-six male Wistar rats were injected s.c. with 2 ml benzene, xylene or saline/kg body weight 3 times a week at 2-3 d intervals for 5 w. The animals were lightly anesthetized and blood was collected by puncture of the retro-orbital plexus before the first administration of the solvents on d 7, 14, 21 and 35 of dosing, and 14 d after dosing was discontinued. Xylene induced leukocytosis as an increase in absolute neutrophil numbers, whereas benzene caused leukocytopenia due to decreases in absolute lymphocyte number. The 2 solvents reduced erythrocyte counts, hematocrit and hemoglobin. Platelet counts were high throughout the dosing with benzene and xylene. Fourteen d after discontinuation of xylene dosing, the rats recovered their initial hematologic values, whereas the animals dosed with benzene did not fully recover leukocytes and erythrocytes. The intoxications with benzene and xylene were not solely hematologic since there was also growth retardation, as shown by reduced weight gain, which did not recover after dosing ceased.

Animals↗

PubMed1998

Metabolism of benzene, toluene, and xylene hydrocarbons in soil

Enrichment cultures obtained from soil exposed to benzene, toluene, and xylene (BTX) mineralized benzene and toluene but cometabolized only xylene isomers, forming polymeric residues. This observation prompted us to investigate the metabolism of 14C-labeled BTX hydrocarbons in soil, either individually or as mixtures. BTX-supplemented soil was incubated aerobically for up to 4 weeks in a sealed system that automatically replenished any O2 consumed. The decrease in solvent vapors and the production of 14CO2 were monitored. At the conclusion of each experiment, 14C distribution in solvent-extractable polymers, biomass, and humic material was determined, obtaining 14C mass balances of 85 to 98%. BTX compounds were extensively mineralized in soil, regardless of whether they were presented singly or in combinations. No evidence was obtained for the formation of solvent-extractable polymers from xylenes in soil, but 14C distribution in biomass (5 to 10%) and humus (12 to 32%) was unusual for all BTX compounds and especially for toluene and the xylenes. The results suggest that catechol intermediates of BTX degradation are preferentially polymerized into the soil humus and that the methyl substituents of the catechols derived from toluene and especially from xylenes enhance this incorporation. In contrast to inhibitory residues formed from xylene cometabolism in culture, the humus-incorporated xylene residues showed no significant toxicity in the Microtox assay.

Journal Article↗