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At least 19 recordsLinked to original sources
PubMed1996

Simultaneous spectrophotometric determination of o-cresol and m-cresol in urine by use of the kinetic wavelength-pair method.

The kinetic wavelength-pair method was applied to the simultaneous determination of o-cresol and m-cresol, based on their oxidative coupling with aniline in the presence of hypochlorite as oxidant and nitroprusside as catalyst. The benzoquinoneanils produced exhibited severe spectral overlap. Resolution of this isomer mixture by using discrete wavelengths was subject to a high degree of error for the determination of m-cresol since the ratios vo-cresol/vm-cresol (where v denotes initial rate for the oxidative coupling reaction) and epsilon o-cresol/epsilon m-cresol (where epsilon is the absorptivity of reaction products) were greater than unity at any given wavelength. Selectivity in the resolution was achieved by measuring the initial rate difference at the wavelength pair 666-566 nm where the contribution of o-cresol was removed, o-Cresol and m-cresol were simultaneously determined at mass ratios between 5:1 and 1:5 at concentrations from 1 to 5 micrograms ml-1, with relative standard deviations of less than 3%. The proposed method was applied to the determination of o-cresol and m-cresol in urine samples, with analytical recoveries ranging between 95 and 105%.

Aniline Compounds↗
PubMed2000

Three types of phenol and p-cresol catabolism in phenol- and p-cresol-degrading bacteria isolated from river water continuously polluted with phenolic compounds.

A total of 39 phenol- and p-cresol-degraders isolated from the river water continuously polluted with phenolic compounds of oil shale leachate were studied. Species identification by BIOLOG GN analysis revealed 21 strains of Pseudomonas fluorescens (4, 8 and 9 of biotypes A, C and G, respectively), 12 of Pseudomonas mendocina, four of Pseudomonas putida biotype A1, one of Pseudomonas corrugata and one of Acinetobacter genospecies 15. Computer-assisted analysis of rep-PCR fingerprints clustered the strains into groups with good concordance with the BIOLOG GN data. Three main catabolic types of degradation of phenol and p-cresol were revealed. Type I, or meta-meta type (15 strains), was characterized by meta cleavage of catechol by catechol 2,3-dioxygenase (C23O) during the growth on phenol and p-cresol. These strains carried C23O genes which gave PCR products with specific xylE-gene primers. Type II, or ortho-ortho type (13 strains), was characterized by the degradation of phenol through ortho fission of catechol by catechol 1,2-dioxygenase (C12O) and p-cresol via ortho cleavage of protocatechuic acid by protocatechuate 3,4-dioxygenase (PC34O). These strains carried phenol monooxygenase gene which gave PCR products with pheA-gene primers. Type III, or meta-ortho type (11 strains), was characterized by the degradation of phenol by C23O and p-cresol via the protocatechuate ortho pathway by the induction of PC34O and this carried C23O genes which gave PCR products with C23O-gene primers, but not with specific xylE-gene primers. In type III strains phenol also induced the p-cresol protocatechuate pathway, as revealed by the induction of p-cresol methylhydroxylase. These results demonstrate multiplicity of catabolic types of degradation of phenol and p-cresol and the existence of characteristic assemblages of species and specific genotypes among the strains isolated from the polluted river water.

Journal Article↗
PubMed1990

Gas chromatographic determination of cresols in the biological fluids of a non-fatal case of cresol intoxication.

A simple and rapid method for analysis of free and conjugated cresols in biological fluids was developed. Prior to and following freeing of the conjugated cresols by acid hydrolysis in a sealed ampoule, free cresols were extracted by Extrelut column extraction, determined by gas chromatography, and confirmed by gas chromatography-mass spectrometry. In a non-fatal case of cresol intoxication a 46-year-old male had ingested about 100 ml of a saponated cresol soap solution. The concentrations of xylenol (2,4- and/or 2,5-dimethylphenol) and p- and m-cresol in the serum sample collected on admission were 15.8 micrograms/g, 43.3 micrograms/g and 73.8 micrograms/g, respectively. The total cresol concentration of 117 micrograms/g in the serum is within the range of fatal concentrations, and it is suspected therefore that the patient's recovery was due to adequate therapy alone.

Chromatography, Gas↗
PubMed1975

Pathways for the degradation of m-cresol and p-cresol by Pseudomonas putida.

A comparison of the oxidation rates of various compounds by whole cells of Pseudomonas putida 3, 5 indicated that m-cresol is metabolized by oxidation to 3-hydroxybenzoate followed by hydroxylation to gentisate, the ring-fission substrate, when grown with 3, 5-xylenol. However, when m-cresol was the growth substrate, similar experiments suggested a different pathway involving a methyl-substituted catechol, and ring-fission by meta cleavage. Assays of ring-fission enzymes in cell-free extracts confirmed that different pathways are induced by the two growth substrates. 3, 5-Xylenol-grown cells contained high levels of gentisate oxygenase and only very small amounts of catechol oxygenase, whereas gentisate ocygenase could not be detected in m-cresol-grown cells, but levels of catechol oxygenase were greatly increased. Extracts of m-cresol-grown cells also contained 2-hydroxymuconic semialdehyde dehydrogenase and hydrolase, whose specificities enable them to metabolize the ring-fission products from catechol, 3-methylcatechol, and 4-methylcatechol. This catechol pathway is also used by m-cresol-grown cells for p-cresol metabolism. In contrast, the results for cells grown with p-cresol point to an alternative pathway involving oxidation to 4-hydroxybenzoate and hydrosylation to protocatechuate as ring-fission substrate. Extracts of these cells contained high levels of protocatechuate oxygenase and only small amounts of catechol oxygenase.

Adipates↗
PubMed1991

p-cresol methylhydroxylase from a denitrifying bacterium involved in anaerobic degradation of p-cresol.

A bacterium, strain PC-07, previously isolated as part of a coculture capable of growing on p-cresol under anaerobic conditions with nitrate as the acceptor was identified as an Achromobacter sp. The first enzyme of the pathway, p-cresol methylhydroxylase, which converts its substrate into p-hydroxybenzyl alcohol, was purified. The enzyme had an Mr of 130,000 and the spectrum of a flavocytochrome. It was composed of flavoprotein subunits of Mr 54,000 and cytochrome subunits of Mr 12,500. The midpoint redox potential of the cytochrome was 232 mV. The Km and kcat for p-cresol were 21 microM and 112 s-1 respectively, and the Km for phenazine methosulfate, the artificial acceptor used in the assays, was determined to be 1.7 mM. These properties place the enzyme in the same class as the p-cresol methylhydroxylases from aerobically isolated Pseudomonas spp.

Alcaligenes↗
PubMed1991

NTP technical report on the toxicity studies of Cresols (CAS Nos. 95-48-7, 108-39-4, 106-44-5) in F344/N Rats and B6C3F1 Mice (Feed Studies).

Cresols are monomethyl derivatives of phenol, and are found as constituents of coal tar, in various industrial solvents and resins, and in some essential oils. In 28-day toxicity studies, F344/N rats and B6C3F1 mice of both sexes were given o-cresol, m-cresol, p-cresol, or m/p-cresol (60:40) at concentrations from 300 ppm to 30,000 ppm in the diet. In 90-day studies, o-cresol or m/p-cresol (60:40) were added to the diet in concentrations as high as 30,000 ppm to F344/N rats and 20,000 ppm (o-cresol) or 10,000 ppm (m/p-cresol) to B6C3F1 mice. In the 28-day studies, all rats survived (5 per sex per dose), but some mice given o-cresol at 30,000 ppm, or m-cresol or p-cresol at 10,000 ppm or 30,000 ppm died before the end of the studies. Feed consumption was depressed during the first study week in all high- dose groups of animals and weight gains were generally less than controls in groups given 10,000 or 30,000 ppm in the four 28-day studies. Increased relative liver weights and kidney weights were noted in both rats and mice given concentrations of cresols as low as 3,000 ppm. However, there were no consistent microscopic changes associated with these weight increases. Bone marrow hypoplasia and uterus, ovary and occasional mammary gland atrophy were seen primarily at the highest dietary concentration, but also at 10,000 ppm with certain cresols. An effect specific to the p- cresol and m/p-cresol studies was atrophy and regenerative changes in the nasal epithelia and forestomach, presumably a direct result of the irritant effects of the chemical or its vapors. Results of reproductive tissue evaluations and estrus cycle characterizations with o-cresol and m/p-cresol gave no indication of adverse effects to the male reproductive system, but the estrus cycle was lengthened in rats and mice receiving the higher concentrations of o-cresol and rats receiving m/p-cresol. In the 90-day studies, no deaths of rats (20 per sex per dose) or mice (10 per sex and dose) could clearly be related to administration of either o-cresol or m/p-cresol. Hematology, clinical chemistry, and urinalysis results were generally unremarkable in all studies, although an accumulation of bile acids in high-dose rats was considered evidence of a deficit in hepatocellular function resulting from ingestion of the chemical. Results of microscopic analyses were consistent with findings in the 28-day studies, and revealed evidence of mild bone marrow hypocellularity in rats and forestomach hyperplasia in mice given diets containing the higher concentrations of o-cresol. Evidence of nasal irritation was present in rats and mice receiving feed containing m/p-cresol. Additional lesions in rats receiving m/p-cresol included bone marrow hypocellularity and uterine atrophy. The cresol isomers exhibited a generally similar pattern of toxicities in rats and mice. Dietary concentrations of 3,000 ppm appeared to be minimal effect levels for increases in liver and kidney weights and deficits in liver function. Histopathologic changes, including bone marrow hypocellularity, irritation to the gastrointestinal tract and nasal epithelia, and atrophy of female reproductive organs, occasionally occurred at 10,000 ppm, but were more common at the high-dose of 30,000 ppm. Synonyms: phenol, 2-methyl-(9CI); 2-cresol; o-cresylic acid; 1-hydroxy-2-methylbenzene; 2-hydroxytoluene; o-hydroxytoluene; 2-methylphenol; o-methylphenol; o-methylphenylol; o-oxytoluene; RCRA Waste Number U052; o-toluol; UN 2076; phenol, 3-methyl-(9CI); 3-cresol; m-cresole; m-cresylic acid; 1-hydroxy-3-methylbenzene; 3-hydroxytoluene; m-hydroxytoluene; m-kresol; 3-methylphenol; m-methylphenol; m-oxytoluene; RCRA Waste Number U052; m-toluol; UN 2076; phenol, 4-methyl- (9CI); 4-cresol; p-cresylic acid; 1-hydroxy-4-methylbenzene; 4-hydroxytoluene; p-hydroxytoluene; p-kresol; 1-methyl-4-hydroxybenzene; p-methylhydroxy- benzene; 4-methylphenol; p-methylphenol; p-oxytoluene; RCRA Waste Number U052; p-toluol; p-tolyl alcohol; UN 2076. (NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.)

Journal Article↗
PubMed2001

Kinetics of the protein-bound, lipophilic, uremic toxin p-cresol in healthy rats.

P-Cresol, a partially lipophilic and protein-bound compound is related to several biochemical alterations in uremia. Because p-cresol kinetics have never been studied, we investigated its kinetic behavior in rats. Results were compared with those obtained with creatinine, a water soluble, non-protein-bound uremic retention solute, which is currently used as a marker of uremic retention. Healthy rats were divided into 3 groups with comparable body weight: (1) a control group (n=6); (2) a group (n=7) which received an intravenous bolus of 3 mg p-cresol; and (3) a group (n=5) which received an intravenous bolus of 18 mg creatinine. Blood samples were collected at 0, 5, 30, 60, 120, 180 and 240 minutes after administration for the determination of p-cresol and creatinine. Urine was collected at 1-hour intervals. p-Cresol concentrations were assessed by HPLC. Pharmacokinetic parameters of p-cresol and creatinine were calculated from the serum concentration-time curves using non-compartmental analysis. Each compound showed a concentration at time point 5 min (p-cresol: 6.7 +/- 1.4 mg/L and creatinine: 141 +/- 12 mg/L) which was comparable with values observed in uremic patients; these concentrations decreased gradually towards min 240 (p-cresol: 0.6 +/- 0.3 mg/L and creatinine: 4 +/- 2 mg/L, p<0.05 vs. 5 min in both cases). No p-cresol was found in the serum of control rats and these rats showed no changes in serum concentration of creatinine. Urinary excretions were strikingly different (p-cresol: 23 +/- 10% and creatinine: 95 +/- 25% of the administered dose, p<0.05). The half-life of p-cresol was twice as long as that of creatinine (1.5 +/- 0.8 vs. 0.8 +/- 0.1 h, p<0.05). Total clearance (CLt) was much higher for p-cresol than for creatinine (23.2 +/- 4.5 vs. 8.1 +/- 0.4 mL/min/kg, p<0.01); renal clearance (CLr), however, was substantially lower for p-cresol (4.8 +/- 2.0 vs. 8.2 +/- 1.9 mL/min/kg, p<0.05). Whereas CLt and CLr were similar for creatinine, CLt of p-cresol largely exceeded its CLr (p<0.05). The volume of distribution (Vd) was also much larger for p-cresol than for creatinine (2.9 +/- 1.4 vs. 0.6 +/- 0.1 L/kg, p<0.01). After injection of p-cresol, an additional chromatographic peak appeared in serum and in urine samples. Although at min 240 serum concentration of p-cresol had decreased to 10% of the peak value, only 23% of the administered amount was excreted in the urine and the CLr was +/- 50% lower compared to that of creatinine. Non-renal clearance and Vd of p-cresol were, however, substantially larger. These data may be of value to explain the different behavior of p-cresol in renal failure and dialysis, compared to creatinine.

Animals↗