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PubMed2005

A multifactorial analysis of concurrent patch-test reactions to nickel, cobalt, and chromate.

BACKGROUND: Previous research indicates that positive patch tests to nickel (II) sulphate, cobalt (II) chloride and potassium dichromate commonly occur together. METHODS: To further examine the relationship between nickel, cobalt, chromate, and the factors that may potentially be related to concurrent sensitizations to two or all three metal allergens, data from the Information Network of Dermatology Departments have been investigated. RESULTS: Women had a higher conditional odds of concurrent nickel-cobalt (OR = 6.80; 95% CI: 5.65-8.19) and nickel-chromate (OR = 2.13; 95% CI: 1.67-2.72) reactions than men. Construction workers had a significantly higher odds of cobalt-chromate reactions (OR = 13.89; 95% CI: 10.36-18.64), while the odds of isolated cobalt allergy was only 0.92 (95% CI: 0.48-1.74). Patients with underlying atopic eczema/dermatitis syndrome had a 40-90% higher chance of any positive outcome, which involved chromate. Polysensitization, defined as the number of positive reactions to standard series substances other than nickel, cobalt, and chromate, was also significantly associated with the concurrent reactions; moreover, steady and significant effect gradients were noted. CONCLUSIONS: This research confirms the occupational nature of cobalt-chromate concurrent reactions, in particular, in construction workers. Polysensitization, which is considered to represent susceptibility to delayed-hypersensitivity in general, is also associated with the concurrent reactions to the metals. Hence, not only coupled exposure, but also individual susceptibility may be responsible for concurrent reactions to metals in man.

Adult↗
PubMed1998

Alcaligenes eutrophus as a bacterial chromate sensor.

In Alcaligenes eutrophus CH34, determinants encoding inducible resistance to chromate (chr) and to cobalt and nickel (cnr) are located adjacent to each other on plasmid pMOL28. To develop metal-sensing bacterial strains, a cloned part of plasmid pMOL28, which contains both determinants, was mutated with Tn5-lacZ. The chr::lacZ fusions were specifically induced by chromium; cnr was induced best by Ni2+ but was also induced by Co2+, Mn2+, chromate, Cu2+, Cd2+, and Zn2+. The broad-host-range IncP1 plasmid pEBZ141, which contains a chr::lux fusion, was constructed. A. eutrophus AE104(pEBZ141), carrying a chr::lux transcriptional fusion, could be used as a biosensor for chromate when cultivated in glycerol as an optimal carbon source. Chromate and bichromate were the best inducers; induction by Cr3+ was 10 times lower, and other ions induced only a little or not at all. Interactions among induction of the chr resistance determinant, chromate reduction, chromate accumulation, and the sulfate concentration of the growth medium were demonstrated.

Alcaligenes↗
PubMed1994

The generation of DNA single-strand breaks during the reduction of chromate by ascorbic acid and/or glutathione in vitro.

The potential role of iron and copper and the involvement of hydroxyl radicals in the DNA cleavage caused by chromate and glutathione (GSH) has been investigated. We have also studied the ability of chromate, on reaction with ascorbate as well as in mixed solutions of ascorbate and GSH, to cause DNA strand breaks. In both fully demetalated and conventional (i.e., metal contaminated) systems, chromate and GSH induced similar numbers of DNA strand breaks. This observation suggests that traces of iron or copper contaminating the reaction mixtures do not play a major role in the DNA cleavage caused by chromate and GSH. A series of hydroxyl radical scavengers exhibited a protective influence on the induction of DNA strand breaks. However, glucose and sucrose, both strong hydroxyl radical scavengers, showed no concentration-dependent inhibition of DNA cleavage. Competition kinetics studies yielded apparent rate constants that were not consistent with hydroxyl radicals being the species responsible for DNA strand breaks. Ascorbate in combination with chromate was also found to induce strand breaks in DNA; this damage could be attributed to reactive intermediates generated during the reduction. When mixed systems of ascorbate and GSH in the presence of chromate were investigated, there were clearly interactions between the two reductants.

Ascorbic Acid↗
PubMed1994

Protective effects of thiol compounds on chromate-induced toxicity in vitro and in vivo.

The effects of thiol compounds (L-cysteine ethyl ester, 2,3-dimercaptosuccinic acid, or 2,3-dimercapto-1-propanesulfonic acid) on the toxicity induced by chromate (potassium dichromate) were investigated in HeLa cells and mice. Chromate-induced cytotoxicity evaluated by inhibition of cell growth and chromium content of the cells was diminished by all of the thiol compounds tested when the cells were incubated in the medium with both chromate and one of the thiol compounds. In mice injected ip with a thiol compound immediately after injection of chromate, mortality, ornithine carbamyl transferase activity in the serum, and chromium content in the liver were diminished remarkably compared with mice injected with chromate alone. These thiol compounds also caused an increase of urinary chromium excretion. These results suggest that the thiol compounds tested are useful for treating chromate-induced toxicity when they are given immediately after intake of the metal.

Animals↗
PubMed1994

Complexing of amino acids to DNA by chromate in intact cells.

Using o-pthaldialdehyde (OPT) fluorescence, the amino acids associated with DNA were studied following exposure of intact Chinese hamster ovary cells to chromate. Rigorous extraction with EDTA, acid, or base was required to release the amino acids cross-linked to the DNA isolated from control or chromate-treated cells by standard procedures (i.e., proteinase K, phenol, etc.). Amino acids resisting extraction from DNA were not studied since analysis was limited to those that could be released by these procedures. There was a chromate dose-dependent increase in amino acids complexed with the DNA that could be released by EDTA, acid, and base, and these amino acids were separated by HPLC and identified. Substantial increases in cysteine, glutamine, glutamic acid, histidine, threonine, and tyrosine were found as a function of increasing concentrations of chromate. There was also a time-dependent increase in complexing of these amino acids to the DNA by chromate. The amino acids found complexed to DNA in intact cells by chromate were thought to originate from reactions of free amino acids or small peptides with the DNA rather than being proteolytic products derived from larger proteins that were cross-linked to the DNA. This was supported by a number of experiments: a) free amino acids or bovine serum albumin (BSA) were cross-linked by chromium to DNA in vitro and the DNA was isolated by standard procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1982

[Investigations of the pathogenesis of lung cancer observed among chromate factory workers].

In order to clarify the relationship between the chromate compound and occurrence of lung cancer, the author studied the characteristics of patients with lung cancer among workers of chromate factory and measured the chromium contents of each tissues obtained from 14 patients at surgery and autopsy. The incidence of the chromate lung cancer was 413 per 100,000 population, which was 16 times that of the general population. All were male. The age ranged from 26 to 74 year old (average 53). The histological type was mostly squamous and small cell carcinoma. Location of carcinoma occurrence was mainly limited to the large bronchi. The average total labor period of patients with lung cancer was 258 months and the latent period was 305 months. The working history of the patients in hexavalent-chromium producing process was longer than that of the control group. Patients with small cell carcinoma was mainly engaged in the monochromate producing process. The labor and latent period of patients with squamous cell carcinoma was longer than those of small cell carcinoma. Measurement of chromium contents in the respiratory system of chromate workers revealed much higher chromium content than in control group. The chromium content of tissues in the non-respiratory system was a little higher than that of the control group. High chromium content itself did not have any relation with the occurrence of lung cancer because the primary location of chromate lung cancer was limited to the large bronchi, not to the peripheral lungs which contained the highest chromium content. The longer was the exposure period, the higher was chromium content in the lung. Chromium content in the upper lobe was higher than that in the lower lobe. From these studies, the author concluded that hexavalent-chromate compound might be the compound responsible for lung cancer occurrence.

Adenocarcinoma↗
PubMed2005

Quantitative phenotyping of chromatic dysfunction in best macular dystrophy.

OBJECTIVES: To quantify chromatic dysfunction in Best disease to reassess the classic categorization of macular chromatic damage and to investigate psychophysical and clinical correlations. METHODS: Color-contrast discrimination was measured using 2 different psychophysical strategies in age-matched control (n = 41) and patient (n = 34) eyes. The first strategy measured performance along 3 main confusion lines (testing cone function), and the second evaluated discrimination ellipses (modified Cambridge Color Test). The main outcome measures were chromatic discrimination variables (confusion line length, ellipse length, angle, and axis ratio) and visual acuity (VA). RESULTS: Significant loss of performance was seen in all color axes in our patients, and it increased monotonically with staging, becoming significant in Fishman stages 2 and 3. The classically assumed preferential type I red-green deficit was true only for stage 4. Substantial chromatic dysfunction occurred even with relatively preserved VA despite that negative correlations between all test variables and VA reached statistical significance. Partial correlation analysis showed that protan/deutan loss was related to VA independent of tritan loss. Statistically significant positive correlations were also found between lesion size and chromatic dysfunction. CONCLUSIONS: Chromatic discrimination is often impaired in Best disease, even when VA is still spared. Our quantitative psychophysical approach shows that the classic categorization as a type I red-green deficit is valid only for disease stage 4.

Adult↗
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↗
PubMed1986

Dynamics of chromatic adaptation in cones of freshwater turtle.

The closer the wavelength of a steady background of monochromatic light is to the peak sensitivity of a cone that is being illuminated, the stronger is the desensitization of that cone; this is chromatic adaptation. A model of the freshwater turtle retina with the neural components of chromatic adaptation via negative feedback circuits is used to simulate and study various aspects of chromatic adaptation. An internal negative feedback circuit resides solely within the cone pedicle and thereby, its adaptive effects are relatively specific, so that univariance is maintained. The cone-L-horizontal cell circuit is an external negative feedback circuit and its adaptive effects are less specific since all 3 chromatic cone types are involved, so that univariance is violated. Chromatic adaptation is the result of the decrease in the cone gain due to the dependency of the gains of the negative feedback circuits on the mean illuminance level. The results of the model are consistent with von Kries law, but the changes in gains of the cones due to chromatic adaptation are dependent on wavelength, intensity of the adapting light and size.

Acclimatization↗
PubMed2002

Nitric oxide controls the light adaptive chromatic difference in receptive field size of H1 horizontal cell network in carp retina.

In carp retina, the receptive field size of the H1-type horizontal cell (HC) network is known to be chromatically selective, as electrophysiological signals are generated by short-wavelength (SW) light stimuli, which spread much less than those for long-wavelength (LW). We have shown previously that the signalling mechanism underlying this chromatic difference operates only in the light-adapted retina and that it involves cGMP as an intermediary messenger. In the present study, the possible role of nitric oxide (NO) as such a control mechanism was investigated. Application of a NO donor (SNP or SNOG) to dark-adapted retinae produced a chromatic difference in the receptive field size, such as in the light-adapted state. This effect was due mainly to a reduction in the spread of signals generated by SW stimuli; LW signalling spread was not altered. No such effect was observed in light-adapted retinae where a chromatic difference in receptive field size was already present. On the other hand, application of the NO 'scavenger' haemoglobin to light-adapted retinae suppressed the chromatic difference. These results are consistent with NO being a light-adaptive retinal neuromodulator involved in the generation of the chromatic difference in H1 cell receptive field size. These results are discussed in the context of two different hypotheses.

Action Potentials↗
PubMed1985

Second-site adaptation in the red-green chromatic pathways.

On different chromatic adapting fields, thresholds were measured with a 1.2 deg flash consisting of simultaneous incremental and decremental red and green components that stimulate the M and L cones in any desired ratio. Thresholds were plotted in normalized coordinates in which the quantal change in the M and L cones due to the flash was divided by the quantal catch due to the field. Detection contours for a wide range of test flashes provide evidence for luminance and chromatic mechanisms that respectively respond to the sum and difference of the M and L cone signals. Field color has little influence on the luminance mechanism but strongly affects chromatic detection, with sensitivity being maximal on yellow fields and declining slightly on green fields and declining strongly on red fields. Similar effects were obtained for long (200 msec) and very brief flashes, although the shape of the contours differed considerably. The results provide evidence for a second adaptation site within the red-green chromatic pathways, similar to the second-site in the S cone pathways. Chromatic fields (green and red) polarize the site and reduce sensitivity to chromatic flashes.

Adaptation, Ocular↗
PubMed1987

Chromatic suppression of cone inputs to the luminance flicker mechanism.

Eisner and MacLeod [J. opt. Soc. Am. 71, 705-718 (1981)] showed that intense green and red chromatic adapting fields may suppress respectively the M and L cone input to the luminance mechanism by a factor considerably greater than Weber's law. We obtained evidence for such chromatic suppression by measuring complete detection contours for different ratios of red and green test lights presented in rapid flicker in the center of a uniform field. The detection contours represent thresholds as the quantal modulation of the M and L cones normalized by the quantal catch owing to the field. Luminance flicker mechanisms were identified by sections of the contours where detection was controlled by a linear sum of the M and L cone test signals. The slope of these sections indicated that intense red fields selectively suppressed the L cone input to the luminance mechanism by a factor greater than Weber's law; evidence was much less firm for an analogous suppression of the M cone input by intense green fields. The shape of the detection contours also suggests that intense red fields, which differentially light-adapt the M and L cones, may produce a moderate temporal phase-shift between the M and L cone signals. The shape of the temporal MTF of the M cone and the L cone input to the luminance mechanism may be determined at the cone stage, with the absolute sensitivity (vertical scaling) being partially dependent on selective chromatic suppression of the cone inputs owing to the intense chromatic field. Luminance and red-green chromatic temporal sensitivity functions are presented in terms of the M and L cone quantal modulations. Chromatic sensitivity progressively rises above luminance sensitivity as temporal frequency is gradually lowered below 15 Hz, with the consequence that 'contrast sensitivity' may be much higher for color than for luminance.

Adaptation, Ocular↗
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↗
PubMed1992

Chromatic adaptation to natural and incandescent illuminants.

A color CRT image display system was used to present adapting backgrounds that were spatially and temporally varied. Three observers adjusted the chromaticity of test stimuli to produce an achromatic appearance under a variety of adapting conditions. The achromatic-appearing chromaticities were used as measures of the observers' states of chromatic adaptation. The spatial configuration of the adapting background was varied to measure the spatial extent of the mechanisms responsible for chromatic adaptation. The temporal configuration of the adapting background was varied to measure the time-course of these mechanisms. The results show that chromatic adaptation is spatially localized with a time-course on the order of 10 sec. Since the mechanisms were shown to be spatially localized, the observed temporal integration across eye movements is required to allow these mechanisms to adjust to the spatially integrated scene chromaticity.

Adaptation, Ocular↗
PubMed1993

Link-specific adaptation in the luminance and chromatic channels.

We present evidence that adaptation occurs in the separate links that connect the receptors to the luminance and the chromatic channels. The relative effectiveness of the L and M cone inputs to the luminance and red/green chromatic channels was determined by using, respectively, heterochromatic flicker photometry and a cancellation technique which maintained a pure yellow. The findings provide evidence for a link-specific adaptation model, wherein one receptor system provides two separate links to the luminance and chromatic channels and the outputs of an individual cone to these two postreceptoral channels can be separately attenuated or weighted at each of these links by colored adapting lights. One line of evidence for link-specific adaptation is that colored adapting fields selectively suppress L and M cone inputs to the red/green chromatic channel by a smaller factor than the luminance channel. A second line of evidence is that there is not only a magnitude difference but also a dynamic difference between adaptive processes operating in the luminance and chromatic channels: the luminance channel has a faster gain change and recovery from adaptation than does the chromatic channel. The results, together with other evidence, make it plausible that an important component of light adaptation in cone vision occurs at the cone-bipolar synapse.

Adaptation, Ocular↗
PubMed1996

Infant motion: detection (M:D) ratios for chromatically defined and luminance-defined moving stimuli.

In order to assess the relative contributions of chromatic vs luminance information to motion processing in infants, we employed a motion:detection (M:D) paradigm. Stimuli consisted of 27 deg by 40 deg, 0.25 c/deg sinusoidal gratings moving at 22 deg/sec (5.6 Hz), and were either chromatically defined or luminance-defined. Contrast thresholds for direction-of-motion (M) were obtained using a directional eye movement technique. Contrast thresholds for detection (D) were obtained using forced-choice preferential looking. M:D threshold ratios were obtained for individual infant subjects, and results were compared to those of adults. As expected, adult M:D threshold ratios were near 1:1 for luminance-defined stimuli, but greater than 1:1 for chromatically defined stimuli. This suggests that, for adults, luminance-defined, but not chromatically defined, stimuli are detected by mechanisms labeled for direction of motion. By contrast, infant M:D ratios for chromatically and luminance-defined stimuli were approximately equal and close to 1:1, suggesting that, for infants, luminance- as well as chromatically defined stimuli are detected by mechanisms that are labeled for direction of motion.

Adult↗
PubMed1980

Effect of lead chromate on chromosome aberration, sister-chromatid exchange and DNA damage in mammalian cells in vitro.

Possible mutagenic activity of lead chromate in mammalian cells was studied using assays for chromosome aberrations and sister-chromatid exchanges in cultured human lymphocytes, and DNA fragmentation as detected by alkaline-sucrose gradient sedimentation in cultured Chinese hamster ovary (CHO) cells. Lead chromate caused dose-related increases in chromosome aberration and sister-chromatid exchange in human lymphocytes. No increase in DNA damage was observed in CHO cells, possibly due to the relative insensitivity of the CHO cells and the limited solubility of lead chromate in tissue culture medium. The mutagenicity of lead chromate in human lymphocytes appears to be entirely due to the chromate ion since chromosome aberrations were induced by potassium chromate but not lead chloride.

Animals↗
PubMed1988

Chromaticity-coded Doppler blood velocity sonagrams: preliminary observations.

This paper describes the application of chromaticity to spectrally analysed Doppler blood velocity signals. Chromaticity enables a particular colour to be assigned to the power/frequency distribution within each instantaneous spectral sweep of a sonagram. Successive spectral sweeps of a sonagram can then be colour-coded in this fashion to produce a chromaticity-coded sonagram. Two chromaticity-coded sonagrams are presented to illustrate various blood flow features. Standard sonagram display formats are also presented for comparison purposes. It appears that the chromaticity-coded sonagram offers the ability to digitally encode the instantaneous power spectral distribution with a single chromaticity vector.

Blood Flow Velocity↗