PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 10472621

[Chromium carcinogenicity].

M Trocha·J Antonowicz·R Andrzejak
View original source ↗Export metadata ↓

Abstract

Chromium belongs to the group of trace elements hich are essential in numerous functions of the human body. Chromium deficiency may be responsible for various dysfunctions, whereas exposure to chromium at higher concentrations is toxic and may lead to the occurrence of neoplastic diseases. Epidemiological studies of chromium exposure proved its carcinogenity, and thus the IARC recognised Cr(VI) and its compounds as one of ascertained carcinogens. Some findings of these studies were reviewed in the first part of this work. The second part presents some molecular aspects of chromium carcinogenity which are still the subject of medical research. The direct and indirect effects of chromium and its compounds on DNA are analysed as are the relationships between the level of chromium oxidation and carcinogenity, and between the presence of reductants and the kind of DNA damage. Methods for the assessment of chromium mutagenity and genotoxicity are also discussed, and special attention is paid to tests of mutation in bacteria and yeast as well as to sister chromatid exchange (SCE) test.

Explore related subjects

Antimutagenic AgentsChromiumDNAHumansMutagensNeoplasmsEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Trocha, J Antonowicz, R Andrzejak. 1999. [Chromium carcinogenicity].. https://pubmed.ncbi.nlm.nih.gov/10472621/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2002

Antioxidant and antimutagenic properties of aqueous extract of date fruit (Phoenix dactylifera L. Arecaceae).

Fruits of the date palm (Phoenix dactylifera L. Arecaceae) are very commonly consumed in many parts of the world and are a vital component of the diet in most of the Arabian countries. This preliminary study documents for the first time its antioxidant and antimutagenic properties in vitro. There was a dose-dependent inhibition of superoxide and hydroxyl radicals by an aqueous extract of date fruit. The amount of fresh extract required to scavenge 50% of superoxide radicals was equivalent to 0.8 mg/mL of date fruit in the riboflavin photoreduction method. An extract of 2.2 mg/mL of date fruit was needed for 50% hydroxyl-radical-scavenging activity in the deoxyribose degradation method. Concentrations of 1.5 and 4.0 mg/mL completely inhibited superoxide and hydroxyl radicals, respectively. Aqueous date extract was also found to inhibit significantly the lipid peroxidation and protein oxidation in a dose-dependent manner. In an Fe(2+)/ascorbate system, an extract of 1.9 mg/mL of date fruit was needed for 50% inhibition of lipid peroxides. In a time course inhibition study of lipid peroxide, at a 2.0 mg/mL concentration of date extract, there was a complete inhibition of TBARS formation in the early stages of the incubation period that increased during later stages of the incubation. Similarly, in the high Fe(2+)/ascorbate induction system a concentration of 2.3 mg/mL inhibited carbonyl formation measured by DNPH reaction by 50%. Moreover, a concentration of 4.0 mg/mL completely inhibited lipid peroxide and protein carbonyl formation. Date fruit extract also produced a dose-dependent inhibition of benzo(a)pyrene-induced mutagenecity on Salmonella tester strains TA-98 and TA-100 with metabolic activation. Extract from 3.6 mg/plate and 4.3 mg/plate was found required for 50% inhibition of His+ revertant formation in TA-98 and TA-100, respectively. These results indicate that antioxidant and antimutagenic activity in date fruit is quite potent and implicates the presence of compounds with potent free-radical-scavenging activity.

Antimutagenic Agents↗
PubMed2002

Quantitative structure--activity relationships of antimutagenic benzalacetones and 1,1,1-trifluoro-4-phenyl-3-buten-2-ones.

The antimutagenic activities (IC(50)) of benzalacetones (BZ) and 1,1,1-trifluo-4-phenyl-3-buten-2-ones (TF) against UV-induced mutagenesis in Escherichia coli WP2s(uvrA trpE) were quantitatively analyzed in terms of physicochemical parameters by regression analyses. Structural requirements for maximal potency were derived from the results of quantitative structure--activity relationship (QSAR) analyses: (1) ring substituents should be electron-withdrawing; (2) 2-OH substituents incapable of intramolecular hydrogen-bonding notably increase the potency; and (3) replacement of CH(3) group by CF(3) in the side chain enhances the activity. Contrary to our expectations, the best correlation lacked hydrophobic effects. Antimutagenic activities against gamma-induced mutagenesis in Salmonella typhimurium TA2638 were also studied for some derivatives in the BZ series, where, in addition to electronic and hydrogen-bonding factors, a hydrophobic term was also significant. Physicochemical meanings of the derived correlations are discussed.

Antimutagenic Agents↗
PubMed2001

Protective effects of vitamins and selenium compounds in yeast.

Antimutagens and anticarcinogens are known to play an important role in decreasing damages induced by oxidants. In this study, we investigated the genotoxic and antimutagenic potential of two selenium compounds (sodium selenite: Na(2)SeO(3); seleno-DL-methionine: C(5)H(11)NO(2)Se) and Vitamins A and E in yeast cells of Saccharomyces cerevisiae. An oxidative mutagen (hydrogen peroxide (H(2)O(2)), HP) was chosen as positive control. We determined the enzymatic activities involved in the protection against oxidative damages (catalase: CAT; superoxide dismutase: SOD; glutathione peroxidase: GPx) in the cytosolic extract of yeast cells. The results demonstrated that selenium compounds exerted both mutagenic and antimutagenic effect at different concentrations. Antimutagenesis was evident both in stationary and in logarithmic phase cells. Catalase, SOD, and GPx were significantly increased in the presence of all the compounds assayed. Vitamins A (retinol) and E (alpha-tocopherol) did not have toxic or mutagenic action.

Antimutagenic Agents↗