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At least 19 recordsLinked to original sources
PubMed1992

Plasmid chromate resistance and chromate reduction.

Compounds of hexavalent chromium (chromates and dichromates) are highly toxic. Plasmid genetic determinants for chromate resistance have been described in several bacterial genera, most notably in Pseudomonas. Resistance to chromate is associated with decreased chromate transport by the resistant cells. The genes for a hydrophobic polypeptide, ChrA, were identified in chromate resistance plasmids of Pseudomonas aeruginosa and Alcaligenes eutrophus. ChrA is postulated to be responsible for the outward membrane translocation of chromate anions. Widespread bacterial reduction of hexavalent chromate to the less toxic trivalent chromic ions is also known. Chromate reduction determinants have not, however, been found on bacterial plasmids or transposons. In different bacteria, chromate reduction is either an aerobic or an anaerobic process (but not both) and is carried out either by soluble proteins or by cell membranes. Chromate reduction may also be a mechanism of resistance to chromate, but this has not been unequivocally shown.

Amino Acid Sequence↗
PubMed1977

The significance of chromate ingestion in patients allergic to chromate.

A double-blind study was carried out to demonstrate the significance of chromate ingestion in the persistence of chromic chromate dermatitis. Each of 31 chromate-allergic patients was given one tablet containing 7.1 mg potassium dichromate, plus a placebo tablet. The dermatitis of 11 of the 31 patients flared after the ingestion of chromate, but not after placebo. 3 patients had equivocal reactions to both tablets; the dermatitis worsened in 2 patients following ingestion of the placebo but not after the chromate tablet. No statistically significant difference could be found between reactivity to chromate and eczema of dyshidrotic morphology. Nor was it possible to correlate the degree of patch test reactivity to the reaction following chromate ingestion. It is concluded that a low-chromate diet is of value in the management of patients with chronic chromate dermatitis.

Administration, Oral↗
PubMed1992

The effect of pupil size on chromostereopsis and chromatic diplopia: interaction between the Stiles-Crawford effect and chromatic aberrations.

Several studies have reported that the magnitude of chromostereopsis changes as the pupil size changes. Einthoven's theory, that chromostereopsis is determined by interocular differences of monocular transverse chromatic aberration, can not easily explain this change. Therefore, several alternative hypotheses have been introduced, most notably by Vos [(1960) Vision Research, 6, 105-107], who argues that shifts in chromostereopsis with pupil size are due to decentration of the peak of the Stiles-Crawford effect (SCE) with respect to the pupil. We tested this hypothesis by measuring chromostereopsis under both scotopic (no SCE) and photopic conditions with centered and decentered artificial pupils. The results show that the SCE plays an important role in the effect of pupil size on chromostereopsis. Similar changes were also measured in monocular chromatic diplopia which supports the hypothesis that the effect of pupil size on chromostereopsis is due to monocular mechanisms.

Adult↗
PubMed1991

Relation between the chromatic difference of refraction and the chromatic difference of magnification for the reduced eye.

We provide a simple model for calculating the chromatic difference of magnification for the human eye. Spectral differences in image size are proportional to the eye's longitudinal chromatic aberration and the axial distance between the entrance pupil and nodal point. We verify that the model provides magnification estimates equal to previously published predictions, and we show the significant increase in this aberration produced by experimental use of artificial pupils.

Humans↗
PubMed1992

Transcriptional inhibition by carcinogenic chromate: relationship to DNA damage.

Hexavalent chromium compounds are carcinogenic to humans, are potent inducers of tumors in experimental animals, and can neoplastically transform cells in culture. In this study, the effects of sodium chromate on the expression of the 78-kDa glucose-regulated protein (GRP78) gene and on general transcription were investigated with respect to the DNA damage induced by this agent. DNA single-strand breaks, DNA-protein cross-links, and chromium-DNA adducts were present in CHO cells immediately after 2 h of treatment with sodium chromate. Subsequently, these types of damage were repaired at different rates. Single-strand breaks were essentially repaired after 8 h. By 24 h posttreatment, no cross-links remained in cells exposed to 30 or 150 microM chromate, although cells treated with the 300-microM concentration still contained cross-links at that time. DNA-chromium adducts remained unrepaired for at least 32 h. The moderate constitutive level of GRP78 mRNA was not affected by chromate. Chromate did, however, suppress induction of this gene by tunicamycin in a concentration-and time-dependent manner. Thirty micromolar sodium chromate (96% survival), which caused the least DNA damage, had no effect on GRP78 induction, general RNA synthesis, or mRNA synthesis. Induction of GRP78 was suppressed immediately and 12 h after treatment with 150 microM chromate (54% survival), although there was a partial recovery of induction at 24 h after treatment, which correlated with the repair of DNA-protein cross-links. In contrast, both total cytoplasmic RNA and mRNA synthesis were suppressed by approximately 60-75% for at least 32 h by 150 microM chromate. At the 300-microM concentration (8% survival), where DNA-protein cross-links persisted beyond 24 h, GRP78 induction was totally suppressed for at least 24 h, while total RNA and mRNA synthesis were suppressed by 80-90% for at least 32 h. Overall, the effects of chromate on GRP78 induction correlated most closely with the presence of DNA-protein cross-links, but suppression of total RNA and mRNA synthesis correlated with the presence of DNA-chromium adducts. These results indicate that chromate exerts differential effects on the induction of the GRP78 gene and on general transcription.

Animals↗
PubMed1991

Chromated steel and contact allergy. Recommendation concerning a "threshold limit value" for the release of hexavalent chromium.

Steel surfaces can be treated with zinc and chromates to prevent the steel from rusting. Cases of allergic contact dermatitis due to the release of hexavalent chromium (Cr64) from chromated surfaces have been reported. The main purpose of the present study was to develop a simple procedure for the determination of leachable Cr64 that could be used in industrial applications to check the quality of chromated products and to establish a "threshold limit value" for such products. Occlusive tests were performed in chromate-sensitive patients using chromated discs, and discs representing a release of 0.6 microgram/cm2 or more elicited positive results in all patients tested. It was proposed that the mean release of Cr64 from chromated parts should not exceed 0.3 microgram/cm2. Approximately 1 out of 4 yellow chromated parts, collected from a chromating plant and a car assembly plant, gave values above this limit. Today, several tests are performed to evaluate the technical quality of the chromate layers. It is suggested that the present method should be added to the test program in order to reduce the risk of causing chromate allergy.

Chromates↗
PubMed1992

Protective effects of thiol compounds on chromate-induced cytotoxicity in HeLa cells.

The effects of several thiol compounds on the cytotoxicity induced by chromate (potassium dichromate) were examined. HeLa cells were incubated in Eagle's minimum essential medium (MEM) with or without the chromate alone, or with both chromate and any one of L-cysteine ethyl ester (LCysEE), L-cysteine methyl ester (LCysME), N-acetyl-L-(+)-cysteine, 2,3-dimercaptosuccinic acid (DMSA), 2, 3-dimercapto-1-propanesulfonic acid (DMPS), or dithiothreitol. After a given period of incubation, the number of viable cells was counted using the trypan blue exclusion test and the chromium content of the cells was estimated by atomic absorption spectrophotometry. The results obtained were as follows. 1) Chromate-induced cytotoxicity evaluated by inhibition of cell growth at 3 days of incubation was diminished by all of the thiol compounds tested when the cells were incubated in MEM with 2.5 to 10.0 microM chromate and 25 to 100 microM thiol compounds. 2) All of the thiol compounds produced a concentration-dependent reduction of chromate when a solution of the thiol compound (12.5 to 100 microM) was mixed with a solution of chromate (10 microM) in distilled water. 3) When cells were incubated in MEM with both 10 microM chromate and 25 to 100 microM thiol compounds, the chromium content of the cells at 6 hr of incubation was decreased in a concentration-dependent manner. 4) When these thiol compounds were added to MEM 1 hr before or after chromate, no or little protective effects of these thiol compounds against chromate-induced cytotoxicity and chromium uptake by the cells were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Division↗
PubMed1992

Peripheral chromatic sensitivity for flashes: a post-receptoral red-green asymmetry.

Thresholds of luminance and red-green chromatic flashes (200 msec) were measured on a yellow adapting field in the fovea and periphery (up to 12 degrees eccentricity for 1 degree flashes and 21 degrees eccentricity for 2 degrees flashes). Chromatic sensitivity (in cone contrast coordinates) is about 7 times higher than luminance sensitivity in the fovea but falls faster with eccentricity, so that luminance and chromatic sensitivities are similar at eccentricities of 20 degrees or less. At eccentricities greater than about 14 degrees, there is a clear asymmetry wherein green chromatic flashes are considerably less detectable than red ones. By measuring complete detection contours for many ratios of incremental and decremental red and green flashes, we isolated the red and green chromatic detection mechanisms, and demonstrated that the red-green asymmetry is not a property of the L- or M-cone response per se, but rather is a property of the post-receptoral, chromatic mechanisms. The peripheral luminance and chromatic mechanisms could be further separated with a suprathreshold luminance flash (a pedestal), since an intense pedestal masks coincident luminance test flashes but facilitates the chromatic flashes. The luminance pedestal approximately linearizes the chromatic detection function (the psychometric function).

Color Perception↗
PubMed1979

Duration thresholds for chromatic stimuli.

The duration necessary to detect chromatic stimuli was measured for wavelengths between 463 and 620 nm. Stimuli were presented either in hue substitution (replacement of white by a chromatic stimulus of matched luminance) or as increments. Two observers viewed a 1 degrees 45' homogeneous white field. A trial consisted of replacement of the central 40' of the field by a chromatic stimulus. In substitution mode the white field was 2.4 cd/m2., the chromatic replacement was of matched luminance using heterochromatic flicker photometry (HFP). In increment mode, the white field was decreased to 1.2 cd/m2., the chromatic replacement remained at 2.4 cd/m2. In substitution mode, duration threshold varied from approximately 3--4 ms for the spectral extremes to 45--66 ms at 570 nm. Detected stimuli were always seen as a change in chromaticity. In increment mode, thresholds were in the 2--4 ms range with no dependence upon spectral composition. Detected stimuli were seen either as changes in chromaticity or brightness. A control experiment indicated that HFP did establish equivalent luminance for the hue substitution mode. We conclude that duration thresholds in substitution mode reveal chromatic processing channels; duration thresholds in increment mode are mediated by chromatic and/or achromatic processing channels.

Color Perception↗
PubMed1979

DNA damage and DNA repair in cultured human cells exposed to chromate.

DNA damage and DNA repair have been observed in cultured human skin fibroblasts exposed to potassium chromate but not to a chromic glycine complex. DNA repair synthesis (unscheduled incorporation of [3H]thymidine (TdR)) was measured in cells during or following exposure to chromate and was significant for chromate concentrations above 10(-6) M. Maximal DNA repair was observed at about 10(-4) M chromate. DNA repair capacity was found to be saturated at this concentration. Chromate was stable for at least 8 h in culture medium and produced approximately a linear increase in repair with duration of exposure. DNA damage as determined by alkaline sucrose gradient sedimentation was detected after treatment for 1.5 h with 5 . 10(-4) M chromate. Exposure to 10(-7) M chromate solution for 7 days inhibited colony formation while acute (1 h) treatment was toxic at 5 . 10(-6) M. The chromic glycine complex was toxic above 10(-3) M for a 1-week exposure but was not observably toxic after a 1-h treatment. These results indicate that chromate and not chromic compounds may be the carcinogenic form for man. The nature of the ultimate carcinogen is discussed. These findings illustrate the utility of the DNA repair technique to study the effects on human cells of inorganic carcinogens and mutagens.

Adult↗
PubMed1992

Clastogenicity of lead chromate particles in hamster and human cells.

Several insoluble compounds of chromium, such as lead chromate, are respiratory carcinogens in experimental animals and suspected to be so in humans. Lead chromate induces neoplastic transformation in cultured cells but the mechanism of genotoxicity is unknown. We examined the effect of lead chromate on the integrity of chromosomes of Chinese hamster ovary (CHO) and human foreskin fibroblasts (HFF) after a 24-h exposure. At 0.4 microgram/cm2, 0.8 microgram/cm2, 2 microgram/cm2 and 8 microgram/cm2 lead chromate particles reduced survival of CHO cells to 86%, 62%, 2% and less than 1% respectively. These concentrations induced a dose-dependent 4-19-fold increase in the percent metaphases with damage. The HFF cells exhibited higher sensitivity in both cytotoxicity and clastogenicity. The spectrum of damage observed for both cell types was primarily achromatic lesions affecting one or both chromatids. To test for particle dissolution effects, CHO cells were treated for 24 h with either clarified medium that had been incubated for 24 h with lead chromate particles, or clarified medium that had been pre-conditioned by CHO cells treated with lead chromate particles for 24 h. No damage was detected in these cells, indicating that extracellular dissolution into ionic lead and chromate did not contribute to the genotoxicity. This is consistent with a previous study in which scanning electron micrographs illustrated internalization of the particles. These results suggest that clastogenesis may be a mechanism for lead chromate induced carcinogenesis.

Animals↗
PubMed1991

Human peripheral spatial resolution for achromatic and chromatic stimuli: limits imposed by optical and retinal factors.

1. The aim of this study was to determine whether optical, receptoral or higher-order neural properties limit spatial resolution (acuity) in human vision, especially in the peripheral regions of the visual field. 2. Both achromatic and chromatic stimuli were used, and measures were taken to ensure that the resolution estimates were not contaminated by the detection of spatial sampling artifacts. Spatial contrast sensitivity functions were measured at retinal locations from 0 to 55 deg along the naso-temporal meridian for: (i) discriminating the direction of drift of luminance-modulated (black-white) sinusoidal stimuli drifting at 8 Hz (achromatic task); and (ii) for detecting isoluminant red-green sinusoidal stimuli drifting at 0.4 Hz (chromatic task). Achromatic contrast sensitivity functions were also measured along the vertical meridian for eccentricities of 8 and 40 deg. Each achromatic function was extrapolated to a contrast sensitivity of one (100% contrast) to estimate achromatic acuity. Chromatic acuities were obtained by expressing chromatic contrast in terms of cone contrasts and using the same method of extrapolation. We compared the results with recent data on human optical properties and retinal anatomy. 3. Both achromatic and chromatic acuity decline with distance from the fovea, but at a faster rate than that dictated by the known optical and/or receptoral properties of the human eye. We conclude that, for stimuli of either achromatic or chromatic contrast, peripheral spatial resolution is limited by post-receptoral mechanisms. Also, chromatic acuity declines more steeply than luminance acuity with eccentricity suggesting that there are additional post-receptoral limitations on colour resolution in the periphery. 4. A clear naso-temporal asymmetry is seen in the resolution whose dependence is qualitatively, but not quantitatively, similar to the Nyquist limits imposed by the asymmetric density of human retinal ganglion cells. We discuss the possibility that in peripheral vision (beyond the optic nerve head) the spacing of ganglion cells may pose a fundamental limit on the resolution of achromatic stimuli, but not chromatic stimuli.

Color Perception↗
PubMed1979

Detection of the mutagenic activity of lead chromate using a battery of microbial tests.

The potential mutagenicity of the carcinogen lead chromate was tested by the following battery of microbial tests: the Escherichia coli PolA+/PolA- survival test; the Salmonella/microsome His+ reversion assay; the E. coli Trp+ reversion test as a plate assay; the E. coli Gal+ forward mutation test; and the Saccharomyces cerevisiae assay for mitotic recombination. Lead chromate is mutagenic in Salmonella and in Saccharomyces and is thus identified as a microbial mutagen by this battery. Metabolic activation by rat liver homogenate (S9) is not required for the mutagenic activity of lead chromate. The most statistically significant, positive result is found with a supplementary assay, the E. coli fluctuation test. To determine whether the lead ion and/or the chromate ion were responsible for the mutagenicity observed, lead chloride and chromium trioxide (chromic acid) were also tested. In E. coli fluctuation test, the ranges of maximal mutagenicity for chromium trioxide and lead chromate overlap at the concentration 10(-5)M, whereas lead chloride shows no mutagenicity and little lethality at concentrations up to 10(-3)M. Thus, it appears that the chromate ion is responsible for the mutagenicity of lead chromate.

Chromates↗
PubMed1992

Prognosis of occupational chromate dermatitis.

To elucidate further the natural history and prognosis of occupational chromate dermatitis, 120 affected patients, diagnosed between 1980 and 1989, were reviewed. The incidence of chromate dermatitis in Western Australia appeared to remain unchanged over the decade. 65% of patients were construction workers with cement-induced chromate dermatitis. Workers at greatest risk of sensitization were those mixing bagged cement at the work site. The median age at onset of symptoms was 34 years, with 48% having been exposed to chromate for 5 years or less. Only 37% presented to the dermatologist within 12 months of developing symptoms. 76% of patients had ongoing dermatitis at the time of review. Although 48% of the study population had completely changed their occupation to avoid chromate exposure, symptoms persisted in 69%. A delayed diagnosis of chromate sensitivity was noted to be a predictor of chronicity. In view of the potential chronicity of chromate dermatitis and its associated social and occupational impairment, we recommend the addition of ferrous sulphate while mixing bagged cement at the work site. This simple technique targets the workers at greatest risk of becoming sensitized.

Adolescent↗
PubMed1992

Chromatic aberration and optical power of a diffractive bifocal contact lens.

Although diffractive contact lenses have been well documented in theory, no definitive experimental data have been reported which confirm that the near image is in fact created by diffraction rather than by refraction. We have tested the diffraction hypothesis for one type of diffractive contact lens (the Hydron Echelon bifocal) experimentally by measuring its longitudinal chromatic aberration in isolation and when worn on the eye. The basis of this test is that, according to theory, diffractive lenses should have chromatic aberration which is opposite in sign to that measured for the eye. Objective measurements of chromatic aberration were made with a focimeter when the lens was in a wet cell. Subjective measurements were made with a Badal optometer when the lens was worn on the eye. Four control experiments were conducted to provide baseline measurements of the eye's chromatic aberration, against which we compared the results obtained for the diffractive contact lens. The data were also compared with conventional measurements of refractive error obtained by standard subjective techniques and by an automated infrared refractor. Our results showed that the longitudinal chromatic aberration of the diffraction image of the Echelon bifocal lens was about one-half that obtained under the four control conditions: for the naked eye, for the nondiffraction image of the Echelon lens, or for either image of a refractive bifocal contact lens (CIBA Bisoft). These results are consistent with the theoretical prediction that the negative chromatic aberration of a diffractive contact lens should partially cancel the positive chromatic aberration of the human eye.(ABSTRACT TRUNCATED AT 250 WORDS)

Color Perception↗
PubMed1991

Simulated bipolar cells in fovea of human retina. III. Effects of chromatic adaptation in bipolar cell spectral responses.

Effects of chromatic adaptation on C-type bipolar cells (BC) in human retinal fovea are studied. Adaptation of the r-g channel is linear for both central fovea and parafovea. Adaptation of the parafovea bl-y channel, on the other hand, is nonlinear, which is accounted for by the slower adaptation rate of blue-sensitive cones with white light intensity as compared to rates of red- and green-sensitive cones. Achromatic adaptation of red- and green-center BCs produces uniform response decreases but without unique yellow loci shifts. Achromatic adaptation of blue-center BCs, on the other hand, does cause shifts of the unique green locus. Shifts of the crossover points for the BC response spectra occur with chromatic adaptation; the unique yellow loci shifts to shorter wavelengths with adapting wavelengths shorter than 550 nm and longer wave-lengths with longer adapting wavelengths than 550 nm. Chromatic adaptation is sufficient to explain the Bezold-Brüke effects; but to fully account for these shifts a novel hypothesis is proposed. For the green and red spectrum regions Bezold-Brücke shifts are due to r-g channel chromatic adaptation, while for the blue spectrum region bl-y channel chromatic adaptation accounts for Bezold-Brücke shifts. The two channels function independently in an either/or manner. The bl-y channel, besides having a unique green locus at 517.7 nm, has a crossover point at about 670 nm. Chromatic adaptation of the bl-y channel produces shifts of the unique red locus, which may account for extraspectral hue shifts.

Acclimatization↗
PubMed1992

Sustained and transient properties of chromatic and luminance systems.

Reaction times were measured to 450 and 650 mm test increments to examine the temporal behavior of the chromatic and luminance systems. A response-terminated random foreperiod paradigm was employed. Stimuli consisted of chromatic test increments upon backgrounds of varying spatial structure. Conditions were chosen which may preferentially favor the reaction time response being mediated by the chromatic or luminance systems. The temporal properties of the chromatic and luminance systems were demonstrated by the shape of the estimated hazard functions of the reaction time distributions. When the white background was spatially coincident with the test field, the hazard functions showed a relatively small peak. As white sectors were added to the annulus surround (introducing spatial transients between test and background fields), however, the hazard functions became more and more peaked. The hazard functions of the luminance system were estimated by assuming that the chromatic and luminance systems function in parallel. We concluded from the results that the chromatic system may be characterized as a quasi-sustained mechanism and the luminance system as a transient mechanism.

Color Perception↗