Induction of Arsenite Tolerance and Thermotolerance by Arsenite Occur by Different Mechanisms

Wang, Zaolin; Hou, Guoying; Rossman, Toby G.

doi:10.2307/3431769

Cited by 5 publications

(2 citation statements)

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“…Further genomic sequencing and identification of chromosomal ars operons in other bacteria will shed light on the evolution of this highly conserved and important bacterial operon. Moreover, recent results have shown this type of arsenic resistance mechanism in mammals (Wang & Rossman, 1993;Wang et al, 1994Wang et al, , 1996, supporting the notion that the protective function of ars operons has been strongly conserved in the course of evolution.…”

Section: Discussionsupporting

confidence: 65%

A chromosomal ars operon homologue of Pseudomonas aeruginosa confers increased resistance to arsenic and antimony in Escherichia coli

Cai¹,

Salmon²,

DuBow³

1998

Microbiology

124

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Operons encoding homologous arsenic-resistance determinants (ars) have been discovered in bacterial plasmids from Gram-positive and Gram-negative organisms, as well as in the Escherichia coli chromosome. However, evidence for this arsenic-resistance determinant in the medically and environmentally important bacterial species Pseudomonas aeruginosa is conflicting. Here the identification of a P. aeruginosa chromosomal ars operon homologue via cloning and complementation of an E. coli ars mutant is reported. The P. aeruginosa chromosomal ars operon contains three potential ORFs encoding proteins with significant sequence similarity to those encoded by the arsR, arsB and arsC genes of the plasmid-based and E. coli chromosomal ars operons. The cloned P. aeruginosa chromosomal ars operon confers augmented resistance to arsenic and antimony oxyanions in an E. coli arsB mutant and in wild-type P. aeruginosa. Expression of the operon was induced by arsenite a t the mRNA level. DNA sequences homologous with this operon were detected in some, but not all, species of the genus Pseudomonas, suggesting that its conservation follows their taxonomic-based evolution.

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Section: Discussionsupporting

confidence: 65%

A chromosomal ars operon homologue of Pseudomonas aeruginosa confers increased resistance to arsenic and antimony in Escherichia coli

Cai¹,

Salmon²,

DuBow³

1998

Microbiology

124

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“…It has been suggested by these investigators that human cells are less resistant to the chronic toxicity of As i due to the lack of an inducible, ef¯ux-mediated tolerance to arsenite (Rossman et al 1997) which has been observed in hamster cells (Wang and Rossman 1993;Wang et al 1996). The inducible arsenite tolerance observed in hamster cells involves de novo mRNA and protein synthesis and appears to be distinct from the ª heat shockº response observed for As i and other stressors (Wang, Hou, and Rossman 1994). Differences in cellular arsenite tolerance could possibly explain the greater susceptibility of humans to the noncancer effects of chronic As i exposure and, perhaps, to the carcinogenic effects as well.…”

Section: Noncancer Effects Of Inorganic Arsenicmentioning

confidence: 98%

Requirements for a Biologically Realistic Cancer Risk Assessment for Inorganic Arsenic

et al. 1999

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A remarkable feature of the carcinogenicity of inorganic arsenic (As i ) is the observation that human exposures to As i have been strongly associated with increases in skin, lung, and internal cancers,but As i does not typically cause tumors in standard laboratory animal test protocols. Considerable controversy has centered on whether there is epidemiological evidence of a ª thresholdº for the carcinogenic effects of As i , or at least of a highly nonlinear dose-response. Saturation of metabolism in the dose-range associated with tumors does not appear to be adequate to produce a major impact on the dose-response for carcinogenicity. If there is a strong nonlinearity, it results from the nature of the carcinogenic mechanism(s) of As i . However, no single hypothesis for the mechanism of As i carcinogenicity has widespread support. A biologically realisticcancer risk assessmentfor As i would require a quantitative description of the dose of active arsenic species in target tissues, the interactions between active arsenic and tissue constituents, and the manner in which these interactions result in tumor formation in multiple organs in humans, but not in experimental animals. Although As i has only infrequently been associated with tumors in animal studies, it has repeatedly been shown to act as a comutagen in vitro and as a cocarcinogen in vivo. As i is clastogenic, producing chromatid aberrations, but does not produce point mutations at single gene loci. Of particular interest, As i has been shown to inhibit repair of DNA single-strand breaks, a possible mechanism for its observed comutagenicity and cocarcinogenicity.We propose a cocarcinogenic mode of action in which As i acts primarily on intermediate cells de® cient in cell cycle control at a late stage in a preexisting carcinogenic process. This interaction enhances genomic fragility and accelerates conversion of premalignant lesions to more aggressive, clinically observable tumors. An indirect effect of As i on DNA repair is consistent with the expectation of a nonlinear dose-response rather than the linear dose-response traditionally assumed for mutagenic carcinogens. However, de® ning the exact nature of this tumor dose-response will require further experimental data on the dose-response for the cellular effects of As i . Because As i carcinogenicity is unlikely to be observed in normal experimental animals not exposed to other carcinogens,studies in animals and cell lines de® cient in cell cycle control should also be considered. Experimental studies speci® cally designed to address the key mechanistic and dose-response issues for As i carcinogenicity are critically needed to support public health policy decisions regarding current environmental exposures to As i .

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Metal Mutagenesis

Rossman¹

1995

Toxicology of Metals

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Induction of Arsenite Tolerance and Thermotolerance by Arsenite Occur by Different Mechanisms

Cited by 5 publications

References 0 publications

A chromosomal ars operon homologue of Pseudomonas aeruginosa confers increased resistance to arsenic and antimony in Escherichia coli

A chromosomal ars operon homologue of Pseudomonas aeruginosa confers increased resistance to arsenic and antimony in Escherichia coli

Requirements for a Biologically Realistic Cancer Risk Assessment for Inorganic Arsenic

Metal Mutagenesis

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