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PubMed1999

Modelling spatial contrast sensitivity functions for chromatic and luminance-modulated gratings.

We extended our detection model of achromatic spatial vision (Rovamo, J., Mustonen, J., & Näsänen, R. (1994a). Modelling contrast sensitivity as a function of retinal illuminance and grating area. Vision Research, 34, 1301-1314) to colour vision by taking into account the fact that due to the spatio-chromatic opponency of retinal ganglion cells and dorsal lateral geniculate nucleus (dLGN) neurons, equiluminous chromatic gratings are not affected by precortical lateral inhibition. We then tested the extended model by using Mullen's experimental data (Mullen, K. J. (1985). The contrast sensitivity of human color vision to red-green and blue-yellow chromatic gratings. Journal of Physiology, 359, 381-400). The band-pass shape of the spatial contrast sensitivity function for luminance-modulated green and yellow gratings transformed to a low-pass shape, resembling the chromatic spatial contrast sensitivity function for red-green and blue-yellow equiluminous gratings, when the effect of precortical lateral inhibition on grating contrast was computationally removed by dividing luminance contrast sensitivities by spatial frequency (i.e. by af, where a = 1 degree). After the removal of this direct effect of lateral inhibition, there still remained a residual shape difference between the spatial contrast sensitivity functions for chromatic and luminance gratings. It was due to indirect reduction of grating visibility by quantal noise high-pass filtered by precortical lateral inhibition. When this indirect effect of quantal noise was also removed, contrast sensitivity for luminance gratings was about twice the sensitivity for chromatic gratings at all spatial frequencies. This was evidently due to the fact that the chromatic contrast of the equiluminous grating at the opponent stage (Cole, G. R., Hine, T. & McIihagga, W. (1993). Detection mechanisms in L-, M-, and S-cone contrast space. Journal of the Optical Society of America A, 10, 38-51) was about half of the luminance contrast of either of its chromatic component. Thus, if the contrast of the equiluminous chromatic grating were not expressed as the Michelson contrast of one chromatic component grating against its own background (Mullen, K. J. (1985). The contrast sensitivity of human color vision to red-green and blue-yellow chromatic gratings. Journal of Physiology, 359, 381-400) but as chromatic contrast at the opponent stage, contrast sensitivity would be the same for chromatic and luminance gratings.

Color Perception↗
PubMed1999

Infant temporal contrast sensitivity functions (tCSFs) mature earlier for luminance than for chromatic stimuli: evidence for precocious magnocellular development?

In order to investigate the development of luminance and chromatic temporal contrast sensitivity functions (tCSFs), we obtained chromatic and luminance contrast thresholds from individual 3- and 4-month old infants, and compared them to previously obtained functions in adults. Stimuli were moving sinusoidal gratings of 0.27 cyc/deg, presented at one of five temporal frequencies: 1.0, 2.1, 4.2, 9.4 or 19 Hz (corresponding speeds: 3.8, 7.7, 15, 34, 69 deg/s). Previous studies, including our own, have shown that adult tCSFs are bandpass for luminance stimuli (peaking at 5-10 Hz), yet lowpass for chromatic stimuli (sensitivity falling at > 2 Hz), and that the two functions cross one another near 4-5 Hz when plotted in terms of cone contrast. In the present study, we find that the shapes and peaks of the luminance tCSF in both 3- and 4-months-olds appear quite similar to those of adults. By contrast, chromatic tCSFs in infants are markedly different from those of adults. In agreement with our earlier report (Dobkins, K. R., Lia, B., & Teller, D. Y. (1997). Vision Research, 37(19), 2699-2716), the chromatic function in 3-month-olds is rather flat, lacking the sharp high temporal frequency fall-off characteristic of the adult function. In addition, the luminance tCSF in 3-month-olds is elevated above the chromatic tCSF, and the two functions do not exhibit an adult-like cross-over within the range of temporal frequencies tested. By 4 months of age, substantial development of chromatic contrast sensitivity takes place at the lowest temporal frequencies. Although still immature, the 4-month-old chromatic tCSF has begun to adopt a more adult-like shape. In addition, similar to adults, luminance and chromatic tCSFs in 4-month-olds cross one another near 5 Hz. In adults, magnocellular (M) and parvocellular (P) pathways are thought to underlie the bandpass luminance and lowpass chromatic tCSF, respectively (e.g. Lee, B. B., Pokorny, J., Smith, V. C., Martin, P. R., & Valberg, A. (1990). Journal of the Optical Society of America (a), 7(12), 2223-2236). Based on this correspondence between psychophysical and neural responses in adults, our results suggest that the relatively slow development of the chromatic tCSF in infants may reflect immature chromatic responses in the P pathway and/or reliance on chromatic responses originating in the M pathway.

Adult↗
PubMed1990

Chromatic mechanisms in striate cortex of macaque.

We measured the responses of 305 neurons in striate cortex to moving sinusoidal gratings modulated in chromaticity and luminance about a fixed white point. Stimuli were represented in a 3-dimensional color space defined by 2 chromatic axes and a third along which luminance varied. With rare exceptions the chromatic properties of cortical neurons were well described by a linear model in which the response of a cell is proportional to the sum (for complex cells, the rectified sum) of the signals from the 3 classes of cones. For each cell there is a vector passing through the white point along which modulation gives rise to a maximal response. The elevation (theta m) and azimuth (phi m) of this vector fully describe the chromatic properties of the cell. The linear model also describes neurons in l.g.n. (Derrington et al., 1984), so most neurons in striate cortex have the same chromatic selectivity as do neurons in l.g.n. However, the distributions of preferred vectors differed in cortex and l.g.n.: Most cortical neurons preferred modulation along vectors lying close to the achromatic axis and those showing overt chromatic opponency did not fall into the clearly defined chromatic groups seen in l.g.n. The neurons most responsive to chromatic modulation (found mainly in layers IVA, IVC beta, and VI) had poor orientation selectivity, and responded to chromatic modulation of a spatially uniform field at least as well as they did to any grating. We encountered neurons with band-pass spatial selectivity for chromatically modulated stimuli in layers II/III and VI. Most had complex receptive fields. Neurons in layer II/III did not fall into distinct groups according to their chromatic sensitivities, and the chromatic properties of neurons known to lie within regions rich in cytochrome oxidase appeared no different from those of neurons in the interstices. Six neurons, all of which resembled simple cells, showed unusually sharp chromatic selectivity.

Animals↗
PubMed2002

Efflux of chromate by Pseudomonas aeruginosa cells expressing the ChrA protein.

The ChrA protein of Pseudomonas aeruginosa plasmid pUM505 confers resistance to chromate. Using an in vitro system, we reported [Alvarez, A.H. et al. (1999) J. Bacteriol. 181, 7398-7400] that chromate resistance is based on energy-dependent efflux of chromate. It is shown here that ChrA determines in vivo efflux of 51CrO(4)(2-) as well. Chromate-loaded cell suspensions of P. aeruginosa strain PAO1 harboring recombinant plasmid pEPL1, which expresses the ChrA protein, showed accelerated efflux of 51CrO(4)(2-) as compared to the plasmidless chromate-sensitive derivative. After a 10-min loading, about 40% of 51CrO(4)(2-) was lost from resistant cells in 15 min. Chromate efflux by resistant cells showed a typical saturation kinetics with an apparent K(m) of 82+/-11 microM chromate and a V(max) of 0.133+/-0.009 nmol chromate min(-1) (mg protein)(-1). Oxyanions sulfate and molybdate inhibited chromate efflux in a concentration-dependent fashion, whereas arsenate and ortho-vanadate had no significant effect on chromate release. Inhibition of chromate extrusion by valinomycin, nigericin, and carbonyl cyanide m-chlorophenylhydrazone, but not by oligomycin or dicyclohexylcarbodiimide, indicated that chromate efflux was driven by the membrane potential.

Anti-Bacterial Agents↗
PubMed1996

Change in cement manufacturing process, a cause for decline in chromate allergy?

Hexavalent chromate in cement is the commonest cause of allergic contact dermatitis, especially among construction workers. Over the past decades, there has been a general decline in the prevalence of chromate allergy among construction workers. We suspect that a change in the constituents of cement, resulting in the lowering of hexavalent chromate, contributed to the decline. Slag (free from hexavalent chromate) from the iron-quenched, blast furnace process has been used as a substitute for clinker (which contains high hexavalent chromate) in manufacturing cement. As a result, the slag has diluted the hexavalent chromate content of cement. Our analytical study showed that slag is free from hexavalent chromate and that the hexavalent chromate of clinker ranged from 6-17 micrograms/g. Substituting slag for clinker resulted in dilution of hexavalent chromate in the cement. The hexavalent chromate content of cement declines proportionately with increasing proportion of slag, e.g., a cement containing 5% slag has a total hexavalent chromate concentration of 17.5 micrograms/g, whereas increasing the proportion of slag to 60% reduced the hexavalent chromate content to 7.1 micrograms/gm in the same cement.

Carcinogens, Environmental↗
PubMed1970

Chromate transport in human leukocytes.

Chromium is a trace metal of importance in human physiology and, in addition, as 51-chromate, has been extensively used as a label in the study of blood cell pool sizes and intravascular kinetics. The transport characteristics of 51-chromate were investigated in normal human leukocytes. Chromate uptake is unidirectional over a 1 hr incubation with extracellular chromate concentrations up to 200 mumoles/liter. Under these conditions, intracellular 51-chromium is in a form in which it is nonexchangeable. Influx is temperature sensitive with a Q(10) of approximately 2 and may be energy dependent since a variety of metabolic poisons strongly inhibit uptake. The unidirectional influx of chromate follows Michaelis-Menten kinetics; the maximum velocity is 52 mmumoles/g dry weight of cells per min and the chromate concentration at which influx velocity is half maximal is 87 mumoles/liter. This transport mechanism is highly specific for chromate; other divalent tetrahedral anions only slightly inhibit influx at concentrations up to 10 times that of chromate. Metavanadate, however, competitively inhibits chromate influx at equimolar concentrations. Exposure of cells to unlabeled chromate leads to inhibition of subsequent influx of 51-chromate. It is suggested that this is due to a primary inhibitory effect of chromate on cellular energy metabolism.

Biological Transport↗
PubMed2000

Absence of a chromatic linear motion mechanism in human vision.

We have investigated motion mechanisms in central and perifoveal vision using two-frame random Gabor kinematograms with isoluminant red-green or luminance stimuli. In keeping with previous results, we find that performance dominated by a linear motion mechanism is obtained using high densities of micropatterns and small temporal intervals between frames, while nonlinear performance is found with low densities and longer temporal intervals [Boulton, J. C., & Baker, C. L. (1994) Proceedings of SPIE, computational vision based on neurobiology, 2054, 124-133]. We compare direction discrimination and detection thresholds in the presence of variable luminance and chromatic noise. Our results show that the linear motion response obtained from chromatic stimuli is selectively masked by luminance noise; the effect is selective for motion since luminance noise masks direction discrimination thresholds but not stimulus detection. Furthermore, we find that chromatic noise has the reverse effect to luminance noise: detection thresholds for the linear chromatic stimulus are masked by chromatic noise but direction discrimination is relatively unaffected. We thus reveal a linear 'chromatic' mechanism that is susceptible to luminance noise but relatively unaffected by color noise. The nonlinear chromatic mechanism behaves differently since both detection and direction discrimination are unaffected by luminance noise but masked by chromatic noise. The double dissociation between the effects of chromatic and luminance noise on linear and nonlinear motion mechanisms is not based on stimulus speed or differences in the temporal presentations of the stimuli. We conclude that: (1) 'chromatic' linear motion is solely based on a luminance signal, probably arising from cone-based temporal phase shifts; (2) the nonlinear chromatic motion mechanism is purely chromatic; and (3) we find the same results for both perifoveal and foveal presentations.

Color Perception↗
PubMed2003

Failure of signed chromatic apparent motion with luminance masking.

It has been suggested that there are two types of chromatic motion mechanisms: signed chromatic motion, in which correspondence across successive frames is based on chromatic content of image regions, and unsigned chromatic motion based on movement of chromatically-defined borders. We investigate whether signed and unsigned red-green chromatic motion are mediated by a genuinely chromatic mechanism. Direction discrimination of signed and unsigned red-green chromatic motion were measured in the presence of a dynamic luminance masking noise. Increasing the luminance noise contrast systematically impaired signed motion, regardless of contrast and speed. This result suggests that signed red-green chromatic motion is derived from a luminance-based signal, rather than a genuinely chromatic motion mechanism. In the case of unsigned chromatic motion, there is no effect of luminance masking noise, indicating there exists a genuine chromatic mechanism for second-order motion perception.

Color Perception↗
PubMed1981

Electron-transport cytochrome P-450 system is involved in the microsomal metabolism of the carcinogen chromate.

The kinetics of chromate reduction by liver microsomes isolated from rats pretreated with phenobarbital or 3-methylcholanthrene with NADPH or NADH cofactor have been followed. Induction of cytochrome P-450 and NADPH-cytochrome P-450 reductase activity in microsomes by phenobarbital pretreatment caused a decrease in the apparent chromate-enzyme dissociation constant, Km, and an increase in the apparent second-order rate constant, kcat/Km, but did not affect the kcat of NADPH-mediated microsomal metabolism of chromate. Induction of cytochrome P-448 in microsomes by 3-methylcholanthrene pretreatment did not affect the kinetics of NADPH-mediated reduction of chromate by microsomes. The kinetics of NADH-mediated microsomal chromate reduction were unaffected by the drug treatments. The effects of specific enzyme inhibitors on the kinetics of microsomal chromate reduction have been determined. 2'-AMP and 3-pyridinealdehyde-NAD, inhibitors of NADPH-cytochrome P-450 reductase and NADH-cytochrome b5 reductase, inhibited the rate of microsomal reduction of chromate with NADPH and NADH. Metyrapone and carbon monoxide, specific inhibitors of cytochrome P-450, inhibited the rate of NADPH-mediated microsomal reduction of chromate, whereas high concentrations of dimethyl-sulfoxide (0.5 M) enhanced the rate. These results suggest that the electron-transport cytochrome P-450 system is involved in the reduction of chromate by microsomal systems. The NADPH and NADH cofactors supply reducing equivalents ultimately to cytochrome P-450 which functions as a reductase in chromate metabolism. The lower oxidation state(s) produced upon chromate reduction may represent the ultimate carcinogenic form(s) of chromium. These studies provide evidence for the role of cytochrome P-450 in the activation of inorganic carcinogens.

Animals↗
PubMed1994

Cell-enhanced dissolution of carcinogenic lead chromate particles: the role of individual dissolution products in clastogenesis.

Lead chromate induces chromosomal damage as a result of extracellular dissolution producing solubilized chromium and lead and we show here that the dissolution process is greatly accelerated by the presence of cells. We have sought to determine which of these ions is involved in lead chromate-induced clastogenicity. Cell-mediated extracellular dissolution of particulate lead chromate resulted in the accumulation of both solubilized chromium and solubilized lead, reaching concentrations in the extracellular medium of 15 and 1.9 microM respectively and reaching concentrations inside the cell of 2700 and 97 microM respectively. Both the extracellular and intracellular accumulation of chromium was time dependent and both the solubilized lead and chromium increased proportionately from a lower dose to a higher dose. Exposing cells to water soluble sodium chromate under conditions which produced similar time-dependent intracellular concentrations of chromium also produced a similar amount and spectrum of chromosome damage as lead chromate. In contrast, exposure to lead glutamate resulted in intracellular lead levels 438-times higher than those produced by lead chromate, but produced no chromosome damage. A higher dose of lead glutamate was weakly clastogenic, but it induced a different spectrum of chromosomal aberrations than lead chromate. Pretreatment of cells with vitamin E had no effect on the uptake of chromium, but reduced both sodium chromate- and lead chromate-induced clastogenesis by 54-93%. Vitamin E pretreatment did not affect lead glutamate-induced clastogenesis. The results of this study indicate that although lead(II) is weakly clastogenic at high doses, hexavalent chromium is the proximate clastogen in lead chromate-induced clastogenesis. Additionally, this is the first report that pretreatment of cells with vitamin E can block clastogenesis induced by particulate chromates.

Animals↗
PubMed1984

Repair of chromate-induced DNA damage in chick embryo hepatocytes.

The repair of DNA damage caused by chromate was examined in chick embryo hepatocytes. Treatment of chick embryo hepatocytes with 5 microM sodium chromate for 2 h caused the formation of DNA strand breaks, DNA interstrand cross-links, and DNA-protein cross-links. The maximal level of strand breaks and DNA interstrand cross-links was observed immediately after the 2 h chromate treatment. After removal of the chromate, strand breaks and DNA interstrand cross-links were completely repaired by 3 h and 12 h, respectively. In contrast, DNA-protein cross-links continued to form reaching a maximal level 3 h after chromate removal. Although the level of DNA-protein cross-links decreased at later times, a significant level persisted 40 h after chromate removal. The effect of these persistent DNA-protein cross-links on gene expression was examined by measuring induction of porphyrin accumulation by propylisopropylacetamide and deferoxamine methanesulphonate, a process known to depend on mRNA synthesis. Induction of porphyrin accumulation was decreased immediately following the 2 h chromate treatment. Only partial recovery of induction was observed even 40 h after chromate removal. The effect of chromate treatment on cellular glutathione levels was monitored. No change in cellular glutathione was observed after a 2 h treatment with 5 microM sodium chromate; however, a three-fold increase was observed 12 h after removal of chromate.

Animals↗
PubMed2003

Luminance mechanisms mediate the motion of red-green isoluminant gratings: the role of "temporal chromatic aberration".

In this paper we use a dynamic noise-masking paradigm to explore the nature of the mechanisms mediating the motion perception of drifting isoluminant red-green gratings. We compare contrast thresholds for the detection and direction discrimination of drifting gratings (1.5 cpd), over a range of temporal frequencies (0.5-9 Hz) in the presence of variable luminance or chromatic noise. In the first experiment, we used dynamic luminance noise to show that direction thresholds for red-green grating motion are masked by luminance noise over the entire temporal range tested, whereas detection thresholds are unaffected. This result indicates that the motion of nominally isoluminant red-green gratings is mediated by luminance signals. We suggest that stimulus-based luminance artifacts are not responsible for this effect because there is no masking of the detection thresholds. Instead we propose that chromatic motion thresholds for red-green isoluminant gratings are mediated by dynamic luminance artifacts that have an internal, physiological origin. We have termed these "temporal chromatic aberration". In the second experiment, we used dynamic chromatic noise masking to test for a chromatic contribution to red-green grating motion. We were unable to find conclusive evidence for a contribution of chromatic mechanisms to the chromatic grating motion, although a contribution at very high chromatic contrasts cannot be ruled out. Our results add to a growing body of evidence indicating the presence of dynamic, internal luminance artifacts in the motion of chromatic stimuli and we show that these occur even at very low temporal rates. Our results are compatible with our previous work indicating the absence of a chromatic mechanism for first order (quasi-linear) apparent motion [Vision Res. 40 (2000) 1993]. We conclude that previous conclusions based on the motion of chromatic red-green gratings should be reassessed to determine the contribution of dynamic luminance artifacts.

Color Perception↗
PubMed1989

Sensitivity of macaque retinal ganglion cells to chromatic and luminance flicker.

1. We have studied the sensitivity of macaque retinal ganglion cells to sinusoidal flicker. Contrast thresholds were compared for stimuli which alternated only in luminance ('luminance flicker') or chromaticity ('chromatic flicker'), or which modulated only the middle- or long-wavelength-sensitive cones ('silent substitution'). 2. For luminance flicker, the lowest thresholds were those of phasic, non-opponent ganglion cells. Sensitivity was maximal near 10 Hz. 3. Tonic, cone-opponent ganglion cells were relatively insensitive to luminance flicker, especially at low temporal frequencies, but were sensitive to chromatic flicker, thresholds changing little from 1 to 20 Hz. Those with antagonistic input from middle- and long-wavelength-sensitive (M- and L-) cones had a low threshold to chromatic flicker between red and green lights. Those with input from short-wavelength-sensitive (S-) cones had a low threshold to chromatic flicker between blue and green. Expressed in terms of cone contrast, the S-cone inputs to blue on-centre cells had higher thresholds than M- and L-cone inputs to other cell types. 4. Phasic, non-opponent cells responded to high-contrast red-green chromatic flicker at twice the flicker frequency. This frequency-doubled response is due to a non-linearity of summation of M- and L-cone mechanisms. It was only apparent at cone contrasts which were above threshold for most tonic cells. 5. M- or L-cones were stimulated selectively using silent substitution. Thresholds of M- and L-cone inputs to both red and green on-centre cells were similar. This implies that these cells' sensitivity to chromatic flicker is derived in equal measure from centre and surround. Thresholds of the isolated cone inputs could be used to predict sensitivity to chromatic flicker. The high threshold of these cells to achromatic contrast is thus, at least in part, due to mutual cancellation by opponent inputs rather than intrinsically low sensitivity. 6. Thresholds of M- and L-cone inputs to phasic cells were similar at 10 Hz, and were comparable to those of tonic cells, suggesting that at 1400 td cone inputs to both cell groups are of similar strength. 7. The modulation transfer function of phasic cells to luminance flicker was similar to the detection sensitivity curve of human observers who viewed the same stimulus. For chromatic flicker, at low temporal frequencies thresholds of tonic cells (red or green on-centre cells in the case of red-green flicker or blue on-centre cells in the case of blue-green flicker) approached that of human observers. We propose the different cell types are the substrate of different channels which have been postulated on the basis of psychophysical experiments. 8. At frequencies of chromatic flicker above 2 Hz, human sensitivity falls off steeply whereas tonic cell sensitivity remained the same or increased. This implies that high-frequency signals in the chromatic, tonic cell pathway are not available to the central pathway respons

Animals↗
PubMed2005

Integration of differing chromaticities in early and midlevel spatial vision.

Using Glass patterns composed of isoluminant dots we have investigated the segregation and integration of chromatic information by the visual system. By measuring pattern detection when the chromaticities of the two elements forming a dot pair are varied (intradipole variation), we characterize integration at an early level of spatial processing. By measuring pattern detection for dot pairs where the within-pair chromaticity is the same but the among-pair chromaticities are varied (interdipole variation) we characterize integration and segregation for a more global, midlevel, spatial processing mechanism. Using isoluminant patterns in which all dots have the same chromaticity, we find that (i) detection thresholds are similar to those for luminance-defined dots, and (ii) an equivalent-contrast metric approximately equates thresholds for various chromaticities, including those along both the cardinal and the intermediate axes of an opponent-color space. When intradipole chromaticity is varied we observe that (i) the ability of visual mechanisms to extract oriented dot pairs decreases with increasing chromaticity differences, and (ii) average bandwidths are similar for cardinal and intermediate directions. For pattern detection with interdipole chromatic variation the visual system does not segregate noise dot pairs from correlated dot pairs on the basis of chromatic differences alone, and appears to integrate oriented dot pairs of differing chromaticities in forming a global percept, even for large color differences. Isoluminant Glass patterns with translational and concentric correlations give similar results. The results are compared with those obtained for contrast variation in luminance-defined Glass Patterns and are discussed in terms of current multistage models of color processing by the visual system.

Adaptation, Ocular↗
PubMed1994

What happens if it changes color when it moves?: the nature of chromatic input to macaque visual area MT.

Neurons in the middle temporal visual area (MT) of macaque cerebral cortex are highly selective for the direction of motion but not the color of a moving stimulus. Recent experiments have shown, however, that the directional selectivity of many MT neurons persists even when a moving stimulus is defined solely by chromatic variation (Charles and Logothetis, 1989; Saito et al., 1989; Dobkins and Albright, 1991 a, b; Movshon et al., 1991; Gegenfurtner et al., 1994). To illuminate the mechanisms by which area MT uses color as a cue for motion correspondence, we recorded from MT neurons while rhesus monkeys viewed an "apparent motion" stimulus in which red/green sine wave gratings underwent contrast reversal each time they were displaced in a particular direction. Under such conditions, correspondence based upon chromatically defined borders conflicts with correspondence based upon conservation of chromatic sign. When our heterochromatic stimuli possessed sufficient luminance modulation, MT neurons responded best to motion in the direction for which the sign of luminance (and chromatic) contrast was preserved. At isoluminance, however, two different chromatic influences were revealed. First, when stimuli underwent small spatial displacements, directional selectivity was elicited by movement of the stimulus in the direction of the nearest chromatically defined border, even though the sign of chromatic contrast at that border alternated over time. Under these conditions, MT neurons apparently exploited information about image borders defined by chromatic contrast while sacrificing information about the colors that make up those borders. By contrast, when chromatically defined borders provided only ambiguous information about direction of motion, MT neurons were capable of using information about the sign of chromatic contrast to detect direction of motion. The results from these experiments suggest the existence of a hybrid mechanism, one in which both signed and unsigned chromatic signals contribute to motion processing in visual area MT.

Animals↗
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↗
PubMed2002

New genes involved in chromate resistance in Ralstonia metallidurans strain CH34.

Chromate resistance in Ralstonia metallidurans CH34 is based on chromate efflux catalyzed by ChrA efflux pumps. The bacterium harbors two chromate resistance determinants, the previously known chr(1) on plasmid pMOL28 (genes chrI, chrB(1), chrA(1), chrC, chrE, chrF(1)) and chr(2) on the chromosome (genes chrB(2), chrA(2), chrF(2)). Deletion of the genes chrI, chrC, chrA(2), chrB(2) and chrF(2) influenced chromate resistance and transcription from a chrBp(1) ::lacZ fusion. Deletion of the plasmid-encoded gene chrB(1) did not change chromate resistance or chrBp(1) regulation. Northern hybridization and primer-extension experiments were used to study transcription of the plasmid-encoded chr(1) determinant. Transcription of chrB(1), chrA(1) and chrC was induced by chromate. The presence of sulfate influenced transcription positively. The chrBp(1), chrAp(1) and chrCppromoters showed some similarity to heat-shock promoters. Transcription of the gene rpoH encoding a putative heat-shock sigma factor was also induced by chromate, but rpoH was not essential for chromate resistance. The ChrC protein was purified as a homotetramer and exerted superoxide dismutase activity. Thus, possible regulators for chromate resistance (ChrI, ChrB(1), ChrB(2), ChrF(1), and ChrF(2)) and an additional detoxification system (ChrC) were newly identified as parts of chromate resistance in R. metallidurans.

Bacterial Proteins↗
PubMed1986

Potassium chromate potentiates frameshift mutagenesis in E. coli and S. typhimurium.

Possible comutagenic effects of chromate on frameshift mutagenesis were studied in bacterial assays. In these experiments, cells were treated with potassium chromate and 9-aminoacridine either singly or in combination. Results were analyzed to detect synergistic, additive and antagonistic responses. Data from these investigations show a clear potentiation of 9-aminoacridine-induced mutagenesis in the presence of chromate in S. typhimurium strain TA1537. Results from cell viability assays shows that the effect is not due to a toxicity artifact. Similar results are obtained in E. coli strains 343/358 (repair-proficient parental strain), 343/415 (recA-deficient), and 343/435 (mismatch-repair-deficient). These data indicate the neither induction of recA-protein nor inhibition of mismatch repair is involved in the action of chromate. In E. coli strain 343/447 (DNA polymerase I deficient), the potentiation was observed at lower concentrations of chromate. This finding suggests that polymerase I functions in recovery of cells from 9-aminoacridine-induced DNA damage and that its absence allows some of this damage to be dealt with in a manner which promotes mutagenesis in the presence of chromate. One possible explanation of these findings is that chromate and 9-aminoacridine react chemically to produce a unique mutagen and that damage caused by this mutagen is repaired via some excision process. However, no reaction between chromate and 9-aminoacridine could be detected by TLC under conditions similar to those in the bacterial assays, even at very high concentrations of both agents. Thus, it seems most likely that the potentiation is due to some action of chromate on repair and/or replication at sites of 9-aminoacridine intercalation. Chromate appears, then, to have significant comutagenic actions in bacterial systems.

Aminacrine↗