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PubMed2002

Relation between colour vision loss and occupational styrene exposure level.

AIMS: To investigate the relation between colour vision loss and the exposure level of styrene. Exposure level included the current exposure concentration, past cumulative exposure, and the maximum exposure level in the past. METHODS: Colour vision was examined by the Lanthony desaturated panel D-15 test for 76 subjects exposed to styrene in a fibreglass reinforced plastics boat plant (as an exposed group) and 102 non-exposed subjects (as a control group). The current exposure level was expressed by the concentration of atmospheric styrene and end shift urinary mandelic acid (MA) and phenylglyoxylic acid (PGA) levels. The individual cumulative exposure index (CEI) was calculated, based on the exposure frequency and urinary MA concentrations measured for the past eight years. RESULTS: The Colour Confusion Index (CCI) of the exposed group showed a significant difference from the age matched controls. However, only a slight significant relation was found between CCI and the concentration of urinary MA plus PGA. In this study, the exposed group was further divided into two subgroups (as sub-MA+PGA groups) by the median of urinary MA plus PGA of each subject. The dividing line between the subgroups was 0.24 g/g creatinine, which was equivalent to an atmospheric concentration of styrene of about 10 ppm. The CCI values of both the sub-MA+PGA groups were significantly higher than that of the control group. The relation between CCI value and the maximum exposure concentration in the past eight years was examined. It was found that the CCI values of the group with the maximum exposure concentration of styrene over 50 ppm were significantly higher than that of the other groups. CONCLUSIONS: Exposure to styrene would impair colour vision even if the exposure concentration was lower than 10 ppm. Furthermore, if the maximum concentration of styrene exposure transiently exceeded 50 ppm in the past, the styrene related damage might remain. Thus, the safe limit of exposure to styrene and the relation between exposure to styrene and the degree of damage to ocular structure, retina, optic nerve, and brain need to be re-examined.

Adult↗
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↗
PubMed2001

Inter- and intra-individual sources of variation in levels of urinary styrene metabolites.

OBJECTIVE: Given the paucity of studies that have examined variability in biological measures of exposure to workplace contaminants, we quantified the intra- and inter-individual sources of variation in urinary levels of mandelic acid (MA) and phenylglyoxylic acid (PGA) among workers exposed to styrene. A secondary objective was to examine effects of job task and the timing of sampling during the workweek on the variation in workers' urinary styrene metabolite levels. METHODS: As part of routine biological monitoring, a total of 1,714 measurements of MA and PGA collected from 331 workers between 1985 and 1999 from eight reinforced-plastics plants were abstracted from laboratory reports. To evaluate sources of variation in levels of urinary styrene metabolites, we applied random-effects models. The influence of job task and day of sampling on metabolite levels was examined using mixed-effects models. RESULTS: PGA levels were characterized by less variation than levels of MA, as were metabolite levels expressed in terms of urinary creatinine concentration. The relative magnitude of the inter-individual to the intra-individual source of variation was generally higher for post-shift urine samples than for pre-shift urine samples. As expected, urinary metabolite levels were highest for laminators and for samples collected at the latter end of the workweek. Owing to the effects of variation from day-to-day, estimates of workers' exposures that rely on single measurements would generally perform poorly in a regression analysis designed to examine effects resulting from chronic exposure. However, the bias in an observed slope coefficient would be diminished if a second or third urine sample were collected. CONCLUSIONS: Quantification of the intra- and inter-individual sources of variation provides useful information that can be used to design optimal sampling strategies, which would allow for the collection of sufficient data to estimate workers' exposures reliably when evaluating health risks associated with occupational contaminants.

Glyoxylates↗
PubMed1994

Kinetics of styrene urinary metabolites: a study in a low-level occupational exposure setting in Singapore.

Biological monitoring of styrene exposure commonly involves measurement of styrene metabolites, mainly mandelic acid (MA) and phenylglyoxylic acid (PGA), in the urine of exposed subjects. Previous studies on the kinetics of styrene metabolites in urine were mostly conducted in a controlled environment on subjects exposed to high concentrations of styrene. In this study, we examined subjects exposed to low levels of styrene in a fiber-reinforced plastics (FRP) plant to see whether the excretion kinetics of styrene metabolites are similar under field conditions. Eight healthy Chinese male volunteers were exposed to styrene for 4 h with a mean environmental concentration of 11 ppm. Urine samples were collected continuously for 20 h after termination of the exposure and concentrations of urinary MA and PCA were determined. The results showed that MA was rapidly excreted in urine after the exposure, with a half-life of 2.1 h or 1.9 h when corrected with urine creatinine. The excretion of PGA followed that of MA and the half-life was 8.1 h or 5.1 h after correction with creatinine. The half-lives are considerably shorter compared to those in previous reports, suggesting that environmental factors, exposure conditions, or ethnic differences may affect the excretion kinetics of styrene metabolites. The fast excretion of styrene metabolites is also consistent with the observation that urine MA and PGA levels correlated better with the half-day time-weighted average (TWA) concentration of environmental styrene than with the whole-day TWA concentration. Our findings thus underscore the need for information on excretion kinetics in order to develop an appropriate biological monitoring scheme for specific exposure settings and subjects.

Adult↗
PubMed2004

Influence of genetic polymorphisms on biomarkers of exposure and genotoxic effects in styrene-exposed workers.

A study on 44 workers exposed to styrene and 44 matched referents was performed in order to examine the influence of genetic polymorphisms in biotransformation and DNA repair enzymes on the levels of N-terminal hemoglobin adducts and genotoxicity biomarkers. Urinary mandelic acid concentration averaged 201.57 mg/g creatinine +/-148.32 in exposed workers, corresponding to a calculated average airborne styrene exposure of 9.5 ppm +/-9.6. Individuals with a high level of N-terminal valine adducts had higher levels of DNA damage, as evaluated by the Comet assay (r = 0.29, P = 0.008). Frequencies of micronucleated mononucleated lymphocytes (MNMC) (0.71 +/- 0.88 vs 0.11 +/- 0.20, P<0.0001), micronucleated binucleated lymphocytes (MNBC) (3.93 +/- 2.75 vs 2.65 +/- 1.94, p = 0.02) and micronucleated nasal epithelial cells (0.52 +/- 0.49 vs 0.23 +/- 0.31, p = 0.04) differed significantly between the exposed and referent groups. In the whole group of 88 individuals, higher frequencies of MNMC were found in individuals possessing the XRCC3 Met(241) allele and those individuals with the XRCC1 Gln( (399) ) allele showed higher frequencies of MNMC and MNCB. In vitro DNA repair capacity, as measured by residual DNA strand breaks in peripheral blood leukocytes after a styrene oxide challenge, was also influenced by styrene exposure, with an apparent induction of early repair mechanisms associated with the intensity of recent exposure and a reduction of late (24 h) repair capacity that was associated with the duration of employment. After 1 h of repair, lower levels of residual DNA damage were found in individuals possessing GSTT1 (P = 0.043). After 24 h of repair, lower residual DNA damage was found in individuals homozygous for XRCC1 Arg(194) (P = 0.013). Multivariate regression analysis indicated that the duration of exposure, smoking habits and polymorphisms of XRCC1 at codon 399 were important variables affecting the genotoxic responses. Our data suggest that DNA damage is formed in workers exposed to low concentrations of styrene, and that genotypes of metabolising and DNA-repair genes are important for the assessment of individual genotoxic risk to styrene. The in vitro DNA repair phenotype assay might be a valuable method to estimate the susceptibility of workers.

Adult↗
PubMed1998

Metabolic interferences in subjects occupationally exposed to binary styrene-acetone mixtures.

OBJECTIVE: To investigate the excretion of styrene metabolites (mandelic acid, MA, and phenylglyoxylic acid, PGA) in workers employed in plastic manufacturing to verify the possible influence of coexposure to acetone on styrene metabolism. METHODS: This study was carried out on 50 workers employed in 3 factories producing polyester buttons. The workers were divided into three groups according to three different levels of acetone exposure. The trend of excretion for metabolites was examined during and after work shifts. Styrene and acetone were monitored on Thursday during the entire work shift by passive dosimeters placed on the lapel of the workers' uniforms, desorbed by carbon disulfide, and analyzed by gas chromatography. Biological monitoring was performed by determination of the urinary metabolites of styrene in urine samples collected on Thursday at the middle and the end of the work shift. MA and PGA were determined by a high-pressure liquid chromatographic method. RESULTS: The styrene concentrations ranged between 16 and 439 mg/m3, and in ten samples they exceeded the TLV-TWA (213 mg/m3). The acetone concentration ranged between 15 and 700 mg/m3 (TLV-TWA 1780 mg/m3), with the mean value being 208 mg/m3. During cleaning operations higher exposures to acetone demonstrated, with concentrations ranging between 500 and 3400 mg/m3. The amounts of MA and PGA determined at the end of workshifts did not significantly differ between the groups with different levels of acetone coexposure. Analysis of variance (ANOVA) between the groups confirmed that MA and PGA excretion did not significantly differ, although the metabolite values measured on the "morning of the day after" appeared higher in those groups with high levels of acetone exposure and were related to the average airborne concentrations of the solvent. In addition, the range and degree of correlation between styrene in air and biological levels of metabolites were modified by coexposure to acetone. CONCLUSIONS: Our data demonstrate that amounts of MA and PGA did not differ in groups with different levels of acetone exposure, but when the acetone air concentration increased the degree of correlation between styrene and MA and PGA decreased. Furthermore, coexposure to acetone levels similar to those described herein may hamper the use of urinary metabolites for the assessment of exposure to styrene, especially on an individual basis.

Acetone↗
PubMed1995

Biomarkers of styrene exposure in lamination workers: levels of O6-guanine DNA adducts, DNA strand breaks and mutant frequencies in the hypoxanthine guanine phosphoribosyltransferase gene in T-lymphocytes.

Occupational exposure to styrene was studied in nine workers of a hand lamination plant in Bohemia. Personal dosimeters were used to monitor the styrene workplace exposure, and the levels of styrene in blood and mandelic acid in urine were measured. Blood samples were taken at four occasions during a 7 month period to determine styrene-specific O6-guanine DNA adducts in lymphocytes and granulocytes, DNA strand breaks and hypoxanthine guanine phosphoribosyltransferase (HPRT) mutant frequency in T-lymphocytes. Seven administrative employees in the same factory (factory controls) and eight persons in a research laboratory (laboratory controls) were used as referents. DNA adduct levels determined by the 32P-postlabelling method in lymphocytes of laminators were remarkably constant and significantly higher (P < 0.0001) than in factory controls at all four sampling times. HPRT mutant frequencies (MF) measured by the T-cell cloning assay were higher in the laminators (17.5 x 10(-6), group mean) than in the factory controls (15.7 x 10(-6), group mean) at three of the four sampling times, but the differences were not statistically significant. However, a statistically significant (P = 0.021) difference between MF in the laminators (18.0 x 10(-6), group mean) and laboratory controls (11.8 x 10(-6), group mean) was observed at sampling time 4 (the only sampling time when this latter group was studied). This result indicates that styrene exposure may induce gene mutation in T-cells in vivo. DNA strand breaks were studied by the 'Comet assay' at the fourth sampling time. The laminators were found to have significantly higher levels of DNA strand breaks than the factory controls (P = 0.032 for tail length, TL; P = 0.007 for percentage of DNA in tail, T%; and P = 0.020 for tail moment, TM). A statistically significant correlation was also found between the levels of lymphocyte DNA adducts and all three DNA strand break parameters (TL P = 0.046; T% P = 0.026 and TM P = 0.034). On the contrary, no significant correlations were found between DNA adduct levels and the HPRT mutant frequencies or between the mutant frequencies and DNA strand breaks. Taken together, these results add further support to the genotoxic and possibly mutagenic effects of styrene exposure in vivo. However, no simple quantitative relationship seems to exist between the levels of styrene-induced DNA damage and frequency of HPRT mutation in T-lymphocytes.

Adult↗
PubMed1999

An evaluation of styrene genotoxicity using several biomarkers in a 3-year follow-up study of hand-lamination workers.

A study employing several biomarkers of styrene exposure and genotoxicity was carried out in a group of lamination (reinforced plastic) workers and controls, who had been repeatedly sampled during a 3-year period. Special attention will be paid to the last sampling (S.VI), reported here for the first time. Styrene concentration in the breathing zone, monitored by personal dosimeters, and urinary mandelic acid (MA) were measured as indicators of external exposure. Blood samples were assayed for styrene-specific O6-guanine adducts in DNA, N-terminal valine adducts of styrene in haemoglobin, DNA single-strand breaks (SSB), determined by use of the single cell gel electrophoresis (Comet) assay), and hypoxanthine guanine phosphoribosyl transferase (HPRT) mutant frequencies (MF) in T-lymphocytes. O6-styrene guanine adduct levels were significantly higher in the exposed group (5.9 +/- 4.9 adducts/10(8) dNp) as compared to laboratory controls (0.7 +/- 0.8 adducts/10(8) dNp; P = 0.001). DNA adduct levels significantly correlated with haemoglobin adducts, SSB parameters and years of employment. Styrene-induced N-terminal valine adducts were detected in the lamination workers (1.7 +/- 1.1 pmol/g globin), but not in the control group (detection limit 0.1 pmol/g globin). N-terminal valine adducts correlated strongly with external exposure indicators, DNA adducts and HPRT MF. No significant correlation was found with SSB parameters. A statistically significant difference in HPRT MF was observed between the laminators (22.3 +/- 10.6/10(6)) and laboratory controls (14.2 +/- 6.5/10(6), P = 0.039). HPRT MF in the laminators significantly correlated with styrene concentration in air, MA and haemoglobin adducts, as well as with years of employment and age of the employees. No significant difference (P = 0.450) in MF between the laminators and the factory controls was observed. Surprisingly, we detected differences in MF between sexes. When data from all measurements were combined, women showed higher MF (geometric mean 15.4 vs. 11.2 in men, P = 0.020). The styrene-exposed group exhibited significantly higher SSB parameters (tail moment (TM), tail length (TL) and the percentage of DNA in the tail (TP)) than the control group (P < 0.001). SSB parameters correlated with indicators of external exposure and with O6-styrene guanine adducts. No significant correlation was found between SSB parameters and haemoglobin adducts or HPRT MF. The data encompassing biomarkers from repeated measurements of the same population over a 3-year period are discussed with respect to the mechanisms of genotoxic effects of styrene and the interrelationship of individual biomarkers.

Adult↗
PubMed1998

Albumin and hemoglobin adducts as biomarkers of exposure to styrene in fiberglass-reinforced-plastics workers.

OBJECTIVE: The purpose of this work was to compare levels of styrene-7,8-oxide (SO) adducts of albumin (Alb) and hemoglobin (Hb) with those of two urinary metabolites of styrene, mandelic acid (MA) and phenylglyoxylic acid (PGA), among workers exposed to styrene in the reinforced-plastics industry and in unexposed subjects. We also wished to determine whether cigarette smoking influenced adduct levels among these subjects. METHODS: A group of 22 male workers was selected on basis of an expectedly high level of exposure to styrene, and a group of 15 controls was selected from hospital blood donors and hospital staff. In the exposed group, MA and PGA were quantified by high-performance liquid chromatography (HPLC) analysis of urine samples collected prior to the work shift. The SO adducts were cleaved from cysteine residues by reaction with Raney nickel to give 1-phenylethanol (1-PE) and 2-phenylethanol (2-PE), which, after derivatization, were measured using gas chromatography-mass spectrometry (GC-MS) in the negative-chemical-ionization (NCI) mode. RESULTS: The estimated mean levels of MA and MA + PGA were 74 and 159 mg/g creatinine, respectively. Using the levels of urinary metabolites, an average styrene concentration of about 100 mg/m3 in the workplace air was estimated. The mean levels of 2-PE and 1-PE adducts in exposed workers were 2.84 and 0.60 nmol/g Alb and 5.44 and 0.43 nmol/g Hb, respectively. When subjects were stratified by level of urinary metabolites [zero (controls), low-level exposure (MA + PGA < or = 159 mg/g creatinine), and high-level exposure (MA + PGA > 159 mg/g creatinine)] and smoking status (smokers versus nonsmokers), a difference in Alb adduct levels was found among the groups (2-PE P = 0.002, I-PE P = 0.052). The difference in 2-PE-Alb levels was related to exposure category, to smoking status, and to their interaction. Correlations at or near a 0.05 level of significance were observed among the workers (n = 22) between individual levels of SO-protein adducts and MA + PGA (2-PE Alb, r = 0.54, 2-PE Hb, r = 0.40). CONCLUSION: Our data suggest that only exposure to relatively high levels of styrene allows a clear relationship to be detected between styrene exposure and SO adducts, due in part to the effects of cigarette consumption and to the high background levels of these adducts observed in unexposed subjects.

Adult↗
PubMed1984

Low dose bromocriptine: a study of acute effects in chronic mediated schizophrenics.

An acute low oral dose (2 mg) of bromocriptine was administered in a randomized double blind fashion to 11 chronic symptomatic mediated schizophrenic patients. There was an overall improvement for the group on the Brief Psychiatric Rating Scale (BPRS) following bromocriptine. Plasma homovanillic acid, 3-methoxy-4-hydroxyphenylglycol, and vanilloyl-mandelic acid concentrations were unchanged after bromocriptine. Bromocriptine concentrations in the plasma showed a large inter-individual variation. There was a significant inverse correlation between plasma bromocriptine concentration and total BPRS score at 60 minutes post-bromocriptine administration. These results suggest a need for further replication in a larger study population and a need for controlled studies with chronic administration of low dose bromocriptine in chronic medicated schizophrenic patients.

Adult↗
PubMed1988

Brain dopamine as a target for solvent toxicity: effects of some monocyclic aromatic hydrocarbons.

Adult male rabbits were exposed to toluene, xylene, styrene, ethylbenzene, vinyltoluene or were dosed with hippuric, methylhippuric, mandelic, phenylglyoxylic, and 7-methyl-mandelic acids. Styrene, vinyltoluene and ethylbenzene caused a marked depletion of striatal and tubero-infundibular dopamine. Such an effect was also caused by treatment with mandelic and phenylglyoxylic acids. These results indicate that dopamine is a target for some solvents of their metabolites, the presence of a lateral vinyl- or ethyl-chain which may be biotransformed into alpha-keto acids being crucial for the effect. Experiments in vitro suggest that dopamine condenses non-enzymatically with reactive carbonylic groups of such and other alpha-keto acids, thus becoming ineffective as neurotransmitter. This mechanism might account for the neurobehavioral and neuroendocrine changes which have been reported in workers occupationally exposed to styrene and to some solvent mixtures.

Animals↗
PubMed2000

Reaction intermediate analogues for mandelate racemase: interaction between Asn 197 and the alpha-hydroxyl of the substrate promotes catalysis.

Mandelate racemase (MR) catalyzes the interconversion of the enantiomers of mandelic acid, stabilizing the altered substrate in the transition state by 26 kcal/mol relative to the substrate in the ground state. To understand the origins of this binding discrimination, carboxylate-, phosphonate-, and hydroxamate-containing substrate and intermediate analogues were examined for their ability to inhibit MR. Comparison of the competitive inhibition constants revealed that an alpha-hydroxyl function is required for recognition of the ligand as an intermediate analogue. Two intermediate analogues, alpha-hydroxybenzylphosphonate (alpha-HBP) and benzohydroxamate, were bound with affinities approximately 100-fold greater than that observed for the substrate. Furthermore, MR bound alpha-HBP enantioselectively, displaying a 35-fold higher affinity for the (S)-enantiomer relative to the (R)-enantiomer. In the X-ray structure of mandelate racemase [Landro, J. A., Gerlt, J. A., Kozarich, J. W., Koo, C. W., Shah, V. J., Kenyon, G. L., Neidhart, D. J., Fujita, J., and Petsko, G. A. (1994) Biochemistry 33, 635-643], the alpha-hydroxyl function of the competitive inhibitor (S)-atrolactate is within hydrogen bonding distance of Asn 197. To demonstrate the importance of the alpha-hydroxyl function in intermediate binding, the N197A mutant was constructed. The values of k(cat) for N197A were reduced 30-fold for (R)-mandelate and 179-fold for (S)-mandelate relative to wild-type MR; the values of k(cat)/K(m) were reduced 208-fold for (R)-mandelate and 556-fold for (S)-mandelate. N197A shows only a 3.5-fold reduction in its affinity for the substrate analogue (R)-atrolactate but a 51- and 18-fold reduction in affinity for alpha-HBP and benzohydroxamate, respectively. Thus, interaction between Asn 197 and the substrate's alpha-hydroxyl function provides approximately 3.5 kcal/mol of transition-state stabilization free energy to differentially stabilize the transition state relative to the ground state.

Alanine↗
PubMed2006

NMR structure of a potent small molecule inhibitor bound to human keratinocyte fatty acid-binding protein.

The NMR structure is presented for compound 1 (BMS-480404) (Ki = 33 (+/-2) nM) bound to keratinocyte fatty acid-binding protein. This article describes interactions between a high affinity drug-like compound and a member of the fatty acid-binding protein family. A benzyl group ortho to the mandelic acid in 1 occupies an area of the protein that fatty acids do not normally contact. Similar to that in the kFABP-palmitic acid structure, the acid moiety in 1 is proximal to R129 and Y131. Computational modeling indicates that the acid moiety in 1 interacts indirectly via a modeled water molecule to R109.

Binding Sites↗
PubMed1996

Conversion of L-lactate oxidase to a long chain alpha-hydroxyacid oxidase by site-directed mutagenesis of alanine 95 to glycine.

A mutant form of L-lactate oxidase (LOX) from Aerococcus viridans in which alanine 95 was replaced by glycine was constructed as a mimic of L-lactate monooxygenase but proved instead to be a mimic of the long chain alpha-hydroxyacid oxidase from rat kidney. A95G-LOX keeps oxidase activity with L-lactate at the same level as wild type LOX but has much enhanced oxidase activity with longer chain L-alpha-hydroxyacids, alpha-hydroxy-n-butyric acid, alpha-hydroxy-n-valeric acid, etc., and also the aromatic alpha-hydroxyacid, L-mandelic acid. Kinetic analysis of the activity with these substrates indicates that the reduction of the enzyme bound flavin by substrates is the rate-limiting step in A95G-LOX. The affinity of pyruvate for the reduced enzyme is increased, and sulfite binding to the oxidized enzyme is weaker in A95G-LOX than in native enzyme. Wild type LOX stabilizes both the neutral and anionic flavin semiquinones with a pKa of 6.1, but A95G LOX stabilizes only the anionic semiquinone form. These results strongly suggest that the environment around the N5-C4a region of the flavin isoalloxazine ring is changed by this mutation.

Alanine↗
PubMed1992

Catecholamines and vitiligo.

The levels of some catecholamine metabolites, namely homovanillic acid (HVA), vanilmandelic acid (VMA), 3-methoxytyramine (MT), normetanephrine (NMN), metanephrine (MN), 3,4-dihydroxy mandelic acid (DOMAC), and 3,4-dihydroxy phenylacetic acid (DOPAC), have been evaluated in the 24 hr urines of 150 patients affected with different types of vitiligo and in 50 healthy age-matched individuals. The patients were divided into three groups according to the different phases of the disease. The first group included subjects affected either with the early active phase or with progressive increase in both number and/or the size of previous lesions. The second group included patients in whom no new lesions had appeared for between 4-8 months. In the third group the white areas had been stable for 1-5 years. The first and second groups showed values of HVA and VMA from 4 to 10 times and from 1/2 to 3 times higher respectively than those of controls, while no significant differences were found between the third group and controls. Our results clearly show that a significant increase of urinary levels of HVA and VMA, deriving respectively from dopamine and from norepinephrine and epinephrine characterizes the onset and the progressive active phases of vitiligo, irrespective of the type of distribution. The increased release of catecholamines from the autonomic nerve endings in the microenvironment of melanocytes in the affected skin areas might be involved in the etiopathogenesis of vitiligo through two main mechanisms: (1) a direct cytotoxic action of catecholamines and/or their o-diphenol catabolites; (2) an indirect action.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1978

Sulphur-containing metabolites of beta-bromostyrene formed by the marmoset, rabbit and rat.

1. The administration of beta-bromostyrene to the rat results in a fall in the level of hepatic glutathione. 2. Marmosets, rabbits and rats dosed with beta-bromostyrene excrete two mercapturic acids. One of these, N-acetyl-S-(2-hydroxy-2-phenyl-1-bromoethyl)-cysteine is readily converted into N-acetyl-S-(1-phenyl-2-bromo-2-ethenyl)-cysteine, the structure of which was established by mass spectrometry. 3. Mass spectrometric evidence suggests that the second mercapturic acid is N-acetyl-S-(1-hydroxy-2-phenylethyl)cysteine. 4. Mandelic acid was detected as a metabolite in all three species.

Animals↗
PubMed1994

Separation of alpha-hydroxy acid enantiomers by high performance capillary electrophoresis using copper(II)-L-amino acid and copper(II)-aspartame complexes as chiral selectors in the background electrolyte.

Optical isomers of some alpha-hydroxy acids, namely 2-, 3-phenyllactic acid, mandelic, p-hydroxy-, m-hydroxy and 3,4-di-hydroxymandelic acid, were separated by means of capillary zone electrophoresis in free solution, using copper (II) complexes with L-amino acid or aspartame ligands in the background electrolyte. The concentration and the pH dependence of the enantiomer separations have been studied in the cases of different chiral ligands and/or analytes. With the use of L-proline as ligand only the optical isomers of 3-phenyllactic acid were resolvable, whereas using L-hydroxyproline the D and L forms of all compounds, except for 2-phenyllactic acid, were separated. Better results were obtained with aspartame as chiral ligand.

Amino Acids↗