Disease relevance of Chrome Orange

• Three renal carcinomas were also found after i.m. treatment with lead chromate [1].
• Sterile and bacterially contaminated emboli containing a lead-chromate pigment (similar to those used in previous studies of septic embolism) (11 dogs) and pure silicone rubber emboli with transversely oriented canals (10 dogs), after brief placement in a bacterial suspension, were associated with intense inflammatory arteritis [2].
• In previous models of mycotic aneurysm, the inflammation attributed to bacterial contamination was probably due to the lead-chromate pigment used [2].
• Embolization with emboli that caused arteritis, that is, bacterial contamination or presence of lead chromate in the embolus (21 dogs), was associated with hemorrhagic infarcts, focal subarachnoid hemorrhage, and increased incidence of acute subdural hemorrhage [3].
• A higher dose of lead glutamate was weakly clastogenic, but it induced a different spectrum of chromosomal aberrations than lead chromate [4].

High impact information on Chrome Orange

• Chronic exposure to lead chromate causes centrosome abnormalities and aneuploidy in human lung cells [5].
• Specifically, a 24-hour lead chromate exposure induced no aneugenic effect, whereas a 120-hour exposure to 0.5 and 1 microg/cm2 lead chromate induced 55% and 60% aneuploid metaphases, respectively [5].
• There was also an increase in aberrant mitosis after chronic exposure to lead chromate with the emergence of disorganized anaphase and mitotic catastrophe [5].
• Transformation of C3H/10T1/2 mouse embryo cells to focus formation and anchorage independence by insoluble lead chromate but not soluble calcium chromate: relationship to mutagenesis and internalization of lead chromate particles [6].
• Kidneys from normal rats were perfusion fixed in situ at physiological pressure, filled with latex microfil containing lead chromate, and embedded in plastic [7].

Chemical compound and disease context of Chrome Orange

• Here we report the cellular and molecular effects of lead chromate and sodium chromate in normal human lung small airway epithelial (HSAE) cells, which may be one of the targets for Cr(VI)-induced lung cancer and respiratory tract toxicity [8].
• In E. coli fluctuation test, the ranges of maximal mutagenicity for chromium trioxide and lead chromate overlap at the concentration 10(-5)M, whereas lead chloride shows no mutagenicity and little lethality at concentrations up to 10(-3)M [9].
• A case of unique acute bone marrow toxicity and pancytopenia following subcutaneous exposure to lead chromate, xylene, and ethylbenzene in a previously healthy patient is reported [10].

Biological context of Chrome Orange

• We found that aneuploid cells increased in a concentration- and time-dependent manner after chronic exposure to lead chromate [5].
• Lead chromate-induced chromosome damage requires extracellular dissolution to liberate chromium ions but does not require particle internalization or intracellular dissolution [11].
• We found that lead chromate was clastogenic in a concentration-dependent manner with 0.1, 0.5, and 1 microg/cm(2), while 5 and 10 microg/cm(2) caused complete cell cycle arrest [11].
• The mechanism of metal-induced morphological transformation was likely not due to the specific base substitution mutations measured in ouabain resistance mutation assays, and for lead chromate, likely not due to this type of base substitution mutation or to frameshift mutations [12].
• DNA damage induced by carcinogenic lead chromate particles in cultured mammalian cells [13].

Anatomical context of Chrome Orange

• 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 [14].
• We investigated these mechanisms in a human lung cell line after exposure to particulate lead chromate [11].
• Lead chromate caused dose-related increases in chromosome aberration and sister-chromatid exchange in human lymphocytes [15].
• Internalization of carcinogenic lead chromate particles by cultured normal human lung epithelial cells: formation of intracellular lead-inclusion bodies and induction of apoptosis [8].
• Lead chromate induces neoplastic transformation in cultured cells but the mechanism of genotoxicity is unknown [16].

Associations of Chrome Orange with other chemical compounds

• 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 [14].
• Carcinogenic arsenic, nickel, and chromium compounds induced morphological and neoplastic transformation but no mutation to ouabain resistance in 10T1/2 mouse embryo cells; lead chromate also did not induce mutation to ouabain or 6-thioguanine resistance in Chinese hamster ovary cells [12].
• All of the cells killed by treatments with lead chromate particles underwent apoptosis as the mode of cell death and this was accurately modeled in cell culture by continuous treatments with low-dose soluble sodium chromate [17].
• 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 [18].
• A survey of occupational exposure to hexavalent chromium in chromate pigment production was undertaken in factories producing lead chromate (PbCrO4) and strontium chromate (SrCrO4) [19].

Gene context of Chrome Orange

• Our study focus was on examining the role of XRCC1 in lead chromate-induced cytotoxicity and structural chromosomal aberrations in CHO cells [20].
• 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 [18].
• We also show that genotoxic concentrations of lead chromate activate the ataxia telangiectasia mutated (ATM) protein, which is thought to play a central role in the early stages of DSB detection and controls cellular responses to this damage [21].
• By using immunofluorescence, we found that lead chromate-induced concentration-dependent increases in phosphorylated H2A.X (r-H2A.X) foci formation with 0.1, 0.5, 1, 5 and 10 microg/cm2 lead chromate inducing a relative increase in the number of cells with r-H2A.X foci formation of 43, 51, 115 and 129%, respectively [21].
• Induction of morphological transformation, anchorage-independent growth and plasminogen activators in non-tumorigenic human osteosarcoma cells by lead chromate [22].

Analytical, diagnostic and therapeutic context of Chrome Orange

• Electron microscopy of golgi-stained material following lead chromate substitution [23].
• Using the single cell gel electrophoresis assay (comet assay), showed that lead chromate-induced concentration dependent increases in DSBs with 0.1, 0.5, 1 and 5 microg/cm2 lead chromate inducing a 20, 50, 67 and 109% relative increase in the tail integrated intensity ratio, respectively [21].
• The investigated workers were exposed to hexavalent Cr, as lead chromate, whereas normal population (control group) was mainly exposed to trivalent Cr [24].

References