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PubMed2002

Frequent microsatellite instability in lung cancer from chromate-exposed workers.

Although chromium has been the most extensively investigated metal with respect to mutagenicity and carcinogenicity, its genetic effects in humans are only partly understood. Our previous study demonstrated that lung cancer from chromate-exposed workers infrequently (20%) displayed p53 gene mutations as well as a particular mutation pattern. In the present study, we examined the replication error (RER) and loss of heterozygosity (LOH) in 38 lung cancers from 28 chromate-exposed workers (chromate lung cancer group) and in 26 lung cancer patients without chromate exposure (non-chromate lung cancer group), using six microsatellite markers containing CA repeats: D3S647 (3p23), D3S966 (3p21.3), D3S1289 (3p21.1), D5S346 (5q21-q22), D9S161 (9p21), and TP53 (17p13.1). The RER phenotype was defined as the presence of microsatellite instability (MSI) at two or more loci. Thirty (78.9%) of 38 tumors in the chromate lung cancer group exhibited RER. In contrast, only four (15.4%) of 26 tumors in the non-chromate lung cancer group exhibited RER. The frequency of RER in the chromate lung cancer group was significantly higher than that in the non-chromate lung cancer group (P < 0.0001). By contrast, the frequency of LOH at 3p, 5q, 9p, and 17p loci in tumors with chromate exposure was not significantly different from that in tumors without chromate exposure. In the chromate lung cancer group, the period of chromate exposure in workers with RER (24.5 +/- 6.7 yr) was significantly longer than that in workers without RER (17.0 +/- 3.5 yr) (P = 0.0046). In addition, a longer period of chromate exposure was associated with a tendency toward a higher frequency of MSI. This finding suggests that MSI may play a role in chromium-induced carcinogenesis. In addition to our previous study of p53 mutations, the present findings suggest that the carcinogenic mechanism of chromate lung cancer may differ from that of non-chromate lung cancer.

Adult↗
PubMed1998

Occupational chromate allergy in Singapore: a study of 87 patients and a review from 1983 to 1995.

BACKGROUND: The prevalence of chromate allergy among all patients tested at the Contact and Occupational Dermatoses Clinic at the National Skin Centre in Singapore had fallen progressively from 1983 to 1989. Chromate has also become a less common occupational allergen because of the decline in the number of cases of allergic contact dermatitis from cement. OBJECTIVE: The aim of this report was to study and update the epidemiology of occupational chromate allergy among workers seen in a tertiary dermatology referral centre in Singapore from 1990 to 1995 and to review the changing trends of occupational chromate allergy in our local setting since 1983. The occurrence of concomitant contact allergens among was also studied. METHODS: All patients diagnosed to have occupational allergic contact dermatitis together with positive reactions to chromate, at the Joint Occupational Dermatosis Clinic at the National Skin Centre in Singapore, between January 1990 to December 1995, were included. Causes of chromate allergy and frequency of occurrence of concomitant contact allergens among construction and nonconstruction workers were compared. RESULTS: Eight hundred and fifty workers were seen during the 6-year-study period. Six hundred and thirty three (74.5%) were diagnosed to have occupational contact dermatitis, of which 257 (40.6%) had allergic contact dermatitis. Eighty-seven (33.8%) of these workers had positive reaction to chromate on patch testing. Ninety-five percent of these workers were men with a mean age of 33.4 years. The construction industry contributed 59% of the workers with chromate allergy. Cement (61%) remained the most common source of chromate allergy in our workers, and chromate from sources other than cement (39%) accounted for the rest. Of workers allergic to chromate from cement, 96% (51 of 53) came from the construction industry. Sixty percent of the workers with chromate allergy had concomitant contact allergens and the coexistence of two or more allergens was significantly more common among nonconstruction workers (53%) than construction workers (22%). The three most common concomitant contact allergens were cobalt (28%), rubber chemicals (21%) and nickel (18%). Nonconstruction workers had significantly higher rates of nickel allergy (36% v 6%) than construction workers (P < .03). Simultaneous reactivity to cobalt and nickel was also significantly more common among nonconstruction workers (22%) than construction workers (6%) (P < .03). CONCLUSION: Chromate has progressively become a less common occupational allergen at the National Skin Centre in Singapore from 1983 to 1989, because of a progressive fall in the number of cases of allergic contact dermatitis from cement. However, our study showed that occupational chromate allergy had now increased from 1990 to 1995, because of an increase in chromate allergy from sources other than cement. Chromate allergy from cement is declining, although still frequent, and sources other than cement are increasing in recent years. Concomitant nickel allergy, as well as simultaneous nickel and cobalt allergies, were more common among nonconstruction workers than construction workers.

Adult↗
PubMed2006

The reduced expression and aberrant methylation of p16(INK4a) in chromate workers with lung cancer.

STUDY OBJECTIVES: It is known that chromium is one of the important inhaled carcinogens that cause lung cancer. Our previous studies revealed a variety of genetic changes in lung cancers from chromate-exposed workers (chromate lung cancer). However, the epigenetic effects of chromium are not understood. MATERIALS AND METHODS: We investigated the methylation of the p16 gene using a methylation-specific PCR method in 30 chromate lung cancers and 38 non-chromate lung cancers, and the expression of the p16 protein using immunohistochemistry in 25 chromate lung cancers. RESULTS: Ten (33%) chromate lung cancers showed methylation of the p16 promoter region. On the other hand, 10 (26%) of the non-chromate lung cancers also showed it. The frequency of p16 methylation in non-chromate lung cancer was 0%, 33% and 30% for low (< or =600), moderate (<600, >1000) and high (> or =1000) Brinkman indexes, respectively. However, the frequency of p16 methylation in chromate lung cancer was constant, irrespective of the Brinkman index. In chromate lung cancer, patients with chromate exposure of less than 15 years never had p16 methylation, while 40% (> or =25 years) or 43% (> or =15, <25 years) of patients with chromate exposure of more than 15 years did. In chromate lung cancer, chromate exposure, not smoking, mainly influenced the p16 methylation. Most of the chromate lung cancers with p16 methylation (85.7%) showed repression of the p16 protein. CONCLUSIONS: We speculate that not only genetic but also epigenetic alterations are involved in the carcinogenesis due to chromium.

Adult↗
PubMed1999

Internalization of carcinogenic lead chromate particles by cultured normal human lung epithelial cells: formation of intracellular lead-inclusion bodies and induction of apoptosis.

Occupational exposure to certain particulate hexavalent chromium [Cr(VI)] compounds, such as lead chromate, has been associated with lung cancer and respiratory tract toxicity. We have previously shown that apoptosis is a major mode of death in cultured rodent cells treated with soluble sodium chromate and particulate lead chromate. 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. Phagocytosed lead chromate particles and intracellular lead-inclusion bodies (LIB) were observed by transmission electron microscopy and confirmed by X-ray analysis. HSAE cells exposed to lead chromate and sodium chromate underwent dose-dependent apoptosis. The cellular uptake and genomic interactions of both Cr and lead (Pb) were examined by inductively coupled plasma mass spectrometry (ICPMS) coupled with a novel, direct-injection high-efficiency nebulizer (DIHEN). Using this approach, we have quantitated a dose-dependent formation of Cr-DNA adducts and DNA-associated Pb in lead chromate-treated HSAE cells. The formation of LIB in normal human lung cells exposed to lead chromate indicates that ionic Pb is released from the particles and thus might contribute to the cell toxicity caused by lead chromate. Internalization and dissolution of lead chromate particles and the interaction of ionic Cr and Pb with DNA, may be components of the mechanism of lead chromate carcinogenesis. Lead chromate-induced apoptosis may be a mechanism to eliminate cells with chromium- and/or lead-damaged DNA.

Apoptosis↗
PubMed1997

Induction of apoptotic cell death by particulate lead chromate: differential effects of vitamins C and E on genotoxicity and survival.

Certain hexavalent chromium compounds are documented human carcinogens. Exposure of cells to particulate forms of chromium results in cell-enhanced dissolution of particles in the extracellular microenvironment and chronic production of chromium oxyanions, which are taken up by the cell through an anion transport system and are genotoxic and clastogenic. It was previously shown that apoptosis is the mode of cell death of nearly all of the Chinese hamster ovary cells (CHO-AA8 cell line), which die after high-dose, short-term treatments with soluble sodium chromate. In this report the mode of cell killing by particulate lead chromate and of low-dose continuous treaments of soluble sodium chromate designed to mimic conditions of ionic chromate uptake after lead chromate exposure was examined. CHO-AA8 cells were treated for 24 hr with doses of sodium chromate or lead chromate which cause a 50% decrease in survival in colony-forming effeciency assays. Longer treatments (up to 72 hr) at the same doses did not decrease survival further than the 24-hr exposure. Morphological changes indicative of apoptosis, as well as internucleosomal DNA fragmentation, were detectable by 24 hr after treatment with lead chromate or soluble sodium chromate. 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. Exposure of cells to hexavalent chromium compounds causes a spectrum of DNA damage which can be selectively altered by pretreatment of cells with antioxidant vitamins prior to chromium exposure. Here we show that ascorbate and alpha-tocopherol markedly inhibited the chromosomal aberrations induced by both particulate and soluble chromate compounds, even though chromium adduct levels were not decreased by either vitamin pretreatment. Cell survival assays showed that ascorbate, but not alpha-tocopherol, protected cells from apoptosis induced by sodium chromate. The results differentiate chromium-induced apoptosis from both chromosomal damage and adduct levels and suggest that other lesions sensitive to ascorbate but not tocopherol are the proximal inducing signal for chromium-induced apoptosis.

Animals↗
PubMed2004

Chromate-reducing properties of soluble flavoproteins from Pseudomonas putida and Escherichia coli.

Cr(VI) (chromate) is a toxic, soluble environmental contaminant. Bacteria can reduce chromate to the insoluble and less toxic Cr(III), and thus chromate bioremediation is of interest. Genetic and protein engineering of suitable enzymes can improve bacterial bioremediation. Many bacterial enzymes catalyze one-electron reduction of chromate, generating Cr(V), which redox cycles, generating excessive reactive oxygen species (ROS). Such enzymes are not appropriate for bioremediation, as they harm the bacteria and their primary end product is not Cr(III). In this work, the chromate reductase activities of two electrophoretically pure soluble bacterial flavoproteins--ChrR (from Pseudomonas putida) and YieF (from Escherichia coli)-were examined. Both are dimers and reduce chromate efficiently to Cr(III) (kcat/Km = approximately 2 x 10(4) M(-1) x s(-1)). The ChrR dimer generated a flavin semiquinone during chromate reduction and transferred >25% of the NADH electrons to ROS. However, the semiquinone was formed transiently and ROS diminished with time. Thus, ChrR probably generates Cr(V), but only transiently. Studies with mutants showed that ChrR protects against chromate toxicity; this is possibly because it preempts chromate reduction by the cellular one-electron reducers, thereby minimizing ROS generation. ChrR is thus a suitable enzyme for further studies. During chromate reduction by YieF, no flavin semiquinone was generated and only 25% of the NADH electrons were transferred to ROS. The YieF dimer may therefore be an obligatory four-electron chromate reducer which in one step transfers three electrons to chromate and one to molecular oxygen. As a mutant lacking this enzyme could not be obtained, the role of YieF in chromate protection could not be directly explored. The results nevertheless suggest that YieF may be an even more suitable candidate for further studies than ChrR.

Amino Acid Sequence↗
PubMedDate not supplied

Kinetics of chromate adsorption on goethite in the presence of sorbed silicic acid.

The adsorption of chromate on mineral surfaces has received much attention due to its toxicity in natural systems. Spectroscopic studies have demonstrated that chromate forms inner-sphere complexes on variable-charge surfaces. However, in natural systems chromate has been observed to be fairly mobile, which has been explained by the presence of naturally occurring ligands competing with chromate for mineral surface sites. Silicic acid is a ubiquitous ligand in soil and water environments and also sorbs strongly to variable-charge surfaces. Yet little research has examined its influence on chromate adsorption to variable-charge surfaces such as goethite. This study examined the influence of silicic acid (0.10 and 1.0 mM) on the adsorption kinetics of chromate (0.05 and 0.10 mM) on goethite over a range of common soil pH values (4, 6, and 8). The rate and total quantity of chromate adsorption decreased in all the experiments except at a pH value of 4 and a chromate concentration of 0.05 mM. The inhibition of chromate adsorption ranged from 3.1% (pH = 4, Si = 0.10 mM, chromate = 0.10 mM) to 83.3% (pH = 8, Si = 1.0 mM, chromate = 0.05 mM). The rate of chromate adsorption decreased with an increase in pH and silicic acid concentration. This was attributed to a reduction in the surface potential of goethite on silicic acid adsorption as well as a competition for surface sites. The presence of naturally occurring ligands such as silicic acid may be responsible for the enhanced mobility of chromate in natural systems and demonstrates the importance of competitive adsorption for evaluating the mobility of trace elements.

Adsorption↗