Genetic effects of chromium compounds

doi:10.1016/0165-1218(83)90128-3

Mutation Research/Genetic Toxicology

Volume 117, Issues 3–4, May–June 1983, Pages 279-300

https://doi.org/10.1016/0165-1218(83)90128-3 Get rights and content

Abstract

Seven different test systems were utilized to investigate the genetic activity of chromium compounds: infidelity of DNA replication in vitro by DNA polα from calf thymus, damage of DNA detected by alkaline elution in treated mammalian cells or in DNA purified and treated in vitro, DNA repair synthesis in mammalian cells in vitro detected by autoradiography or scintillation counting after labelling with [³H]dThd, gene mutations in the Salmonella typhimurium Ames test, gene mutations (6TG resistance) in cultured hamster cells, sister-chromatid exchanges in different rodent cell cultures, and transformation to anchorage-independent growth of hamster cells in vitro (soft-agar assay).

Potassium dichromate and chromium chloride were used as water-soluble Cr(VI) and Cr(III) salts. Several reference mutagens (EMS, MMS, MMC, 4NQO) were included in the single tests as positive controls.

Cr(VI) was active in all the tested systems, except in the induction of DNA damage and DNA repair synthesis in cultured cells. Cr(III), on the other hand, was absolutely inactive unless a direct interaction with purified DNA was permitted by the test conditions.

The relevance of data from the various tests to the understanding of the mechanisms of the genotoxic activity of chromium is discussed. Effects other than the direct interaction of Cr(III) with DNA are inferred, which can cause infidelity of the DNA polymerase functions.

References (54)

V. Bianchi et al.
Mechanisms of chromium toxicity in mammalian cell cultures
Toxicology
(1980)
V. Bianchi et al.
Scintillometric determination of DNA repair in human cell lines: a critical appraisal
Mutation Res.
(1982)
V. Bianchi et al.
Effects of hexavalent chromium on the adenylate pool of hamster fibroblasts
Toxicology
(1982)
P. Debetto et al.
Effects of potassium dichromate on ATP content of mammalian cells cultured in vitro
Chem.-Biol. Interact.
(1982)
G.R. Douglas et al.
Effect of lead chromate on chromosome aberrations, sister chromatid exchanges and DNA damage in mammalian cells in vitro
Mutation Res.
(1980)
J.E. Gruber et al.
Metabolism of the carcinogen chromate by rat liver microsomes
Biochem. Biophys. Res. Comm.
(1978)
N. Kanematsu et al.
Rec assay and mutagenicity studies on metal compounds
Mutation Res.
(1980)
A. Leonard et al.
Carcinogenicity and mutagenicity of chromium
Mutation Res.
(1980)
W.D. Macrae et al.
Sister chromatid exchanges induced in cultured mammalian cells by chromate
Chem.-Biol. Interact.
(1979)
G. Marin
Origin and rate estimation of the spontaneous loss of anchorage dependence of growth in BHK 21 cells
Exp. Cell Res.
(1980)

M. Miyaki et al.

Effect of metal cations on misincorporation by E. coli DNA polymerases

Biochem. Biophys. Res. Comm.

(1977)

E.R. Nestmann et al.

Detection of the mutagenic activity of lead chromate using a battery of microbial tests

Mutation Res.

(1979)

R.F. Newbold et al.

The cytotoxic, mutagenic and clastogenic effects of chromium containing compounds on mammalian cells in culture

Mutation Res.

(1979)

H. Nishioka

Mutagenic activities of metal compounds in bacteria

Mutation Res.

(1975)

F.L. Petrilli et al.

Metabolic deactivation of hexavalent chromium mutagenicity

Mutation Res.

(1978)

M. Stella et al.

Clastogenic effects of chromium on human lymphocytes in vitro and in vivo

Mutation Res.

(1982)

G. Tamino et al.

Effects of trivalent and hexavalent chromium on physicochemical properties of mammalian cell nucleic acids and synthetic polynucleotides

Chem.-Biol. Interact.

(1981)

M.J. Tsapakos et al.

The carcinogen chromate induces DNA cross-links in rat liver and kidney

J. Biol. Chem.

(1981)

H. Tsuda et al.

Chromosomal aberrations and morphological transformation in hamster embryonic cells treated with potassium dichromate in vitro

Mutation Res.

(1977)

G. Warren et al.

Mutagenicity of a series of hexacoordinate chromium(III) compounds

Mutation Res.

(1981)

R.F. Whiting et al.

DNA damage and DNA repair in cultured human cells exposed to chromate

Chem.-Biol. Interact.

(1979)

B.N. Ames et al.

Methods for detecting carcinogens and mutagens with the Salmonella/mammalian microsome mutagenicity test

Mutation Res.

(1975)

C. Balbi et al.

Effetti specifici di ioni Cr sul DNA: confronto delle interazioni fra Cr(III) e DNA purificato con le parallele interazioni che avvengono nella cellula vivente

Boll. Soc. It. Biol. Sp.

(1981)

V. Bianchi et al.

The scintillometric evaluation of DNA repair synthesis can be distorted by changes of thymidine pool radioactivity

Chem.-Biol. Interact.

(1982)

G. Brambilla et al.

DNA crosslinking in mammalian cells treated with potassium dichromate

C.E. Campbell et al.

Isolation and characterization of Chinese hamster cell mutants resistant to the cytotoxic effects of chromate

Somatic Cell Genet.

(1981)

B.C. Casto et al.

Enhancement of viral transformation for evaluation of the carcinogenic or mutagenic potential of inorganic metal salts

Cancer Res.

(1979)

Cited by (149)

Carbon nano-structures and functionalized associates: Adsorptive detoxification of organic and inorganic water pollutants
2022, Inorganic Chemistry Communications
Deterioration of water quality is a desperate threat worldwide. Industrial development regularly added a vast amount of organic and inorganic contaminants to water. Therefore, eradicating these contaminants is highly essential for the well-being of biotic components. Adsorption-assisted technologies are among the most benign and principally used due to their higher efficiencies at lower costs and independence of complex technological supports. Carbon nanomaterials, such as activated carbons, carbon nanotubes, graphene-based materials, and carbon dots have been broadly adopted as adsorbents because of their outstanding surface characteristics. Researchers worked a lot on activation procedures and chemicals to achieve an ultrahigh surface area (above 3000 m²/g) to increase the adsorption efficiency. Further, cross-linked carbon nanotubes exhibited much-selected adsorption to organics. Carbon dots, a new type of carbon-based nanomaterials emerged as excellent adsorbents when introduced into the polymers matrix and provided promising platforms for the removal of metal ions. Also, graphene oxide and other oxidized forms of carbon being rich in functional groups are reported to exhibit excellent adsorption capacities as high as 2564 mg/g at 25 °C for basic and cationic compounds.
Here, we reviewed the various types of pollutants found in aquatic biota with some basics on fundamentals and mechanistic features of adsorption, adsorption efficiency regulating factors. The article emphasized the performances of carbon nanomaterials and associated nanocomposites for the adsorption of various pollutants. The review also addresses the essential issues for the technical development and commercial application of carbon-assisted materials as nano adsorbents for water decontamination.
Selected molecular mechanisms of metal toxicity and carcinogenicity
2021, Handbook on the Toxicology of Metals: Fifth Edition
This chapter will summarize some of the molecular responses exhibited by cells that come into contact with toxic metals. We will consider the transport of toxic metals into cells and how this interferes with the transport of essential metals. Toxic metals also interfere with the intracellular action of essential metals and may cause toxicity and cancer by this mechanism. Some metals have very specialized effects on enzymes, and there are proteins that can bind toxic metals such as metallothionein, which will also be discussed. A number of metals are also slightly mutagenic or genotoxic and these effects will be reviewed. Since most metals that are carcinogenic, such as arsenic (As), beryllium (Be), cadmium (Cd), and nickel (Ni), with the exception of chromium, do not interact with DNA and are not mutagenic, we discuss other mechanisms such as epigenetic effects to account for their carcinogenic activity, as well as how they affect the expression of genes. Metals also interfere with cell signaling and we will discuss the hypoxic signaling pathway, in particular, as well as those involving PI3K, Akt, reactive oxygen species mitogen-activated protein kinase, NF-κB, NF-AT, and AP-1. Finally, the basis of the interaction of toxic metals with all cellular constituents is their coordination with biological ligands, which will be addressed throughout the chapter.
Carcinogenicity of metal compounds
2021, Handbook on the Toxicology of Metals: Fifth Edition
Compounds of four metals including nickel, chromium, cadmium, and beryllium, and one metalloid and its compounds—arsenic, have been confirmed as human carcinogens by International Agency for Research on Cancer (IARC). Most of these epidemiological studies were done retrospectively in humans occupationally exposed to compounds of these metals. There are only a few environmental studies in humans exposed to any of these metal compounds in which possible speciation of the metal compound is considered. The carcinogenicity of these compounds has been confirmed in vitro and in vivo. This chapter gives the background of metal carcinogenicity. Epidemiological studies, experimental models, and mechanism of carcinogenicity are summarized for each metal. In addition, mechanical information about the carcinogenicity of air pollution is briefly discussed in this chapter. The reader is referred to more detail in the individual metals chapters in Volume II and to Chapter 11, Volume I, Selected Molecular Mechanisms of Metal Toxicity and Carcinogenicity, and to Chapter 6, Volume I, Metals and Air Pollution, for more detail in air pollution.
Carcinogenicity of metal compounds
2021, Handbook on the Toxicology of Metals: Volume I: General Considerations
Compounds of four metals including nickel, chromium, cadmium, and beryllium, and one metalloid and its compounds—arsenic, have been confirmed as human carcinogens by International Agency for Research on Cancer (IARC). Most of these epidemiological studies were done retrospectively in humans occupationally exposed to compounds of these metals. There are only a few environmental studies in humans exposed to any of these metal compounds in which possible speciation of the metal compound is considered. The carcinogenicity of these compounds has been confirmed in vitro and in vivo. This chapter gives the background of metal carcinogenicity. Epidemiological studies, experimental models, and mechanism of carcinogenicity are summarized for each metal. In addition, mechanical information about the carcinogenicity of air pollution is briefly discussed in this chapter. The reader is referred to more detail in the individual metals chapters in Volume II and to Chapter 11, Volume I, Selected Molecular Mechanisms of Metal Toxicity and Carcinogenicity, and to Chapter 6, Volume I, Metals and Air Pollution, for more detail in air pollution.
Selected molecular mechanisms of metal toxicity and carcinogenicity
2021, Handbook on the Toxicology of Metals: Volume I: General Considerations
This chapter will summarize some of the molecular responses exhibited by cells that come into contact with toxic metals. We will consider the transport of toxic metals into cells and how this interferes with the transport of essential metals. Toxic metals also interfere with the intracellular action of essential metals and may cause toxicity and cancer by this mechanism. Some metals have very specialized effects on enzymes, and there are proteins that can bind toxic metals such as metallothionein, which will also be discussed. A number of metals are also slightly mutagenic or genotoxic and these effects will be reviewed. Since most metals that are carcinogenic, such as arsenic (As), beryllium (Be), cadmium (Cd), and nickel (Ni), with the exception of chromium, do not interact with DNA and are not mutagenic, we discuss other mechanisms such as epigenetic effects to account for their carcinogenic activity, as well as how they affect the expression of genes. Metals also interfere with cell signaling and we will discuss the hypoxic signaling pathway, in particular, as well as those involving PI3K, Akt, reactive oxygen species mitogen-activated protein kinase, NF-κB, NF-AT, and AP-1. Finally, the basis of the interaction of toxic metals with all cellular constituents is their coordination with biological ligands, which will be addressed throughout the chapter.
Selected Molecular Mechanisms of Metal Toxicity and Carcinogenicity
2015, Handbook on the Toxicology of Metals: Fourth Edition
This chapter will summarize some of the molecular responses exhibited by cells that come into contact with toxic metals. We will consider the transport of toxic metals into cells and how this interferes with the transport of essential metals. Toxic metals also interfere with the intracellular action of essential metals and may cause toxicity and cancer by this mechanism. Some metals have very specialized effects on enzymes and there are proteins that can bind toxic metals such as metallothionein, which will also be discussed. A number of metals are also slightly mutagenic or genotoxic and these effects will be reviewed. Since most metals that are carcinogenic, such as arsenic (As), beryllium (Be), cadmium (Cd), and nickel (Ni), with the exception of chromium (Cr), do not interact with DNA and are not mutagenic, we discuss other mechanisms such as epigenetic effects to account for their carcinogenic activity, as well as how they affect the expression of genes. Metals also interfere with cell signaling and we will discuss the hypoxic signaling pathway, in particular, as well as those involving PI3K, Akt, reactive oxygen species mitogen-activated protein kinase (MAPK), NF-κB, NF-AT, and AP-1. Finally, the basis of the interaction of toxic metals with all cellular constituents is their coordination with biological ligands, which will be addressed throughout the chapter.

View all citing articles on Scopus

^☆: Supported by grants from the National Research Council of Italy (C.N.R., Progetto Finalizzato ‘Controllo della Crescita Neoplastica’) and the Venetia Region (‘Centro Regionale di Alta Specializzazione in Cancerogenesi Ambientale’).

View full text

Genetic effects of chromium compounds☆

Abstract

Toxicology

Mutation Res.

Toxicology

Chem.-Biol. Interact.

Mutation Res.

Biochem. Biophys. Res. Comm.

Mutation Res.

Mutation Res.

Chem.-Biol. Interact.

Exp. Cell Res.

Biochem. Biophys. Res. Comm.

Mutation Res.

Mutation Res.

Mutation Res.

Mutation Res.

Mutation Res.

Chem.-Biol. Interact.

J. Biol. Chem.

Mutation Res.

Mutation Res.

Chem.-Biol. Interact.

Methods for detecting carcinogens and mutagens with the Salmonella/mammalian microsome mutagenicity test

Mutation Res.

Effetti specifici di ioni Cr sul DNA: confronto delle interazioni fra Cr(III) e DNA purificato con le parallele interazioni che avvengono nella cellula vivente

Boll. Soc. It. Biol. Sp.

The scintillometric evaluation of DNA repair synthesis can be distorted by changes of thymidine pool radioactivity

Chem.-Biol. Interact.

DNA crosslinking in mammalian cells treated with potassium dichromate

Isolation and characterization of Chinese hamster cell mutants resistant to the cytotoxic effects of chromate

Somatic Cell Genet.

Enhancement of viral transformation for evaluation of the carcinogenic or mutagenic potential of inorganic metal salts

Cancer Res.