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Results for “Chromium Compounds”

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At least 127 records · Page 7Linked to original sources
PubMed1992

Induction of DNA strand breaks in peripheral lymphocytes by soluble chromium compounds.

1. Incubation of human lymphocytes with sodium dichromate (CrVI) at 37 degrees C for 3 h resulted in a dose-dependent increase in DNA strand breaks without concurrent cytotoxicity. In contrast, chromium acetate hydroxide (CrIII) failed to induce DNA strand breaks at sub-cytotoxic concentrations. 2. DNA strand breaks were also detected in the peripheral lymphocytes of Wistar rats, 24 h after intratracheal instillation of sodium dichromate (1.3 and 2.5 mg kg-1). Instillation of chromium acetate hydroxide (up to 21.8 mg kg-1) failed to induce DNA strand breaks in peripheral lymphocytes. In accord with previous studies, hexavalent chromium was found to be more readily absorbed from the lungs into the peripheral blood than chromium in its trivalent form. 3. The results of this study indicate that fluorometric analysis of DNA unwinding (FADU) in peripheral lymphocytes might be a convenient method of measuring an important biological effect of chromium in occupationally-exposed workers.

Animals↗
PubMed1991

Complexing of actin and other nuclear proteins to DNA by cis-diamminedichloroplatinum(II) and chromium compounds.

Actin was found to be the major protein crosslinked to the DNA of intact Chinese hamster ovary cells that were treated with either potassium chromate (hexavalent) or cis-diamminedichloroplatinum(II) (cis-platinum). This protein was identified as actin by its mol. wt (45 kd), its isoelectric point (pI = 5.4), positive reactivity with an actin antibody, and by protease mapping. Additionally, a purified actin standard migrated to the same location in a two-dimensional gel system as p45. Actin comprised approximately 20% of the protein component in chromate-induced DNA-protein crosslinks. In addition, to actin, several other major proteins (e.g. 53 kd, pI = 5.2, 50 kd, pI = 9) were crosslinked to DNA following exposure to cis-platinum or chromate. These proteins were abundant in the nuclear matrix fraction. Hexavalent chromate is the toxicologically active form because it is readily taken up into cells by an anion transport system. In contrast, trivalent chromium is considerably less toxic because it cannot enter the cell; however, most of the hexavalent form is eventually reduced to the trivalent form inside the cell. Previous studies have suggested that the trivalent form of chromium participates in complexing DNA with proteins. DNA-protein crosslinks were formed in isolated nuclei or in mixtures of purified DNA and protein incubated with trivalent chromium. However, the formation of these complexes required at least 16 h of incubation to exchange the parent compound ligands. Hexavalent chromate did not form these complexes in vitro under similar conditions. Incubation of trivalent chromium with purified actin and DNA resulted in DNA-actin crosslinks as detected by an electrophoretic mobility different from that of either free actin or DNA when the complex was transferred from a gel to nitrocellulose and stained for protein. These studies describe a new technique for detecting DNA-protein complexes and demonstrate that actin-DNA structures in intact cells create sites that selectively react with metal DNA-protein crosslinking agents.

Actins↗
PubMed1989

Role of epidemiologic studies in evaluating the carcinogenicity of chromium compounds.

Epidemiologic and animal studies have identified intermediately-soluble chromates as human carcinogens. Epidemiologic studies also provide moderately strong evidence to conclude that chromates do not cause cancer at sites other than the respiratory tract. This information, combined with the evidence from animal studies and in vitro experiments, has led to the conclusion that chromates do not present a carcinogenic risk from ingestion. Unfortunately, epidemiologic studies have not provided definitive answers to other questions: (i) does trivalent chromium present a cancer risk?; (ii) is there a threshold for carcinogenic effects?; and (iii) what is the appropriate model for predicting cancer risk? Mechanistic research with supporting evidence from animal studies has provided the most useful information to answer these questions. Working hypotheses are: (i) trivalent chromium is not a carcinogen; (ii) there are probably substantial differences in carcinogenic potency between chromates, with the water-soluble compounds having lower potency than intermediately-soluble compounds; (iii) only respiratory tract cancers are caused by exposure to chromates, and ingestion and chromates does not constitute a carcinogenic risk; (iv) there is probably a threshold for carcinogenic effects from chromium due to detoxification mechanisms and lack of bioavailability of low doses; and (v) currently used models for quantitative risk assessment (e.g. the low dose linearized multi-stage model) are inappropriate to predict low dose cancer risks from exposure to chromates.

Carcinogens↗
PubMed1980

Intestinal absorption of 5 chromium compounds in young black ducks (Anas rubripes).

An in vivo intestinal perfusion technique was used to measure the absorption rates of five Cr compounds in black ducks. Cr was absorbed from saline solutions of KCr(SO4)2 and CrO3 at a rate about 1.5 to 2.0 times greater than from solutions of Cr, Cr(NO3)3, and Cr(C5H7O2)3. These results suggest the ionic form of Cr in solution may be an important factor in determining absorption of Cr compounds from the small intestine.

Animals↗