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Hexavalent chromium uptake by sensitive and tolerant mutants of Schizosaccharomyces pombe.

Lysine and leucine auxotrophic, heterothallic (h+, h-) strains of Schizosaccharomyces pombe were used to obtain chromium (VI)-sensitive and -tolerant mutants by ultraviolet radiation-induced and nitrosoguanidine-induced mutagenesis. The minimal inhibitory concentrations of K2Cr2O7 on YEA media were 225 microM for the wild-type strain CW-6, 125 microM for the sensitive mutant CS-6.51 and 275 microM for the tolerant mutant CT-6.66. The mutants exhibited cross-sensitivity of various patterns to Cd2+, Cu2+, Ni2+, Zn2+ and VO3-(4). Cr(VI) was added to the actively growing cultures and the total chromium (TOCr) content of the cells was determined. The sensitive mutant exhibited a high bioaccumulation ability, with a dry biomass of 810 micrograms g-1 after 30 min, while the tolerant mutant had a significantly lower ability than the wild-type strain. In PIPES buffer, washed, lysine-starved biomasses were treated with 75 microM Cr(VI) and after 2 h, the TOCr and the organically bound chromium (OBCr) were determined. Under these conditions, the sensitive and tolerant mutants had the same TOCr content, 50% of which was OBCr. The wild-type strain exhibited a lower TOCr content than that of its mutants and only 35% of this was OBCr. The Cr(VI)-sensitivity was due to a significantly increased uptake of Cr(VI).

Chromium↗

Nickel, cobalt and chromium in consumer products: a role in allergic contact dermatitis?

In spite of the improved awareness of the potential for nickel, cobalt and chromium to cause skin allergy, the incidence of sensitization to them is generally on the increase, especially for nickel. We review data from the literature and industry on transition metal contamination of consumer products and assess the hazard to man. Consumer products are defined as personal care items and detergent/cleaning products used regularly in domestic work. The analytical data demonstrate that consumer products are a relatively minor source of contact with nickel, cobalt or chromium. The traces found in consumer products will not be the primary cause of sensitization to these metals: levels will be too low and exposure too brief. A person sensitized to these metals has many other more significant sources of daily contact such as earrings, jewelry and metal objects. It is therefore necessary to focus on decreasing the high exposure to these transition metals from other sources rather than on possible trace amounts found in consumer products. Current good manufacturing practice ensures that trace nickel, cobalt and chromium concentrations in consumer products are less than 5 ppm of each metal. It is recommended that this be accepted as a standard for maximum concentrations and that the target should be to achieve concentrations as low as 1 ppm.

Chromium↗

Pulmonary deposition following inhalation of chromium-cobalt grinding dust in rats and distribution in other tissues.

Twenty rats were exposed to dust particles of chromium-cobalt alloy abrasives produced in dental material handling. The exposure was carried out in chambers for periods up to 107 days at concentrations of particulate matter of about 10-50 mg/m3. The content of chromium and cobalt in autopsy specimens of lung, liver, kidney and trachea was measured with nuclear techniques. The alloy particles were found to be markedly accumulated in lung tissue. Increased levels of chromium and cobalt were also observed in the trachea. In addition, a moderate increase of cobalt in liver and kidney was demonstrated. The lungs of six exposed rats were examined microscopically. The main part of the dust particles was observed within macrophages. Only a minor fraction of particles were seen in the bronchial lumen close to the epithelial surface. The majority of dust-filled macrophages were located in groups within the bronchial wall or in the interstitium close to the terminal broncheoli. No fibrosis, dysplasia or tumor formation occurred. No acute adverse effects in the lungs were observed.

Air Pollutants↗

Release of cobalt from cobalt chromium alloy constructions in the oral cavity of man.

The release of cobalt from a cobalt chromium alloy construction with a major palatal connector (palatal strap) in the maxilla was determined for 10 test subjects. The concentration of cobalt in unstimulated whole saliva and tongue scrapings was estimated 21, 14 and 7 d respectively before and 1, 2, 3, 10, 20 and 30 d after insertion of the cobalt chromium alloy construction. The method used to quantify the cobalt content was flameless atomic absorption spectrophotometry (AAS). The results showed that the median cobalt concentration in saliva and tongue scrapings increased after the insertion of the cobalt chromium alloy construction, with the highest values occurring in the first 2 d after insertion. The tongue scrapings, in general, showed higher cobalt median values than saliva did at all times of estimation. The sampling method described in the present study seems to be useful in long-term investigations in man, where numerous sample collections in the oral cavity are required in order to determine metal content. The risk of negative biologic effects on the human organism caused by the cobalt release from the alloy is discussed.

Adult↗

Experimentally induced lipid peroxidation after exposure to chromium, mercury or silver: interactions with carbon tetrachloride.

Chromium, along with other heavy metals, induces an increased production of malondialdehyde (MDA), an indicator of lipid peroxidation, in liver and kidney tissue of NMRI male mice. After acute intoxications MDA levels remain high for 60 min. and thereafter return to normal in the kidney whereas MDA levels in liver are still increased 48 hr after exposure. Exposure of mice to chromium, mercury, or silver and another stimulator of lipid peroxidation, carbon tetrachloride, showed synergism between inorganic mercury and CCl4. Pre-exposure to chromium, organic mercury, or silver at selected doses did not enhance CCl4-toxicity as measured by organ content of MDA.

Animals↗

The determination of leachable chromium from chromicized catgut sutures.

Application of the British Pharmacopoeia (BP) Analytical procedure for the determination of leachable chromium to samples of catgut sutures yielded fading coloured solutions and was considered to constitute a poor basis for an analytical method. The United States Pharmacopeia (USP) method and an adaptation of the American Public Health Association (APHA) method were explored and found to give linear responses over the concentration range of interest. Both these methods were applied to a series of samples and the results obtained were different as the APHA method measures total chromium while the USP procedure determines only chromium (VI).

Animals↗

Nutritional ergogenic aids: chromium, exercise, and muscle mass.

Athletes who want to develop muscle mass have sought various ways to reach this goal. We are all too familiar with the abuse of anabolic steroids and growth hormone. Given the concern for such abuses, athletes and coaches are seeking new and safer means to achieve the same end. Within the last couple of years, advertisements for chromium supplements have been prominently displayed in body-building and strength-training magazines. These supplements are purported to be a safe alternative to anabolic steroids and are said to promote an increase in muscle mass. This brief review will focus on the theoretical basis for believing that chromium supplements will increase muscle mass, and on the current research regarding the relationship of chromium and exercise.

Chromium↗

Serum cholesterol reduction by chromium in hypercholesterolemic rats.

The addition of chromium (III) to the drinking water of rats in a normal laboratory environment on a hypercholesterolemic diet resulted in lower serum cholesterol concentrations whether the dietary carbohydrate was either sucrose or starch. However, rats fed the sucrose diet with chromium in drinking water had serum cholesterol concentrations similar to those of rats fed the starch diet without chromium in drinking water.

Animals↗

Enhanced exopolymer production and chromium stabilization in Pseudomonas putida unsaturated biofilms.

Chromium-contaminated soils threaten surface and groundwater quality at many industrial sites. In vadose zones, indigenous bacteria can reduce Cr(VI) to Cr(III), but the subsequent fate of Cr(III) and the roles of bacterial biofilms are relatively unknown. To investigate, we cultured Pseudomonas putida, a model organism for vadose zone bioremediation, as unsaturated biofilms on membranes overlaying iron-deficient solid media either containing molecular dichromate from potassium dichromate (Cr-only treatment) or with deposits of solid, dichromate-coated hematite (Fe+Cr treatment) to simulate vadose zone conditions. Controls included iron-deficient solid medium and an Fe-only treatment using solid hematite deposits. Under iron-deficient conditions, chromium exposure resulted in lower cell yield and lower amounts of cellular protein and carbohydrate, but providing iron in the form of hematite overcame these toxic effects of Cr. For the Cr and Fe+Cr treatments, Cr(VI) was completely reduced to Cr(III) that accumulated on biofilm cells and extracellular polymeric substances (EPSs). Chromium exposure resulted in elevated extracellular carbohydrates, protein, DNA, and EPS sugars that were relatively enriched in N-acetyl-glucosamine, rhamnose, glucose, and mannose. The proportions of EPS protein and carbohydrate relative to intracellular pools suggested Cr toxicity-mediated cell lysis as the origin. However, DNA accumulated extracellularly in amounts far greater than expected from cell lysis, and Cr was liberated when extracted EPS was treated with DNase. These results demonstrate that Cr accumulation in unsaturated biofilms occurs with enzymatic reduction of Cr(VI), cellular lysis, cellular association, and extracellular DNA binding of Cr(III), which altogether can facilitate localized biotic stabilization of Cr in contaminated vadose zones.

Biofilms↗

Respiratory health of workers exposed to low levels of chromium in stainless steel production.

OBJECTIVES: To determine whether occupational exposure to chromite, trivalent chromium, or hexavalent chromium causes respiratory diseases, an excess of respiratory symptoms, a decrease in pulmonary function, or signs of pneumoconiosis among workers in an integrated chain of stainless steel production. METHODS: This cross sectional study was carried out in 1993 and the inclusion criterion was a minimum of eight years of employment in the same production department. A self administered questionnaire was collected, and spirometry, measurement of diffusing capacity, chest radiography, and laboratory tests were carried out by a mobile research unit. RESULTS: There were 221 workers in the exposure groups and 95 in the control group. The average duration of employment was 18 years. No significant differences in the odds ratios (ORs) of the symptoms were found between the exposure and the control groups. In a logistic regression analysis age and smoking significantly explained the occurrence of most of the respiratory symptoms. The smokers in the chromite group had significantly lower forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and diffusing capacity than the corresponding values of the control group. The analysis of variance between study groups, smoking, and exposure time, without modelling for interactions, showed that the chromite group had lower values for FVC, FEV1, and diffusing capacity than the other groups. The occurrence of small opacities was more frequent on the chest radiographs of the workers in the chromite group. CONCLUSIONS: An average exposure time of 18 years in ferrochromium and stainless steel production and exposure to dusts containing low concentrations of hexavalent or trivalent chromium do not lead to any respiratory changes detectable by lung function tests or radiography nor to any increase in symptoms of respiratory diseases. The lung function values were lower and the occurrence of radiological findings was more frequent among the workers from the chromite mine than among the controls. The difference was partly caused by differences in age and smoking habits, but evidently also partly by higher exposures more than two decades ago or by the fibrous components of the dust.

Adult↗

Nickel, chromium, manganese, iron and aluminum levels in human cataractous and normal lenses.

Atomic absorption spectrophotometry was used to detect lenticular nickel, chromium, manganese, iron and aluminum levels in 37 senile cataractous and 9 normal human lenses. The nuclear parts of the lenses were used for the study in both groups. It was found that the concentrations of nickel and iron were significantly higher, and those of chromium, manganese and aluminum were significantly lower in human cataractous lenses than those in normal human lenses. None of the elements showed a significant difference according to sex in both groups. As remarkable differences in chromium, manganese, iron, aluminum and nickel levels exist in cataractous lenses, all the five elements may play some roles in cataractogenesis.

Aged↗

Role of chromium in barley in modulating the symptoms of diabetes.

In adult diabetic rats, a diet containing barley had a modulating effect on the symptoms of diabetes (blood glucose concentration and water consumption) when compared with a starch or sucrose-based diet. It was postulated that the beneficial effect of barley might be explained by its very high content of chromium (5.69 micrograms/g). Supplementation of the sucrose-based diet with an amount of trivalent inorganic chromium calculated to be equivalent to the available chromium in the barley-based diet abolished the differences in response to the diabetic state.

Animals↗

Successful induction of allergic contact dermatitis to mercury and chromium in mice.

Availability of reproducible mouse models for allergic contact dermatitis (ACD) to the metal allergens nickel, mercury and chromium, would be of great value for pathogenetic and preventive studies. We explored epicutaneous sensitization to nickel, mercury and chromium in mice in which oral grooming of the sensitization site was prevented by a plaster cast around the abdomen and lower thorax. This procedure was based on earlier findings that oral ingestion of allergen could prevent contact sensitization. The present results show that BALB/c mice can be readily sensitized to mercury and chromium using this epicutaneous casting method, without the further use of adjuvants. With nickel, however, neither this method, nor conventional methods involving the use of Freund's complete adjuvant (FCA) were effective.

Animals↗

Toxic effects of chromium acetate hydroxide on cells cultivated in vitro.

Many human activities, particularly industrial ones, result in an ever-growing production of toxic waste materials. The dynamics of the toxic effects of chromium acetate hydroxide, which is found in high concentrations in a waste sediment produced in the Czech Republic, were assessed by using a battery of in vitro tests carried out on two cell lines: L-929 (mouse fibroblasts) and Hep 2 (human laryngeal cells). Various markers of cell damage were assessed by phase-contrast, video and fluorescence microscopy, fluorometry, and DNA analysis. Chromium acetate hydroxide, over a concentration range of 1-0.02mol/l induced immediate cell death by fixation, whereas, at 0.002mol/l, the treated cells died in a much slower, more discrete manner. All the detected markers of cell damage, whether immediate or slow, clearly demonstrated that the cells died by necrosis. On the other hand, test concentration of 0.001mol/l appeared to constitute a threshold at which no pathological changes of Hep 2 cells were observed over 96 hours. We conclude that chromium acetate hydroxide has a high toxic potential in vitro, which should be considered when studying the toxicity of waste materials containing it.

Animals↗

Direct interaction with cellular targets as the mechanism for chromium carcinogenesis.

The carcinogenic activity of chromium appears to be due to its direct interaction with cellular targets and not to nonspecific solid-state carcinogenesis. Chromium was evaluated at 2 valences, Cr+3 (as CrC13) and Cr+6 (as K2Cr2O7), for its toxicity, transforming activity, and ability to induce chromosomal aberrations in tertiary cultures of mouse fetal cells. The ID50 (dose for 50 percent inhibition of cell growth) of Cr+3 was approximately 4 times greater than that of Cr+6 after 96 h of exposure, and about 29 times greater than that of Cr+6 after 1 h of exposure. At equitoxic concentrations, both chromium valences induced the same degree of morphologic changes and alterations of growth behavior, but Cr+6 produced more chromosomal aberrations. Using autoradiography in an established cloned line of mouse cells, unscheduled DNA synthesis was observed in cells previously exposed to Cr+6 but not in cells previously exposed to Cr+3.

Animals↗

[Effects of metals (silver, nickel, cobalt and chromium) on the reactive oxygen species generating capacity of human neutrophils and on the serum opsonic activity].

Many metal materials are used in clinical medicine and the number used is increasing. However, there are a few papers concerning the biological effects, especially effects of clinically used metals on cellular immunity. In this paper, silver (Ag), nickel (Ni), cobalt (Co), and chromium (Cr), clinically commonly used metals, the effects of which on neutrophilic activity have already reported using the luminol-dependent chemiluminescence (LDCL) method, were examined to determine their influence on the reactive oxygen species (ROS) generating capacity of human neutrophils and on a serum opsonic activity. Silver suppressed the ROS generating capacity of neutrophils in a dose-dependent manner but did not affect the serum opsonic activity. Nickel also suppressed the ROS generating capacity of neutrophils but, at some concentrations, caused the serum opsonic activity to increase. In contrast, Cobalt increased both the ROS generating capacity of neutrophils and the serum opsonic activity. Like silver, chromium did not affect the serum opsonic activity and suppressed the ROS generating capacity of neutrophils. However, the suppression of ROS generating by chromium occurred differently from that of silver. In the cases of nickel and cobalt, effects of these metals on hemolyzing activity of serum complements (CH-50) were measured and consumption of complements was observed at the same metal concentration at which serum opsonic activity was elevated. In this paper, we report that some metals influence not only the ROS generating capacity of neutrophils but also the serum opsonic activity, results thought to be important for more details studies of the effects of metals on cellular immunity.

Cells, Cultured↗

Increased serum corticosterone and glucose in offspring of chromium(III)-treated male mice.

Preconceptional carcinogenesis occurs in animals and is suspected for humans--for example, after occupational metals exposure. Several characteristics in animal models, including high frequency and non-Mendelian inheritance patterns, have suggested an epigenetic mechanism, possibly involving hormone changes in offspring. To test this hypothesis, we treated male mice with chromium(III) chloride, a preconceptional carcinogen, 2 weeks before mating, in two separate experiments. Their 10-week-old offspring showed highly significant increases in average serum corticosterone and glucose, compared with control offspring. Average serum levels of insulin-like growth factor 1 (IGF1) showed more modest possible increases. A previous microarray experiment identified hepatic insulin-like growth factor binding protein 1 (IGF BP1) gene expression as consistently changed in correlation with serum corticosterone levels. In the present study, hepatic IGF BP1 mRNA correlated with serum IGF1 in male offspring of chromium-treated fathers, but not in controls; serum glucose correlated positively with hepatic IGF BP1 in chromium-group offspring but negatively in controls. These results support the hypothesis that preconceptional exposure effects may alter hormones, metabolism, and control of tissue gene expression, probably through epigenetic mechanisms. Risk of neoplasia may be influenced by these changes.

Animals↗

Metabolic pathways of carcinogenic chromium.

The products of hexavalent chromium [Cr(VI)] reduction by glutathione (GSH) alone or in the presence of equimolar quantities of aspartate (Asp) and/or glutamate (Glu) and a chromium-containing material extracted from bovine liver were studied by ultraviolet-visible spectrum (UV-vis) studies, electrospray mass spectrometry (ES-MS), electron paramagnetic resonance (EPR), and nuclear magnetic resonance (NMR). Reduction of chromate by GSH was followed by UV-vis and NMR, revealing the formation of a paramagnetic complex in which GSH acts as a ligand. ES-MS and EPR measurements provided unequivocal evidence of a dimeric Cr(V)(2)GSH(2) species in which the two metal ions are bridged by the Gamma-Glu carboxylate. The analysis of the (1)H and (13)C shifts experienced by GSH protons and the values of paramagnetic contributions to proton spin-lattice relaxation rates provided a set of constraints for structural determination. The same experiments were repeated in the presence of an equimolar concentration of Asp, revealing the formation of a dimeric Cr(V) paramagnetic complex in which the two metals are now bridged by Asp. Nuclear magnetic resonance dispersion profiles show that water is not displaced by Asp and that the correlation time of this complex is slowed by the increased complexity. When Glu is also included in the solution in equimolar concentration to GSH and Asp, data are consistent with the formation of many mono- and dinuclear species, with the three ligands competing with each other. Finally, the spectroscopic investigation of the chromium-containing material extracted from bovine liver revealed the presence of a complicate mixture of Cr(IV) or Cr(V) complexes, among which some Cr(V)-GSH species are present alone or with other ligands in the metal coordination sphere.

Aspartic Acid↗