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At least 19 recordsLinked to original sources
PubMed1977

Toxicity and mutagenicity of hexavalent chromium on Salmonella typhimurium.

Four hexavalent and two trivalent chromium compounds were tested for toxicity and mutagenicity by means of the Salmonella typhimurium/mammalian-microsome test. All hexavalent compounds yielded a complete inhibition of bacterial growth at doses of 400 to 800 mug/plate, a significant increase of his(+) revertant colonies at doses ranging from 10 to 200 mug, and no effect at doses of less than 10 mug. The distinctive sensitivity of the four Salmonella strains tested (TA1535, TA1537, TA98, and TA100) suggested that hexavalent chromium directly interacts with bacterial deoxyribonucleic acid by causing both frameshift mutations and basepair substitutions. The latter mutations, which are prevalent, are amplified by an error-prone recombinational repair of the damaged deoxyribonucleic acid. On the average, 1 mumol of hexavalent chromium yielded approximately 500 revertants of the TA100 strain, irrespective of the compound tested (sodium dichromate, calcium chromate, potassium chromate, or chromic acid). The mutagenic potency of the hexavalent metal was not enhanced by adding the microsomal fraction of rat hepatocytes, induced either with sodium barbital or with Aroclor 1254. The two trivalent compounds (chromium potassium sulfate and chromic chloride), with or without the microsomal fraction, were neither toxic nor mutagenic for the bacterial tester strains.

Chromates↗
PubMed1978

Comparative toxicity of trivalent and hexavalent chromium to rabbits. III. Biochemical and histological changes in testicular tissue.

The administration of trivalent and hexavalent chromium compounds produced inhibition of the activity of succinic dehydrogenase, adenosine triphosphatase and acid phosphattase accompanied by cellular degeneration with complete absence of spermatocytes in the testis of rabbits. The biochemical and histological changes were more marked in the animals treated with the trivalent chromium than those exposed to hexavalent chromium and were progressive with the duration of exposure.

Acid Phosphatase↗
PubMed1977

Comparative toxicity of trivalent and hexavalent chromium to rabbits. II. Morphological changes in some organs.

Toxicity of trivalent and hexavalent chromium compounds was investigated in experimental rabbits to ascertain health hazards among industrial workers of miners occupationally exposed to such chemicals. Brain, kidney and myocardium showed a tendency to accumulate chromium irrespective of its valency state; the morphological changes were more marked in animals exposed to hexavalent chromium. However, no definite co-relation could be observed between the concentration of the metal and the degree of histological changes in these organs.

Animals↗
PubMed1979

A simple analytical technique for the determination of hexavalent chromium in welding fumes and other complex matrices.

A systematic study of analytical methods for the determination of hexavalent chromium showed that currently existing techniques are unsatisfactory when used with welding fumes, the s-diphenylcarbazide method proposed by the U.S. National Institute for Occupational Safety and Health permitting less than 1% recovery of hexavalent chromium from synthetic welding fumes of known composition. A new (carbonate leaching) technique is proposed which permits better than 80% recovery of both soluble and insoluble chromium (VI). This technique is then used as part of a general method for the determination of total chemical composition as distributed among sample fractions of different solubility. The method is specifically designed for use in the analysis of small samples and is especially suitable for the routine evaluation of health risks as found in the work environment.

Air Pollutants↗
PubMed1978

Comparative studies of chromosomal aberration and mutagenicity of the trivalent and hexavalent chromium.

The comparative cytogenetic and mutagenic effects between trivalent and hexavalent chromium were investigated. Five chromium compounds, K2Cr2O7 and K2CrO4 containing Cr6+, and Cr(CH3COO)3, Cr(NO3)3 and CrCl3 containing Cr3+, were examined for their ability to induce chromosomal damage in cultures of human leukocytes, for their reactivity with DNA by a rec-assay system and for mutagenicity in the E. coli Hs30R test system. Chromosome-breaking activity was significantly higher for the compounds with hexavalent than trivalent chromium, the efficiency being in the decreasing order K2Cr2OM greater than K2CrO4 greater than Cr(CHCOO)3 greater than Cr(NO3)3, CrCl3. In the rec-assay and mutation assay, hexavalent (K2Cr2O7 and K2CrO4) and trivalent Cr(CH3COO)3) compounds gave positive results, their mutagenic potential being higher in the same order of clastogenic magnitude.

Cells, Cultured↗
PubMed1979

Chromosomal aberrations and sister-chromatid exchanges in Chinese hamster cells treated in vitro with hexavalent chromium compounds.

Chinese hamster cells (CHO line) were treated in vitro for 30--39 h with hexavalent chromium compounds (K2Cr2O7 and Na2CrO7), at concentrations ranging from 0.1 to 1.0 microgram of Cr6+ per ml, in medium containing BUdr. Chromosomal aberrations and sister-chromatid exchanges were scored on BUdr-labelled 2nd division metaphases, collected at the end of treatment and stained with Giemsa. Treatment with mitomycin C 0.009--0.030 microgram/ml) was carried out as a control for the responsiveness of the cell system to chromosomal damage. Both chromium compounds induced marked mitotic delays. Chromosomal aberrations were increased about 10-fold by exposure to Cr6+ (1.0 microgram/ml). The principal aberrations observed were single chromatid gaps, breaks and interchanges, whose frequencies increased proportionally to the concentration of chromium. Dicentric chromosomes, isochromatid breaks, chromosome and chromatid rings were also induced. The frequenyc of sister-chromatid exchanges was hardly doubled 30 h after exposure to Cr6+ at 0.3 microgram/ml, whereas it was trebled 39 h after treatment, in the cells whose division cycle had been slowed down by chromium.

Animals↗
PubMed1978

Effect of copper and tri- and hexavalent chromium on the work of an activated sludge.

The effect of metals (Cu2+, Cr3+, Cr6+) on the work of an activated sludge grown in crude oil refining or synthetic wastes was examined. The activated sludge method was found to be applicable for the purification of wastes carrying up to 0.8 mgCu2+/1,15mgCr3+/1, or 20mgCr6+/1. Higher concentrations of these metals inhibited the work of the activated sludge which was evident in inferior purification and reduced intensity of respiration of the activated sludge microorganisms.

Bacteria↗
PubMed2026

Mechanisms of Hexavalent Chromium-Induced Reproductive Toxicity: A Focus on the Ovary and Placenta.

Hexavalent Chromium (Cr(VI)) is a Group A carcinogen, mutagen, and teratogen. Cr(VI) has been used by more than 50 industries, and its contamination of drinking water is widespread across the United States (U.S.). Epidemiological data of women who lived in Willits, California, U.S., indicate that environmental exposure to Cr(VI) adversely affects pregnancy outcomes and the health of their immediate offspring, resulting in a low birth rate, pregnancy loss, and spontaneous abortion, and their children (F1 offspring) experienced birth defects. However, the molecular mechanisms behind Cr(VI)-induced reproductive and developmental toxicity are poorly understood. Cr(VI) enters cells through anion transporters and is rapidly reduced to Cr(III) by endogenous antioxidants within the cell. Cr(III) forms adducts with DNA, which can block DNA replication and transcription; abnormal repair can lead to DNA double-strand breaks, mutations, micronucleus formation, chromosomal abnormalities, and increased genomic instability. Cr(VI) induces oxidative stress via the Fenton reaction, generating free radicals, and depleting antioxidants, thereby promoting apoptosis via p53-dependent and independent pathways, resulting in follicular atresia and accelerated reproductive aging. Antioxidant supplementation with resveratrol, vitamin C, and edaravone mitigates Cr(VI) toxicity in the ovary. Cr(VI) disrupts meiosis in metaphase II oocytes by causing DNA strand breaks, altering F-actin dynamics, disturbing microtubules, and leading to chromosome missegregation. Gestational exposure to Cr(VI) also disrupts placental function through multiple mechanisms by targeting trophoblast lineages. The current review focuses on genotoxicity, oxidative stress, and other mechanisms by which Cr(VI) disrupts the female reproductive and endocrine systems, with particular emphasis on the ovary and placenta.

Hexavalent chromium↗
PubMed1977

Urinary chromium as an indicator of the exposure of welders to chromium.

Five welders working with high alloy Cr-Ni steel and one working with mild steel were followed during one work week. The chromium concentration in air was measured concomitantly with urinary chromium determinations. The water-soluble chromium concentrations in air exceeded 0.05 mg/m3 during welding with coated electrodes, but metal inert-gas (MIG) welding produced much lower concentrations. The proportion of water-soluble hexavalent chromium in the air was usually more than 50% of the total chromium concentration during welding with coated electrodes, whereas less than 10% of the chromium produced during MIG welding was in a water-soluble. Since water-soluble chromium (hexavalent) is the more important biologically, the determination of both water-soluble and water-insoluble chromium concentrations is emphasized instead of the measurement of the total concentration. The urinary chromium concentration proved to be a good indicator of short-term exposure to water-soluble chromium when exposure was above the current threshold limit value of 0.05 mg/m3, concentrations of more than 30 microgram/g of creatinine representing an exposure level higher than the threshold limit value.

Adult↗
PubMed1978

Oxidation of inactive trivalent chromium to the mutagenic hexavalent form.

Soluble trivalent chromium compounds (chromium potassium sulfate, chromium nitrate, chromium chloride, neochromium and chromium alum) were inactive for Salmonella typhimurium TA100, even at milligram amounts per plate. No effect could be detected either in the absence or in the presence of rat-liver, lung or muscle microsomal fractions, of rat-muscle mitochondria (with or without ATP), of oxidized glutathione (GSSG), or of human serum, plasma or erythrocyte lysates. Conversely, addition of a strongly oxidizing agent (potassium permanganate) resulted in toxic effects in plates incorporating more than 40--80 microgram of compounds and elicited a dose-effect mutagenic response at 10--40 microgram per plate. These effects could be ascribed to oxidation of chromium from the trivalent to the active hexavalent state. Insoluble chromite, as tested in the spot test, was spontaneously mutagenic, owing to contamination of the industrial product with hexavalent chromium. The results obtained may be useful to interpret the findings of carcinogenicity tests and to predict health hazards linked to chromium.

Chromium↗
PubMed1978

Effects of potassium dichromate on nucleic acid and protein syntheses and on precursor uptake in BHK fibroblasts.

Treatments for 1 to 4 hr with 10-4 m potassium dichromate, a soluble hexavalent chromium salt with a strong oxidizing power, markedly reduce DNA and RNA accumulation rates in hamster fibroblasts grown in vitro (BHK line), as shown by quantitative spectrophotometric determinations. Such inhibitory action is not immediately evident on the basis of the incorporation rates of labeled nucleosides into DNA and RNA, as dichromate affects also the relative concentrations of labeled precursors in the intracellular pool. Dichromate first stimulates and then inhibits nucleoside (mostly thymidine) uptake, whereas amino acid uptake is immediately inhibited. Actual rates of macromolecular syntheses have been calculated by taking into account the induced changes of soluble precursor concentrations; sucn normalized rates point out that dichromate induces a sudden blockage of DNA replication, whereas RNA and protein syntheses are secondarily inhibited. The observed cytotoxic effects of dichromate are tentatively referred to the oxidation of cell components by hexavalent chromium and thereby to the interaction of reduced trivalent chromium with specific biological ligands on cell membrane and on DNA.

Cells, Cultured↗
PubMed1979

[On the suitability of migration inhibition techniques in the in-vitro-diagnostics of chromium allergy (author's transl)].

1. Under the conditions of cell culture potassium dichromate is reduced to trivalent chromium (diphenylcarbacid/fotometry). Trivalent chromium reacts with proteins more strongly than the hexavalent chromium (gelchromatography/atom absorption spectrophotometry) and presumably represents the actual hapten. 2. Because of this in-vitro-conjugation chromium salts are suitable in their unconjugated form for applying in migration inhibition tests (capillary/Clausen technique). 3. In migration inhibition tests potassium dichromate showed a better antigenicity than chromium chloride. The capillary method was more sensitive than the Clausen technique when using the same test concentration. 4. Correlations between the degree of the patch test and the value of the migration inhibition did not exist.

Allergens↗
PubMedDate not supplied

[Permeability of physiological barriers for chromium and its balance in the body when administered with water or food].

In experiments set up on albino male-rats by using Cr51 the permeability of physiological barriers to hexad stable chromium (sodium chromate), introduced with water per os in doses of 2.5 and 2250 gamma/kg was studied and the chromium balance in the rats' organism with an addition of the same doses of trivalent (chromium sulfide) chromium to the ration investigated. With all the tested additions of stable hexad chromium in water Cr51 is prevalently retained in the stomach and intestines. With an addition of 2.5 gamma/kg of stable chromium to the ration and without chromium addition to the ration it is only 7.8--9.5 per cent of the introduced Cr51 that is excreted in 4 days, the respective figures with additions of 24 gamma/kg and 2250 gamma/kg being 59.7 and 54.5 per cent. An addition of 2.5 gamma/kg of chromium to the ration is physiologically justified, for with this dose the retention in the barriers and excretion of chromium with this dose do not increase, whereas higher doses of tri- and hexavalent chromium are non-physiological, since with these doses the retention of chromium by physiological barriers sharply increases and so doses its elimination from the organism.

Animals↗