Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CHROMATES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1993

Inhibition of lead chromate clastogenesis by ascorbate: relationship to particle dissolution and uptake.

Chromium metal salts are considered to be human carcinogens, especially the salts of low solubility. Lead chromate, a highly insoluble chromium metal salt, has been shown to be tumorigenic, genotoxic and clastogenic. In this study, the roles of particle-cell contact, particle dissolution and particle uptake in the clastogenic activity of lead chromate were investigated. Using Pb51CrO4 it was found that lead chromate particles (1.2 microns mean diameter, -28 mV surface charge) were slightly soluble in water; solubility increased 2-fold when particles were incubated in culture medium, but was not increased further by the addition of serum. The extracellular concentration of chromium increased 7-fold when lead chromate was incubated in the presence of Chinese hamster ovary (CHO) cells compared with culture medium alone. The intracellular concentration of ionic chromium increased in a dose-dependent manner following exposure of CHO cells to clastogenic doses of lead chromate reaching estimated levels as high as 1.2 mM per cell. Treatment of cells with lead chromate particles in the presence of a nontoxic dose of vitamin C blocked uptake of ionic chromium and eliminated the clastogenic activity of the particles. Transmission electron microscopy showed that lead chromate particles were internalized by CHO cells in phagocytic vacuoles in as little as 1 h; internalization was unaffected by co-treatment with vitamin C. It was demonstrated that particle-cell contact was required for lead chromate-induced clastogenesis. These data show that although phagocytic particle uptake occurs, particle-cell contact and extracellular dissolution are responsible for the clastogenic activity of lead chromate. These data also demonstrate that the genotoxicity of particulate hexavalent chromates can be blocked by vitamin C.

Animals↗
PubMed1993

Lung cancer mortality among a cohort of male chromate pigment workers in Japan.

In 1975, five manufacturers of chromate pigment in Japan were examined in a study of the carcinogenicity of chromates. These companies were producing lead chromate, zinc chromate, molybdate orange and/or strontium chromate. The current study covers a cohort of 666 workers involved in the manufacture of chromate pigment for at least 1 year between 1950 and 1975. The workers were followed up for 15-40 years, until 1989. Many previous reports have found an excess lung cancer risk among workers involved in the manufacture of chromate pigments and chromate chemicals. In the current study, subjects were classified on the basis of years worked, years of observation, characteristics of company, type of work engaged in for the longest period of time, and involvement in the manufacture of zinc chromate. Mortality was compared with that of all Japanese males by means of the person-year method. The route of exposure was primarily inhalation through the respiratory system. None of the results showed statistically significant differences that would suggest an excess risk for malignant neoplasms, particularly lung cancer, among workers engaged in the manufacture of chromate pigment in Japan.

Cause of Death↗
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↗
PubMed2006

Effect of chromate stress on Escherichia coli K-12.

The nature of the stress experienced by Escherichia coli K-12 exposed to chromate, and mechanisms that may enable cells to withstand this stress, were examined. Cells that had been preadapted by overnight growth in the presence of chromate were less stressed than nonadapted controls. Within 3 h of chromate exposure, the latter ceased growth and exhibited extreme filamentous morphology; by 5 h there was partial recovery with restoration of relatively normal cell morphology. In contrast, preadapted cells were less drastically affected in their morphology and growth. Cellular oxidative stress, as monitored by use of an H2O2-responsive fluorescent dye, was most severe in the nonadapted cells at 3 h postinoculation, lower in the partially recovered cells at 5 h postinoculation, and lower still in the preadapted cells. Chromate exposure depleted cellular levels of reduced glutathione and other free thiols to a greater extent in nonadapted than preadapted cells. In both cell types, the SOS response was activated, and levels of proteins such as SodB and CysK, which can counter oxidative stress, were increased. Some mutants missing antioxidant proteins (SodB, CysK, YieF, or KatE) were more sensitive to chromate. Thus, oxidative stress plays a major role in chromate toxicity in vivo, and cellular defense against this toxicity involves activation of antioxidant mechanisms. As bacterial chromate bioremediation is limited by the toxicity of chromate, minimizing oxidative stress during bacterial chromate reduction and bolstering the capacity of these organisms to deal with this stress will improve their effectiveness in chromate bioremediation.

Adaptation, Physiological↗
PubMed2006

Surfactant protein B gene variations and susceptibility to lung cancer in chromate workers.

BACKGROUND: Hexavalent chromium has been extensively investigated regarding its mutagenicity and carcinogenicity; however, its mechanism for initiating and enhancing the development of lung cancer is still obscure. Biomarkers of exposure, effect or susceptibility are required for risk assessment and for epidemiologic research studies especially in occupational settings. Since the surfactant protein system (SP) is very important for normal lung function and for mediating local airway conditions and in the clearance of the upper respiratory tract from the occupational and environmental dusts, we hypothesize that SP genes may represent good candidates to study susceptibility for lung cancer. METHODS: Using PCR genotyping methods with gel electrophoresis and confirmation of results with precise DNA fragment size measurement on microchip electrophoresis, we analyzed SP-B intron-4 polymorphism in 230 subjects who were classified into groups; chromate-related lung cancer, control chromate workers who had not developed lung cancer, control individuals with non chromate-related adenocarcinoma or squamous cell carcinoma of the lungs, or healthy Japanese control individuals. RESULTS: Our results indicated that the SP-B variants (deletion/insertion) were significantly overrepresented (61.3%) in the chromate-related lung cancer group than other groups (X2 = 47.6; DF = 4, P = 0.0001). There was a significant difference between the chromate lung cancer group and both of the control groups, healthy individuals and chromate workers who did not develop lung cancer, showing odds ratios (OR) with 95% confidence intervals (CI) of 21.9 (7.3-65.7) and 19.0 (3.78-95.4), respectively. Compared with 46 non chromate-related SCC of the lung, the SP-B variants were significantly overrepresented in the chromate-related SCC (18/28; 64.3%) than the non-chromate SCC (11/46; 23.9%) of the lung samples (X(2) = 10.27, P = 0.01), OR with 95% CI is 5.73 (2.05-16.01). CONCLUSION: These findings indicate a very strong association of the SP-B intron-4 variants with mechanisms that may enhance lung cancer susceptibility, especially in workers who are employed in chromate industry. Moreover, confirmation of such results may help to suggest adding the SP-B intron-4 typing to be one of the screening tests of the pre-placement medical examination to confirm that the worker has no variations of the SP-B gene before being engaged in a chromium-related industry, with the intention of providing proper medical counseling.

Carcinogens, Environmental↗
PubMed2000

A central mechanism of chromatic contrast.

The color appearance of a light can be altered by introducing a second, surrounding field. This phenomenon, called chromatic induction, is attenuated by chromatic variation within a remote region outside the surround [Shevell & Wei (1998). Vision Research, 38, 1561-1566]. We now consider the locus of the neural mechanism mediating the attenuation caused by the remote chromatic contrast. In the first experiment, the magnitude of chromatic variation within the remote region is changed either: (i) in the same eye that views the patch judged in color; or (ii) in only the opposite eye. The measurements are virtually the same in both cases, which implies attenuation of chromatic induction is mediated by a central, binocular mechanism. In the second experiment, the patch with its immediate inducing surround is changed in binocular disparity relative to the remote region with chromatic variation. The patch and surround, seen together in one depth plane, are perceived to be in front of, behind, or in the same plane as the remote region with chromatic variation. Attenuation of chromatic induction is strongest when the patch and surround are in the same depth plane as the remote region. This change of color appearance with disparity is consistent with a central binocular process. Overall, the color-appearance measurements are explained by monocular encoding of chromatic differences at edges, and a central binocular mechanism of chromatic-contrast gain control.

Color Perception↗
PubMed1998

Chromatic induction: border contrast or adaptation to surrounding light?

Chromatic induction from a surrounding light is measured with an additional remote field outside the surround. Chromatic induction from the surround into a central test field is found to be attenuated by a remote inhomogeneous 'checkerboard', composed of squares at two different chromaticities. A uniform remote field, on the other hand, either at the average or at the most extreme chromaticity of the 'checkerboard', has a weaker effect on chromatic induction than the inhomogeneous field, implying that chromatic contrast within the remote region is a critical factor. The complete set of experiments is accounted for by chromatic contrast gain control: chromatic induction, mediated by a neural signal for contrast at the edge of the test, is attenuated by contrast within the remote region. A contrast gain control set by variation in chromaticity over a broad area can contribute to the stable color appearance of surfaces embedded within complex scenes by minimizing chromatic induction from locally adjacent regions.

Adaptation, Ocular↗
PubMed1997

Uptake of chromate in sulfate deprived wheat plants.

Terrestrial plants have been proposed for the removal of chromate from waste waters. Since chromate seems to be absorbed in roots by the same transport system as sulfate, sulfate-deprivation pretreatment and sulfate absence during chromate uptake were tested in wheat in order to increase chromium uptake efficiency. At 1 and 5 microg CrO(2-)(4) ml(-1) the highest chromate uptake was observed when plants suffered 5 days of sulfate deprivation pretreatment and absence of sulfate during chromate uptake. However, only at the lower concentration chromate net uptake was rapidly replaced by net efflux presumably due to toxic effects. At 5 microg CrO(2-)(4) ml(-1), the uptake of chromate was also enhanced by sulfate-deprivation pretreatment alone or lack of sulfate-competition. We conclude that sulfate is a strong inhibitor of chromate uptake, and when plants are going to be used to remove chromate from waste waters, sulfate-chromate interaction should be considered.

Journal Article↗
PubMedDate not supplied

Determination of chromate adulteration of human urine by automated colorimetric and capillary ion electrophoretic analyses.

Various chemicals can be added to urine specimens collected for drug analysis to abnormally elevate ionic concentrations and/or interfere with either immunoassay urine drug-screening procedures or gas chromatographic-mass spectrometric confirmation techniques. One such adulterant, "Urine Luck" (formula 5.3), has been identified in our previous research to contain potassium dichromate. Screening of suspected adulterated specimens and confirmation of the adulterant are important for forensic drug screening. The application and comparison of automated colorimetric and capillary ion electrophoretic techniques for the detection, confirmation, and quantitation of chromate adulteration of urine specimens were the purpose of this investigation. Thirty-six urine specimens suspected of adulteration were analyzed for chromate by colorimetric analysis with diphenylcarbazide. Duplicate aliquots were analyzed for chromate by capillary ion electrophoresis. Results of the colorimetric chromate analyses revealed a mean chromate concentration of 929 microg/mL with a standard error of 177 microg/mL and a range of 30 to 5634 microg/mL. Results of the capillary ion electrophoresis chromate analyses revealed a mean chromate concentration of 1009 microg/mL with a standard error of 218 microg/mL and a range of 20 to 7501 microg/mL. The correlation coefficient between the capillary ion electrophoretic and colorimetric chromate results was r = 0.9669. Application of the automated diphenylcarbazide colorimetric technique provides rapid determination of chromate adulteration of a urine specimen. Capillary ion electrophoresis offers a separation technique to confirm the presence of chromate in suspected adulterated specimens. The excellent correlation between these methods substantiates their application to forensic testing as screening and/or confirmation techniques.

Colorimetry↗
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↗
PubMed1982

Chromate lung cancer with special reference to its cell type and relation to the manufacturing process.

The manufacturing process of the chromate industry can be classified into five steps. The main hazardous pollutants of the first step are trivalent chromate compounds, and those of the second and third steps are hexavalent chromate compounds. Analysis of the detailed working history of chromate workers with bronchogenic carcinoma, yielded the following results: the work history of chromatic lung cancer patients in the first step, which produced mainly trivalent chromate dust, was rather short. Patients with small cell carcinoma were engaged mainly in the second step (98.1% of the total working months), where they were heavily exposed to hexavalent chromate dusts. Patients with squamous cell carcinoma were engaged rather evenly in the second and fourth steps, and somewhat longer in the third step. Comparisons of the exposure periods revealed that the working history of small cell carcinoma patients was significantly shorter than that of squamous cell carcinoma patients. There were many more heavy smokers among the squamous cell carcinoma group as compared to the small cell carcinoma patients. Based on these results, it is concluded that the cell type of occupational lung cancer was mainly small cell carcinoma when the exposure to carcinogenic agents was heavy, and that the carcinogenicity of chromate was derived mainly from hexavalent chromate rather than trivalent compounds.

Adult↗
PubMed2005

Microsatellite instability and protein expression of the DNA mismatch repair gene, hMLH1, of lung cancer in chromate-exposed workers.

Our previous studies of lung cancer in chromate-exposed workers (chromate lung cancer) have revealed that the frequency of replication error (RER) in chromate lung cancer is very high. We examined whether the RER phenotype of chromate lung cancer is due to an abnormality of DNA mismatch repair protein. We investigated the expression of a DNA mismatch repair gene, hMLH1, and hMSH2 proteins using immunohistochemistry and microsatellite instability (MSI) in 35 chromate lung cancers and 26 nonchromate lung cancers. Lung cancer without MSI or with MSI at one locus was defined as "RER(-)," lung cancer with MSI at two loci was defined as "RER(+)," and lung cancer with MSI at three or more loci was defined as "RER(++)." The repression rate of hMLH1 and hMSH2 proteins in chromate lung cancer was significantly more than that of nonchromate lung cancer (hMLH1: 56% vs. 20%, P = 0.006, hMSH2: 74% vs. 23%, P < 0.0001). In chromate lung cancer, the repression rate for hMLH1 was 43% in RER(-), 40% in RER(+), and 90% in the RER(++) group. The repression rate of hMLH1 protein in the RER(++) group was significantly higher than that in the RER(-) and RER(+) groups (P = 0.039). The inactivation of hMLH1 expression strongly correlated with the microsatellite high instability phenotype in chromate lung cancer. The genetic instability of chromate lung cancer is due to the repression of hMLH1 protein.

Adaptor Proteins, Signal Transducing↗
PubMed2005

A comparison of hepatocyte cytotoxic mechanisms for chromate and arsenite.

In the following, we have compared the cytotoxic mechanisms of the chromate CrO(4)(2-) and arsenite AsO(2)(-). Chromate (Cr (VI)) cytotoxicity was associated with reactive oxygen species (ROS) formation, lipid peroxidation and loss of mitochondrial membrane potential, which were prevented by catalase, antioxidants and ROS scavengers. Hepatocyte glutathione was also rapidly oxidized. Chromate reduction was inhibited in glutathione depleted hepatocytes, and glutathione depleted hepatocytes were also much more resistant to chromate induced cytotoxicity, ROS formation and lipid peroxidation. This suggests that chromate is reductively activated by glutathione. Chromate cytotoxicity also involved lysosomal injury and protease activation, which were prevented by lysosomotropic agents, endocytosis inhibitors, protease inhibitors and ROS scavengers. On the other hand, arsenite cytotoxicity was associated with much less oxidative stress, and lysosomal damage did not occur. However, arsenite cytotoxicity was also associated with loss of mitochondrial membrane potential, which in contrast to chromate cytotoxicity was inhibited by the ATP generators fructose, xylitol and glutamine. Arsenite induced cytotoxicity, mitochondrial membrane potential decline and also ROS formation were significantly increased by inactivating hepatocyte methionine synthase or hepatocyte methyl transferase. However, methyl donors such as betaine, methionine or folic acid prevented arsenite but not chromate cytotoxicity, and this suggests that arsenite is detoxified by reductive methylation. In conclusion, chromate induced cytotoxicity could be attributed to oxidative stress and lysosomal damage, whereas arsenite induced cytotoxicity could be attributed to mitochondrial toxicity and ATP depletion.

Animals↗
PubMed2000

Frequent cyclin D1 expression in chromate-induced lung cancers.

Ex-chromate workers are frequently afflicted with lung cancers, especially central-type squamous cell carcinomas (SCCs) of the lung. However, little is known about the molecular and cellular biologic characteristics of chromate-induced lung cancers. We investigated expression of cyclin D1, bcl-2, and p53 proteins in chromate-induced lung cancers by immunohistochemistry, compared with those in lung cancers from nonexposed individuals and those in individuals with pneumoconiosis. Of 19 chromate-induced lung cancers, 16 tumors were SCCs, including 11 central and 5 peripheral types. Eleven (69%) of 16 chromate SCCs showed cyclin D1 expression. In contrast, cyclin D1 expression was observed in only 3 (12%) of 26 SCCs from nonexposed individuals and 6 (16%) of 37 SCCs that developed in patients with pneumoconiosis, respectively. The frequency of cyclin D1 expression proved to be significantly higher in chromate-induced SCCs than in SCCs from nonexposed individuals and from those with pneumoconiosis (P < .001). When comparisons were extended to all histologic types of lung cancer, cyclin D1 expression was observed significantly more often in chromate-induced lung cancers than in lung cancers from nonexposed subjects and those from patients with pneumoconiosis (11 [58%] of 19 v 5 [10%] of 52, P < .001, and 7 [11%] of 63, P < .001, respectively). Frequencies of bcl-2 and p53 expression were not significantly different among lung cancers from ex-chromate workers, nonexposed individuals and those with pneumoconiosis. The current study suggests that cyclin D1 expression may be involved in the development of chromate-induced lung cancers, although its underlying mechanism remains to be determined.

Adenocarcinoma↗
PubMed1983

The carcinogen chromate causes DNA damage and inhibits drug-mediated induction of porphyrin accumulation and glucuronidation in chick embryo hepatocytes.

DNA damage by chromate in chick embryo hepatocytes has been correlated with the effect of chromate on inducible cell functions. Treatment of chick embryo hepatocytes with chromium(VI) in the form of sodium chromate resulted in the rapid uptake of chromate and the induction of DNA lesions in a time- and concentration-dependent manner. DNA interstrand cross-links, strand breaks and DNA-protein crosslinks, as measured by the alkaline elution technique, were observed after treatment of the hepatocytes with chromate concentrations (2.5- 0 microM) which did not affect cell viability. The effect of chromate on inducible cell functions was measured by assaying propylisopropylacetamide-induced accumulation of porphyrin and glucuronidation of phenol red by intact cells. Chromate inhibited propylisopropylacetamide-induction of porphyrin accumulation and phenol red glucuronidation in a time- and concentration-dependent manner which paralleled DNA damage. DNA damage was removed and inducibility of porphyrin accumulation by propylisopropylacetamide plus deferoxamine methanesulfonate was restored 21 h following a 2 h pretreatment with chromate. Chromium(III) in the form of chromic nitrate at concentrations up to 25 times those used with chromate had no effect on DNA damage or the induction of porphyrin accumulation and phenol red glucuronidation by propylisopropylacetamide in the cultured chick hepatocytes.

Animals↗
PubMed2004

Chromator, a novel and essential chromodomain protein interacts directly with the putative spindle matrix protein skeletor.

We have used a yeast two-hybrid interaction assay to identify Chromator, a novel chromodomain containing protein that interacts directly with the putative spindle matrix protein Skeletor. Immunocytochemistry demonstrated that Chromator and Skeletor show extensive co-localization throughout the cell cycle. During interphase Chromator is localized on chromosomes to interband chromatin regions in a pattern that overlaps that of Skeletor. However, during mitosis both Chromator and Skeletor detach from the chromosomes and align together in a spindle-like structure. Deletion construct analysis in S2 cells showed that the COOH-terminal half of Chromator without the chromodomain was sufficient for both nuclear as well as spindle localization. Analysis of P-element mutations in the Chromator locus shows that Chromator is an essential protein. Furthermore, RNAi depletion of Chromator in S2 cells leads to abnormal microtubule spindle morphology and to chromosome segregation defects. These findings suggest that Chromator is a nuclear protein that plays a role in proper spindle dynamics during mitosis.

Amino Acid Sequence↗
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↗
PubMed1993

What happens if it changes color when it moves?: psychophysical experiments on the nature of chromatic input to motion detectors.

Several lines of evidence indicate that the processing of motion by the primate visual system continues even when a moving stimulus differs from its surroundings by color alone. To illuminate the mechanisms by which our visual system uses color as a token for motion correspondence, we have developed an "apparent motion" paradigm in which red/green sine-wave gratings undergo reversal of chromatic contrast sign each time they are displaced in a particular direction. Under such conditions, correspondence based upon conservation of chromatic sign conflicts with correspondence based upon chromatically-defined borders. When these heterochromatic stimuli also possess luminance modulation, motion is always perceived in the direction in which the sign of luminance contrast is preserved. At isoluminance, however, two very different chromatic influences on motion detection are revealed. First, when stimuli undergo small spatial displacements, motion is perceived in the direction of the nearest chromatically-defined border even when the sign of chromatic contrast at that border alternates over time. Under these conditions, motion detectors apparently exploit information about image borders defined by color while sacrificing information about the colors that make up those borders. By contrast, when spatial displacement is large, motion is more apt to be perceived in the direction for which sign of chromatic contrast is preserved. In this instance, information about the polarity of chromatic contrast facilitates motion detection. These results suggest that chromatic signals contributing to motion detection are of two distinct types. This conclusion has implications for the degree of crosstalk between magnocellular and parvocellular processing streams in the primate visual system and it reinforces our understanding of how image features affect the way we see things move.

Color Perception↗