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PubMed1993

Measurements of chromatic and achromatic afterimages.

Several types of measurement were made of the negative afterimages formed by viewing chromatic and achromatic sine-wave conditioning gratings that were stabilized on the retina. We varied the spatial frequency, contrast, and duration of the conditioning stimulus and the interval between its offset and the afterimage measurement. Different methods of measuring afterimage contrast were also compared. We conclude that (1) an isoluminant chromatic stimulus creates an isoluminant chromatic afterimage; (2) afterimage contrast is linearly related to conditioning contrast; (3) chromatic and achromatic afterimages have similar low-pass spatial-frequency characteristics; (4) both types of afterimage build up and decay exponentially, with a (1/e) time constant of 4-8 s; (5) most important, both chromatic and achromatic afterimages raise the threshold for a chromatic flashed grating, but neither affects the threshold for an achromatic flashed grating; (6) we can explain these results by postulating that negative afterimages are subserved only by the sustained, or parvocellular, pathways.

Afterimage↗
PubMed1998

Chromatic rod-cone interaction during dark adaptation.

Chromatic rod-cone interaction in mesopic vision was investigated by measuring chromaticity coordinates of spectral lights 3 deg extrafoveally during long-term dark adaptation, under conditions where the eye was chromatically adapted. It was concluded that (a) the chromaticity shift obtained between the cone-plateau period and the dark-adapted state is due, at least under some conditions, to rod signals elicited by the test stimulus, (b) the chromaticity points of cone-mediated colors may change in different directions in the chromaticity diagram as an effect of the rod intrusion, (c) cone-cone and rod-cone color-mixture processing may, at least under some conditions, be different, and (d) chroma-related processes of rods and cones tend to suppress each other, with rods dominating at low and cones at high mesopic intensities.

Color↗
PubMed1991

Effects of chromatic and luminance contrast on reading.

Reading performance was measured for drifting text defined by chromatic contrast with various amounts of luminance contrast present. With 0.12 luminance contrast added, reading performance was unaffected by the presence of chromatic contrast over a range of character sizes varying 30-fold. When luminance contrast was reduced to near the threshold for reading, chromatic contrast sustained reading rates of nearly 300 words per minute, almost as high as those found with high luminance contrasts. Low-pass filtering of chromatic text had a proportionately greater effect on small characters, as would be predicted from the lower bandwidth of chromatic visual channels. Arguments are presented suggesting that reading rates for equiluminant text are sustained by luminance transients introduced by transverse chromatic aberrations of the eye.

Color Perception↗
PubMed2004

The impact of suppressive surrounds on chromatic properties of cortical neurons.

Stimulation of the suppressive surround of a cortical neuron affects the responsivity and tuning of the classical receptive field (CRF) on several stimulus dimensions. In V1 and V2 of macaques prepared for acute electrophysiological experiments, we explored the chromatic sensitivity of the surround and its influence on the chromatic tuning of the CRF. We studied receptive fields of single neurons with patches of drifting grating of optimal spatial frequency and orientation and variable size, modulated along achromatic or isoluminant color directions. The responses of most neurons declined as the patch was enlarged beyond the optimal size (surround suppression). In V1 the suppression evoked by isoluminant gratings was less than one-half that evoked by achromatic gratings. Consequently, many cells were most sensitive to achromatic modulation when patches just covered the CRF but were most sensitive to isoluminant modulation when patches were enlarged to cover the suppressive surround. Non-oriented neurons that were strongly chromatically opponent generally lacked suppressive surrounds. In V2 most neurons showed equal surround suppression from isoluminant gratings and achromatic gratings. This makes the relative sensitivity of V2 neurons to achromatic and isoluminant gratings mainly independent of the size of the grating. We also measured the chromatic properties of the CRF in the presence of differently colored surrounds. In neither V1 nor V2 did the surround alter the chromatic tuning of the CRF. Cortical mechanisms sensitive to chromatic contrast seem to provide little input to the suppressive surrounds of V1 neurons but substantial input to those of V2 neurons.

Animals↗
PubMed2005

Chromatic organization of ganglion cell receptive fields in the peripheral retina.

This study addresses the chromatic properties of receptive fields in the subcortical visual pathway of primates. There is agreement that, in the central visual field, many cells belonging to the parvocellular (PC) division of the subcortical pathway show red-green opponent responses, that a subgroup of cells belonging to the koniocellular (KC) pathway shows blue-yellow opponent responses, and that magnocellular (MC) pathway cells show only weak signs of chromatic input. However, the chromatic properties of ganglion cells in the peripheral retina are poorly understood. Here, we measured the temporal-chromatic properties of ganglion cells in extracellular in vivo recordings from peripheral macaque retina. We show that the chromatic responsivity of peripheral KC ("blue-on") and MC cells is very similar to that of their counterparts in the foveal retina. Cone-opponent responses are expressed only at low temporal frequencies (<10 Hz) in the majority of peripheral PC cells, and some peripheral PC cells show non-opponent response properties. With these exceptions, the chromatic properties of ganglion cells are essentially preserved throughout the first 50 degrees of visual eccentricity. The main change seen in passing from foveal to peripheral retina is that all ganglion cell classes become more responsive to high temporal-frequency modulation.

Action Potentials↗
PubMed2000

Natural history of Ctenus medius Keyserling, 1891 (Araneae, Ctenidae) I: observations on habitats and the development of chromatic patterns.

Ctenus medius Keyserling, 1891 is a common species in several spots of Mata Atlântica, however there is a great lack of studies in all aspects of its natural history. This work aims to elucidate aspects of ecotope preference compared to large spiders, and to provide data on the development of chromatic patterns during its life cycle. The observations on the behavior of C. medius were done in the campus of Centro Universitário de Barra Mansa (UBM) by means of observations and nocturnal collections using cap lamps. For observations on the development of chromatic patterns, spiderlings raised in laboratory, hatched from an oviposition of a female from campus of UBM, and others spiderlings collected in field were used. The field observations indicate that: C. medius seems to prefer ecotopes characterized by dense shrub vegetation or herbal undergrowth; Lycosa erythrognatha and L. nordeskioldii seems to prefer open sites; Phoneutria nigriventer seems to prefer shrub vegetation and anthropogenic ecotopes as rubbish hills; Ancylometes sp. seems to prefer ecotopes near streams. Concerning chromatic patterns, it was observed that males and females show well distinct patterns during the last two instars, allowing distinction by sex without the use of a microscope. Through chromatic patterns it was also possible to draw a distinction between C. medius and C. ornatus longer that 3 mm cephalothorax width. 69 specimens of C. medius (males and females) collected in the campus of UBM did not show a striking polymorphism in chromatic pattern, but one among 7 adult females collected in National Park of Itatiaia, showed a distinct chromatic pattern.

Animals↗
PubMed1984

Colorimetry for the stain technologist. II. The specification of chromaticity difference.

This paper describes the calculation of chromaticity difference. The text has been written specifically for the stain technologist and is largely self-contained. The concept of a uniform chromaticity scale (UCS) is described. A UCS is a diagram in which equal perceived differences in chromaticity are represented by equal distances anywhere on the diagram. UCSs are developed by transformations of the CIE 1931 chromaticity diagram, and may be linear (projective) or nonlinear. The effectiveness of the various transformations has been assessed using published data on discrimination of chromaticity. The usefulness of chromaticity difference calculations is illustrated by histological examples, including Romanowsky stained blood cells and Papanicolaou stained cells from the uterine cervix. Six UCSs are used in these examples, two projective and four nonlinear.

Animals↗
PubMed1996

Chromatic and achromatic visual evoked potentials in Parkinson's disease.

Chromatic and achromatic visual evoked potentials (VEP) were evaluated in 39 patients with idiopathic Parkinson's disease (PD) (age 64.0 +/- 8.6 years) and 43 healthy controls (age 62.8 +/- 8.7 years). The following pattern-reversal checkerboard stimuli were performed: (1) achromatic with luminance contrast 86% (achr.hk.) (2) achromatic with luminance contrast 20% (achr.lk.); (3) chromatic isoluminant blue-yellow (by.); (4) chromatic isoluminant red-green (rg.). The mean latencies N70, P100, and N135 of chromatic and achromatic VEP were significantly delayed in patients with PD as compared to controls. The highest rate (41.0%) of pathological findings could be demonstrated by achromatic stimulation (luminance contrast 86%). Isolated abnormalities of chromatic VEP (in combination with normal achromatic VEP) were found in 5 (12.8%) patients. The delay of VEP-latencies was significantly correlated with the severity of motor symptoms in PD patients. We conclude that VEP are valuable tools to demonstrate a dysfunction of the visual system in PD. Although chromatic VEP are less sensitive than achromatic VEP, the combination of both will increase the diagnostic yield. Therefore, there seems to exist a variety of individual characters of visual impairment in PD.

Adult↗
PubMed1997

Mutations of the p53 gene in human lung cancer from chromate-exposed workers.

We examined p53 mutations in 20 cancer samples from 19 chromate workers with lung cancer by Polymerase chain reaction-Single strand conformation polymorphism analysis and direct sequencing. Six missense mutations were identified in 4 (20%) of the 20 chromate lung cancer samples. Fewer mutations were found in the patients with lung cancers who had been exposed to chromate than in those who had not. However, the pattern of p53 mutations in lung cancer patients exposed to chromate differed from that of common lung cancers in 3 respects. There were no apparent G to T transversions, which are common base changes in lung cancers. Half of the mutational sites (3/ 6) had changes of AT base-pairs, and 2 of 4 mutational tumor samples had double missense mutations. Our results suggested that chromate exposure may induce point mutation of the p53 gene.

Adenocarcinoma↗
PubMed1991

Bacterial interactions with chromate.

Hexavalent chromium compounds (chromates and dichromates) are highly toxic and are considered as mutagens and carcinogens. These compounds are discharged frequently to the environment as a result of diverse industrial processes. Some microorganisms are able to reduce hexavalent chromium to the less toxic trivalent form. Chromate pollution has promoted the selection of bacterial strains possessing chromate resistance determinants, usually carried by plasmids. Strains combining both abilities, i.e. resistance to and reduction of chromate, are potentially useful for detoxifying chromate polluted waste waters.

Bacteria↗
PubMed1988

Biological monitoring of occupational exposure in the chromate pigment production industry.

A survey of occupational exposure to hexavalent chromium in chromate pigment production was undertaken in factories producing lead chromate (PbCrO4) and strontium chromate (SrCrO4). Sampling pre and post-shift in a factory where SrCrO4 production had just started showed the optimum strategy for biological monitoring is the measurement of urinary chromium, in urine samples taken at the end of Friday shift and pre-shift the following Monday. However, short-term uptake may be assessed under these circumstances by the increase in urinary chromium over a shift. Body burden, representing long-term chromate exposure is best assessed by measuring chromium in whole blood or pre-shift urinary chromium at the beginning of the working week. Exceptionally high levels of chromium in blood (387-4160 nmol l-1) and urine (41-1250 nmol nmol-1 creatinine) as well as skin and nasal lesions, were discovered amongst the workforce at the strontium chromate plant. These contrasted with occupationally unexposed levels of less than 20 nmol l-1 and less than 1 nmol nmol-1 creatinine, respectively, and led to the continuation of the biological monitoring programme. At the same time, improved working practices and respiratory protection equipment were introduced. A steady elimination of chromium from whole blood with a half-life of approximately 24 days was found. This elimination rate was confirmed over a 14 day period when the workforce were completely removed from exposure. The study confirms the usefulness of biological monitoring in assessing the uptake of hexavalent chromium and control of exposure.

Chromates↗
PubMed1991

The effects of potassium chromate and citrinin on rat renal membrane transport.

Both chromate and citrinin have been shown to produce acute renal damage. Although both substrates act on the proximal tubule in the rat, they affect different parts of that nephron segment. As with most nephrotoxicants, the mechanism(s) or subcellular target(s) for citrinin or chromate is unknown. The availability of methodology for isolation of functional membrane vesicles has afforded the opportunity to study the plasma membrane as a target for the effects of citrinin and chromate. Whether studied solely with in vitro conditions or after administration to the rat, chromate exhibited its primary action on the basolateral (BL) membrane vesicles. This was exhibited by a reduction in the p-aminohippurate (PAH) overshoot. At both 3 and 16 hr after treatment (40 mg/kg, sc) there was a significant, but relatively modest, effect on glucose transport by brush border (BB) vesicles. Citrinin, when studied in vitro, inhibited PAH transport (BL vesicles), but had only equivocal effects on BB glucose transport. However, after pretreatment of the rats with citrinin (60 mg/kg, ip), both BL and BB membrane vesicle function was reduced markedly at 3 hr. By 16 hr, an overshoot had returned for both transport substrates, although the glucose overshoot was still significantly below control. These data demonstrate that both citrinin and chromate alter proximal tubular cell membrane function and do so relatively early after administration to the rat. This effect suggests that alteration of membrane function by these nephrotoxicants is an early, if not initiating, event in the production of acute tubular necrosis.

Animals↗
PubMedDate not supplied

Mitochondrial reduction of the carcinogen chromate: formation of chromium(V).

Incubation of chromate with isolated rat liver mitochondria in vitro resulted in the uptake and reduction of chromium(VI), as well as the formation of chromium(V) species. Chromate was rapidly taken up and reduced by intact mitochondria. The rate of reduction of chromate by intact mitochondria was increased upon addition of succinate or malate plus glutamate, substrates for the electron-transport chain, but was decreased upon addition of cyanide, an inhibitor of the electron-transport chain. Incubation of chromate with mitochondria in the presence or absence of malate, glutamate, and succinate resulted in a steady increase in the level of chromium(V) over time. The extent of chromium(V) formation was increased upon addition of malate, glutamate, and succinate but was inhibited upon addition of the electron-transport chain inhibitors, antimycin, cyanide, or rotenone, to whole mitochondria. High levels of glutamate plus malate inhibited chromium(V) formation; however, high concentrations of succinate or sulfate had no effect. These studies suggest that the chromate-reductase activity in mitochondria is due to the electron-transport chain as well as other mitochondrial reducing systems which are insensitive to inhibitors of the electron-transport chain. Since chromium(VI) is effectively metabolized by mitochondria in vitro and chromium(V) "reactive intermediates" are formed in the process, mitochondria may play a role in chromium(VI) carcinogenesis.

Animals↗
PubMed1999

Survival and chromate reducing ability of Pseudomonas aeruginosa in industrial effluents.

The ability of a chromate-reducing Pseudomonas aeruginosa strain, isolated from tannery effluent, to survive and reduce chromate in the effluent of a tannery and an electroplating unit was evaluated. The test strain survived in the native tannery effluent but numbers fell sharply in the native electroplating effluent. Supplementation with a carbon (C), nitrogen (N) and phosphorus (P) source supported bacterial multiplication and chromate reduction in both types of effluents with almost equal efficiency. Chromate reduction, however, was not observed in the absence of C, N or P supplement, or in the chromate-reducing strain.

Biodegradation, Environmental↗
PubMedDate not supplied

Effect of chromates on ciliated cells of rat tracheal epithelium.

Exposure to chromates is an occupational hazard that may result in disease of the respiratory tract. Specific subcellular effects of exposure to this chemical that might be the basis for observed pathologic findings were assessed in tracheal organ culture and excised whole tracheas. Chromate concentrations of 10 mg/ml or more were found to induce ciliostasis within 20 minutes and to kill cells within 24 hours. Levels between 10mug/ml and 100 mug/ml were not ciliostatic but resulted in cytotoxicity after a delay of several hours. Ultrastructural alterations associated with chromate-induced cytotoxicity are similar to the progressive degenerative changes that result from other chemical injuries. An inhibitory effect of chromate on protein synthesis, RNA synthesis, or succinic dehydrogenase activity could not be demonstrated. The data suggest that damage to the plasmalemma by chromates may be responsible for the observed change.

Animals↗
PubMed1994

The generation of apurinic/apyrimidinic sites in isolated DNA during the reduction of chromate by glutathione.

We have obtained evidence for the induction of apurinic/apyrimidinic sites (AP-sites) in isolated DNA treated with chromate and glutathione using agents that cleave the DNA phosphate backbone at AP-sites (putrescine, Lys-Trp-Lys and exonuclease III). In the presence of glutathione (5 mM) the level of AP-sites rose with increasing concentrations of chromate (75-200 microM). Neither chromate nor glutathione alone nor the final product of the reaction between chromate and glutathione were capable of inducing the lesion. Thus, an intermediate species generated during the reduction process seems to be the cause of the damage. In view of the known mutagenicity of AP-sites our findings might be of some importance in relation to the mechanisms involved in chromate carcinogenicity.

Amino Acid Sequence↗
PubMed1995

Glutathione and free amino acids form stable complexes with DNA following exposure of intact mammalian cells to chromate.

Exposure of cells to carcinogenic Cr(VI) compounds results in the formation of several types of DNA lesions such as strand breaks, DNA-protein crosslinks and uncharacterized DNA-Cr adducts. Hexavalent chromium compounds are positive in most bacterial and eukaryotic mutagenic systems, although the nature of DNA modifications underlying the chromium-induced mutagenesis is not known. Hexavalent chromate(VI) is very active in cellular systems because it is actively transported into cells, but intracellularly it is ultimately reduced to Cr(III). Here we show that exposure of Chinese hamster ovary (CHO) cells to potassium chromate(VI) leads to the formation of stable complexes between DNA and amino acids or glutathione. Cysteine, glutamic acid and histidine were the major amino acids crosslinked to DNA in chromate-treated cells. Incubation of purified DNA in the presence of EDTA dissociated SDS stable amino acid-DNA complexes, which indicates that these DNA adducts are most likely to represent ternary coordination complexes mediated by Cr(III) rather than covalent linkage between amino acids/glutathione and DNA. The amino acids that were found complexed with DNA purified from chromate-exposed cells did not orginate from previously crosslinked proteins during DNA isolation, but represented authentic reactions of free amino acids and glutathione with chromium and DNA in cells. Ternary complexes of glutathione or amino acids with Cr(III) and DNA were estimated to account for as much as 50% of DNA-bound chromium following exposure to < or = 25 microM chromate.

Amino Acids↗
PubMed2006

XRCC1 protects against particulate chromate-induced chromosome damage and cytotoxicity in Chinese hamster ovary cells.

Water-insoluble hexavalent chromium compounds are well-established human lung carcinogens. Lead chromate, a model insoluble Cr(VI) compound, induces DNA damage, chromosome aberrations, and dose-dependent cell death in human and Chinese hamster ovary (CHO) cells. The relationship between lead chromate-induced DNA damage and chromosome aberrations is unknown. Our study focus was on examining the role of XRCC1 in lead chromate-induced cytotoxicity and structural chromosomal aberrations in CHO cells. Three different cell lines were used: AA8 (parental), EM9 (XRCC1 mutant), and H9T3 (EM9 complemented with human XRCC1 gene). Cytotoxicity was significantly higher in EM9 cells when compared to AA8 and H9T3 cells, indicating that XRCC1 is important for protecting cells from lead chromate particles-induced cell death. The frequency of damaged metaphase cells was not affected by XRCC1 deficiency. However, the total amount of Cr(VI)-induced chromosome damage was exacerbated by XRCC1 deficiency, and the spectrum of damage changed dramatically. Chromatid and isochromatid lesions were the most prominent aberrations induced in all cell lines. XRCC1 was essential to reduce the formation of chromatid lesions, but not for isochromatid lesions. In addition, XRCC1 deficiency resulted in a dramatic increase in the number of chromatid exchanges, indicating that XRCC1 is involved in protection from lead chromate-induced chromosome instability.

Animals↗