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PubMed2001

Toxicity and bioaccumulation of arsenic and chromium in epigean and hypogean freshwater macroinvertebrates.

Lethal toxicity levels of two inorganic water pollutants, chromium (Cr6+) and arsenic (As3+), were determined toward six freshwater macroinvertebrate species collected from a single field site. Crustaceans were represented by two amphipod species, an epigean one (Gammarus fossarum) and a hypogean one (Niphargus rhenorhodanensis), and by an isopod species (Asellus aquaticus). There were two insect larvae, Heptagenia sulphurea (Ephemeroptera) and Hydropsiche pellucidula (Trichoptera) and a snail, Physa fontinalis. Median lethal concentrations (LC50s) were determined over 96-h and 240-h periods for chromium and over a 240-h period for arsenic. Arsenic bioaccumulation was studied, too. The macroinvertebrates tested showed a wide range of sensitivity and bioaccumulation. A comparison between 96-h and 240-h experiments demonstrated that there was an increase in toxicity values following a longer time exposure for chromium. Also chromium was more toxic toward crustaceans than arsenic; conversely, arsenic was more toxic for the insect larvae and snail tested here. The lethal concentrations determined for the two metals were discussed and compared to results from other toxicity studies. The use of such macroinvertebrates, collected in the field and tested for longer exposure periods than within the standardized 96-h tests, should provide more suitable results for monitoring the general environmental quality of freshwater systems.

Animals↗
PubMed2004

Effect of chromium(VI) action on Arthrobacter oxydans.

Arthrobacter species is of interest because of its high potential for bioremediation. Bacteria can detoxify chromium, by either reduction or accumulation inside the bacteria and/or absorption of chromium(VI) (CrVI) on their surface, and efflux pump. The possible pathway of Cr(VI) reduction by Arthrobacter oxydans isolated from Columbia basalt rocks at a US DOE highly contaminated site (USA) has been considered in the present study. FTIR absorption spectroscopy showed that these bacteria reduce Cr(VI). In the present study the threshold Cr(VI) nontoxic concentration (35 microg/mL) for A. oxydans growing in liquid medium was estimated. Complete uptake of this concentration was achieved in about 10 days after chromium addition into the medium. At this concentration an increase in the protein isolated from the cell wall of A. oxydans was observed. This increased protein predominated independently of the growth phase at which Cr(VI) was added. Thermal analysis was used to identify any influence of Cr(VI) on the DNP complex of A. oxydans. According to the data obtained it can be supposed that Cr(VI) reduction predominantly occurs on the bacterial surface and that cell wall represents a permeable barrier for these bacteria at the non-toxic chromium action.

Arthrobacter↗
PubMed1997

Reference values of urinary chromium in Italy.

OBJECTIVES: The paper describes the results of a polycentric study for the assessment of reference values of urinary chromium (U-Cr) in the Italian population. METHOD: A total of 890 subjects (58.3% males and 41.7% females) were selected on the basis of standardized criteria in eight different areas of Italy. Urinary chromium was determined on morning spot samples collected using standardized procedures. The U-Cr was determined independently by three laboratories using an Electrothermic atomization-Atomic Absorption Spectrometry (ETA-AAS) method with a detection limit of 0.05 microgram/l, adopting-for the statistical analysis-the median value of the results of the three laboratories. The between-laboratories within-subjects standard deviation was 0.049 microgram/l. Due to the high proportion (approx, 28%) of undetectable chromium levels, the geometric mean (GM) and geometric standard deviation (GSD) were estimated using a procedure of linear interpolation. The analysis of the effects of some variables (sex, age, center, residence, smoking and drinking habits) on the U-Cr values, was also performed, by multiple regression analysis after logarithmic transformation, using GM and SD. RESULTS: The reference value of U-Cr was of 0.08 microgram/l as an estimated GM, whereas the expected distribution ranged from not detectable (nd) (95% CI = nd-0.06) to 0.24 microgram/l (95th percentile; 95% CI = 0.20-0.31). Among the variables studied, only geographical area and sex significantly influenced the U-Cr levels. In subjects selected in the provinces of Bari and Venice values of U-Cr were significantly lower than those determined in subjects residing in other areas. CONCLUSIONS: From our investigation the reference values for U-Cr were lower than those obtained in previous investigations. In addition it confirms a further reduction in U-Cr levels following the previous decline reported in the 1970s and 1980s. In over 20 years U-Cr values in the general population dropped from values greater than 1 microgram/l to values between 0.5 and 0.2 microgram/l. The reasons of this progressive decline cannot be attributed in our opinion to a reduced intake of the metal, but mainly to the improvement in analytical instrumentation and methods. A further decrease may be ascribed to a more accurate definition of the reference groups and to a better control of pre-analytical factors. Considering that the reference values for U-Cr are much lower than those determined some decades ago, toxicological studies in order to verify the significance of biological limit values currently suggested for chromium seem to be necessary.

Adult↗
PubMed2002

Effects of mercury and chromium upon longevity of Diplostomum sp. (Trematoda: Diplostomidae) cercariae.

Laboratory experiments were carried out to examine the impact of mercury and chromium upon survival of Diplostomum sp. cercariae. Freshly emerged cercariae were exposed to solutions of either mercury, at concentrations ranging between 0.1 and 100 microg/l, or chromium at concentrations from 2 microg/l to 2 mg/l. The mortality patterns and mean survival times (MSTs) of the exposed parasites were determined by the Kaplan-Meier estimator and were compared (log-rank test) with corresponding patterns and estimators of the unexposed controls. Mercury concentrations > or = 10 microg/l caused statistically significant changes in the mortality pattern of Diplostomum sp. cercariae and reduced MST by at least 9 h compared with the control group, in which MST was 42 h. Cercariae exposed to chromium solutions had statistically significant changes in mortality pattern only at a concentration of 2 mg/l and exhibited a reduction in MST of 8 h compared with the control (MST = 41 h). The results show for the first time that longevity of Diplostomum sp. cercariae can be reduced by direct exposure to heavy metals. Ecotoxicological effects of mercury are manifested at lower concentrations than those of chromium, and thus potentially have a higher impact on parasite populations and communities.

Animals↗
PubMed2004

Chromium recycling of tannery waste through microbial fermentation.

An Aspergillus carbonarius isolate, selected from an established microbial culture collection, was used to study the biodegradation of chromium shavings in solid-state fermentation experiments. Approximately 97% liquefaction of the tannery waste was achieved and the liquid obtained from long-term experiments was used to recover chromium. The resulting alkaline chromium sulfate solution was useful in tanning procedures. A proteinaceous liquid was also obtained which has potential applications as a fertilizer or animal feed additive and has several other industrial uses. The A. carbonarius strain proved to be a very useful tool in tannery waste-treatment processes and chromium recovery in the tanning industries.

Aspergillus↗
PubMed2006

The effects of combined treatment with niacin and chromium on the renal tissues of hyperlipidemic rats.

In this study, 12 months old female Swiss albino rats were used. They were randomly divided into four groups. The animals of group I were fed with pellet chow. Group II were fed with pellet chow and treated with 250 microg/kg CrCl3 x 6H2O and 100 mg/kg niacin for 45 days. Group III were fed a lipogenic diet consisting of 2% cholesterol, 0.5% cholic acid and 2% sunflower oil added to the pellet chow, and given 3%alcoholic water for 60 days. Group IV were fed with the same lipogenic diet for 60 day sand treated by gavage technique to rats at a dose of 250 micro/kg CrCl3 x 6H2O and 100 mg/kg niacin for 45 days, 15 days after experimental animals were rendered hyperlipidemic. At the 60th day, renal tissue and blood samples were taken from the animals. The sections were examined under light and electron microscopy. The degenerative changes were much more in the hyperlipidemic rats than the control group. The changes in renal tissue were also observed in hyperlipidemic animals given niacin and chromium. In the hyperlipidemic rats, renal glutathione levels decreased and renal lipid peroxidation levels, and serum urea and creatinine levels were increased. But, renal glutathione levels increased and lipid peroxidation levels and serum urea and creatinine levels decreased in hyperlipidemic rats given niacin and chromium. The purpose of this study was to investigate whether a protective effect of a combination of niacin and chromium is present on the renal tissue of hyperlipidemic rats or not. In conclusion, we can say that niacin and chromium do not have a protective effect on the morphology of the renal tissue of hyperlipidemic rats, except a protective effect on their biochemical parameters.

Animals↗
PubMed1984

Effect of chromium(III) on poly(dG-dC) conformation.

The interaction of chromium(III) with poly(dG-dC) inhibits the B to Z transition and results in the condensation of the polymer at high Cr/nucleotide ratios. At low Cr/nucleotide ratios chromium(III) enhanced the ability of ethanol to induce the B to Z transition of poly(dG-dC). The effects of chromium(III) on the conformation of DNA may be related to the carcinogenicity of chromium compounds.

Chromium↗
PubMed1979

The urinary excretions of iron and chromium by children with burns and scalds.

There is a wide variation in the urinary output of chromium by children who have been burned or scalded. It seems possible that when the excretion of chromium is increased this may be related to an increased plasma concentration of glucose which may follow injury, and when the excretion of chromium is reduced this may be related to a low body content of chromium. During the first seven days after injury there is a significant increase in the excretion of iron. Likewise the iron/chromium ratio is also raised over the first seven days. The overall loss of iron during the first twelve days or thereabouts is probably not sufficient to require nutritional supplements over this period.

Burns↗
PubMed1989

Environmental chemistry of chromium.

The processes that control the environmental chemistry of chromium include redox transformation, precipitation/dissolution, and adsorption/desorption reactions. Commonly occurring reductants, such as ferrous iron and organic material, can transform Cr(VI) to Cr(III), but manganese oxides are the only inorganic oxidants found in the environment that cause the rapid oxidation of Cr(III) to Cr(VI). In the trivalent state, chromium readily forms compounds such as Cr(OH)3 and (Cr,Fe)(OH)3. These solids show amphoteric solubility behavior, with hydroxo complexes being the dominant aqueous species of Cr(III). The relatively low solubilities of Cr(OH)3 and (Cr,Fe)(OH)3 limit Cr(III) concentrations to less than the drinking water limit over much of the pH range of environmental interest. In the hexavalent state, the formation of the Ba(S,Cr)O4 solid solution controls the dissolved chromium concentrations in environments that contain BaSO4. In the absence of solubility-controlling Cr(VI) solids, Cr(VI) concentrations in acidic to slightly alkaline conditions are expected to be limited by adsorption. Iron oxides are the most important absorbents for aqueous Cr(VI) species in most soil environments. Although these processes are complex and interrelated, each must be considered to predict the aqueous concentrations, mobility, and toxicity of chromium in the environment.

Adsorption↗
PubMed1989

Analytical chemistry of chromium.

The determination of chromium in most biological materials is extremely difficult because of the very low levels present. Easily accessible samples, for example biological fluids such as serum, urine, etc., usually have chromium concentrations well below 1 ng g-1. The only widely available analytical method with sufficient sensitivity is graphite furnace atomic absorption spectrometry (GFAAS), yet values reported in the early literature were wildly divergent. Man appeared to be excreting several times the amount of chromium he was absorbing from his diet. This dilemma was resolved in 1978 when it was shown that all previous chromium analytical results were probably wrong (too high), due to limitations of the instrumentation used up until then. Subsequent instruments with improved background correction capabilities have removed this limitation. However, making determinations at the sub-parts-per-billion level remains a formidable task in terms of contamination control.

Chromium↗
PubMed1989

Acute and chronic systemic chromium toxicity.

Although chromium and compounds containing it have been recognized as having potential severe adverse effects on health for more than 160 years, understanding of the systemic toxicology and true hazard of these compounds is still not complete. A review of the current state of knowledge is attempted in this paper, with appropriate attention given to the complications of multiple valence states and solubility. Selected chromium compounds, particularly hexavalent ones, are carcinogens, corrosives, delayed contact sensitizers, and have the kidney as their primary target organ. But chromium is also an essential element for humans. The body clearly possesses some effective detoxification mechanisms for some degree of exposure to hexavalent chrome compounds. The significant features of acute and chronic chromium toxicity are presented in view of these considerations.

Air Pollutants↗
PubMed1994

Competitive binding of chromium, cobalt and nickel to serum proteins.

The competitive binding of chromium, cobalt and nickel chloride salts to murine serum proteins was studied in vitro. Individual metal salt solutions and combinations were incubated with 1:20 dilution of murine serum proteins for 24 h. Then free metal was removed by dialysis. The protein bound metal ions were analysed by graphite furnace atomic absorption spectroscopy. This study determined the saturation binding of cobalt and nickel to serum proteins. Murine serum is mostly saturated when cobalt or nickel is added at the concentration of 2 mol of metal to 1 mol of albumin. Chromium and cobalt have similar protein binding affinity, chromium and cobalt bind to protein in proportion to the added concentration ratio. However, nickel shows significant competition for chromium and cobalt binding moieties. This study provides a reference for future research on the biological role and properties of corrosion products.

Animals↗
PubMed1996

Titanium, chromium and cobalt ions modulate the release of bone-associated cytokines by human monocytes/macrophages in vitro.

Osteolysis has become a major cause of aseptic loosening in total joint arthroplasty (TJA). Titanium, cobalt and chromium are commonly used in orthopaedic implants (e.g. joint prostheses). The release of bone-associated cytokines has been associated with the development of osteolysis in patients with prostheses. We evaluated the effects of these metals on the release of bone-associated cytokines (IL-1 beta, IL-6, TNF-alpha and TGF-beta 1) by human blood monocytes/macrophages and monocyte-like U937 cells upon lipopolysaccharide (LPS) stimulation, the cell proliferation, and their cytotoxic effects on these cells in vitro. We found that the release of IL-1 beta was enhanced by titanium, chromium and cobalt, the release of TNF-alpha was enhanced by titanium and chromium, and the release of IL-6 was enhanced by titanium. All three metal ions inhibited the release of TGF-beta 1. We also found that titanium and chromium, but not cobalt, enhanced blood monocyte/macrophage proliferation in response to LPS while only titanium enhanced U937 cell proliferation in response to LPS. The metals in concentrations ranging from 0.01 to 100 ngml-1 did not stimulate the cells to secrete detectable cytokines in the absence of LPS. Furthermore, a 4-h pre-exposure of blood monocytes/macrophages or U937 cells to the metals did not alter cytokine release when the metals were removed from the media prior to the addition of LPS. Similarly, a 4-h pre-exposure of blood monocytes/macrophages or U937 cells to LPS did not alter cytokine release when LPS was removed from the media prior to the addition of the metals. The metals did not reduce cell viability and induce cell injury after 72h incubation with the cells. The data suggest that the three metals at clinically relevant concentrations modulated cytokine expression, whereas they did not induce any cytotoxic effects. A metal-induced enhancement of bone-resorbing cytokine release with a concomitant inhibition of bone-forming cytokine release may be an important factor in the development of osteolysis, which can severely compromise the outcome of TJA.

Biocompatible Materials↗
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↗
PubMed1987

Intracellular chromium reduction.

Two steps are involved in the uptake of Cr(VI): (1) the diffusion of the anion CrO4(2-) through a facilitated transport system, presumably the non-specific anion carrier and (2) the intracellular reduction of Cr(VI) to Cr(III). The intracellular reduction of Cr(VI), keeping the cytoplasmic concentration of Cr(VI) low, facilitates accumulation of chromate from extracellular medium into the cell. In the present paper, a direct demonstration of intracellular chromium reduction is provided by means of electron paramagnetic (spin) resonance (EPR) spectroscopy. Incubation of metabolically active rat thymocytes with chromate originates a signal which can be attributed to a paramagnetic species of chromium, Cr(V) or Cr(III). The EPR signal is originated by intracellular reduction of chromium since: (1) it is observed only when cells are incubated with chromate, (2) it is present even after extensive washings of the cells in a chromium-free medium; (3) it is abolished when cells are incubated with drugs able to reduce the glutathione pool, i.e., diethylmaleate or phorone; and (4) it is abolished when cells are incubated in the presence of a specific inhibitor of the anion carrier, 4-acetamido-4'-isothiocyanatostilbene-2-2'-disulfonic acid.

Animals↗
PubMed1986

Chromium-associated 32P-labeling of proteins.

The incubation of proteins with chromium (Cr3+ or Cr6+) in the presence of 32P ([gamma-32P]ATP or H3(32)PO4) at room temperature for 10-30 min resulted in the labeling of these proteins with 32P. The 32P-labeled proteins could be separated by SDS-polyacrylamide gel electrophoresis and identified by exposure to X-ray film. The characteristics of this procedure included: the optimal chromium concentration was 100 microM; the minimum requirement of each protein was 1 microgram; the optimal pH value was between 6 and 8; metal ions such as V5+, Mn2+ and Fe3+ strongly inhibited the effect of chromium, whereas Ca2+ and Mg2+ had little effect. It was concluded that chromium binds to the proteins and forms a complex with 32P to achieve the 32P-labeling of the proteins. This technique can be applied for the rapid preparation of 32P labels on protein markers for gel electrophoresis and for the identification of unknown protein species.

Autoradiography↗
PubMed1989

Nick translation studies on DNA strand breaks in pBR322 plasmid induced by different chromium species.

Single strand breaks are DNA defects caused by various chemicals. DNA strand breaks induced in vitro by chromium(VI) during the reduction of this chromium species with glutathione or hydrogen peroxide were examined. Using DNA agarose gel electrophoresis and a nick translation assay, strand breaks were detected only when chromium(VI) was reduced by hydrogen peroxide. The reduction of chromium(VI) by an excess of glutathione led to no alteration in the DNA agarose gel electrophoresis pattern of the double-stranded plasmid pBR322 DNA and in the nick translation assay, indicating that no strand breaks had occurred under these conditions. No strand breaks could be detected during the reduction by hydrogen peroxide after the addition of superoxide dismutase. This indicates that hydroxyl radicals from peroxochromium complexes may be a relevant reactive species involved in chromate genotoxicity.

Chromium↗
PubMed1996

Embryotoxicity of orally administered chromium in mice: exposure during the period of organogenesis.

Administration of chromium (VI)(250, 500 and 750 ppm as potassium dichromate) via drinking water during organogenesis (days 6-14 of gestation) in mice revealed embryo- and fetotoxic effects. Reduced fetal weight, retarded fetal development, number of fetuses (live and dead) per mother and high incidences of dead fetuses and resorptions in treated mothers in the highest dosed group were evident. No significant gross structural abnormalities were observed in any of the fetuses of chromium (VI)-treated mothers. Significant incidences of reduced ossification were found in the highest dosed group. Chromium levels were increased in a dose-dependent manner in maternal blood, placenta and fetuses. The present study suggests a risk to the developing embryo if the mother is exposed to a sufficiently high concentration of chromium (VI) through drinking water during the period of organogenesis.

Abnormalities, Drug-Induced↗