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At least 19 recordsLinked to original sources
PubMed1992

Reduction of chromium(VI) to chromium(V) by rat liver cytosolic and microsomal fractions: is DT-diaphorase involved?

Incubation of rat liver cytosolic or microsomal fractions with chromium(VI) led to a dramatic decrease in chromium(VI) mutagenicity, as determined by the Ames Salmonella assay using the TA100 tester strain. The cytosol-dependent decrease in chromium(VI) mutagenicity was found to be counteracted in the presence of dicumarol, an inhibitor of the cytosolic enzyme NAD(P)H:quinone oxidoreductase (DT-diaphorase). In order to determine whether DT-diaphorase is a significant factor in enzymatic reduction of chromium(VI) in rat liver tissue, cytosolic and microsomal fractions were analyzed for NAD(P)H-dependent chromium (VI) reductase activity leading to chromium(V) formation by using electron paramagnetic resonance (EPR) spectroscopy. Reaction of chromium(VI) with NADH or NADPH in the presence of either cytosolic or microsomal fractions led to the formation of stable chromium(V)--NAD(P)H complexes. When glucose 6-phosphate (G6P) was present in the reaction as part of a NADPH-generating system, stable chromium(V)--G6P complexes were formed in addition to the chromium(V)--NAD(P)H complexes. The chromium(V) complexes had g values of 1.980-1.982 and superhyperfine splitting constants of 0.8-0.9 characteristic of bis(diol)oxochromium(V) complexes. Inhibition of 90% of the cytosolic DT-diaphorase activity by dicumarol led to only partial (20-22%) inhibition of chromium(V) formation. Visible and EPR spectroscopic studies showed that purified DT-diaphorase had no detectable chromium(VI) reductase activity and did not catalyze formation of chromium(V). Inhibition of 69% of microsomal aryl hydrocarbon hydroxylase activity by ketoconazole led to partial (10%) inhibition of chromium(V) formation. These results indicate that intracellular NAD(P)H-dependent enzymatic reduction of chromium(VI) in rat liver cannot be attributed to the activity of any one enzyme in the cytosolic or microsomal fractions. DT-diaphorase appears to play an indirect role in decreasing chromium(VI)-induced mutagenicity in Salmonella, possibly through interaction with other redox active cellular components. The involvement of diols such as sugars and pyridine nucleotides in stabilizing intracellularly generated chromium(V) is discussed.

Animals↗
PubMed1991

Reaction of chromium(VI) with glutathione or with hydrogen peroxide: identification of reactive intermediates and their role in chromium(VI)-induced DNA damage.

The types of reactive intermediates generated upon reduction of chromium(VI) by glutathione or hydrogen peroxide and the resulting DNA damage have been determined. In vitro, reaction of chromium(VI) with glutathione led to formation of two chromium(V) complexes and the glutathione thiyl radical. When chromium(VI) was reacted with DNA in the presence of glutathione, chromium-DNA adducts were obtained, with no DNA strand breakage. The level of chromium-DNA adduct formation correlated with chromium(V) formation. Reaction of chromium(VI) with hydrogen peroxide led to formation of hydroxyl radical. No chromium(V) was detectable at 24 degrees C (297 K); however, low levels of the tetraperoxochromium(V) complex were detected at 77 K. Reaction of chromium(VI) with DNA in the presence of hydrogen peroxide produced significant DNA strand breakage and the 8-hydroxydeoxyguanosine adduct, whose formation correlated with hydroxyl radical production. No significant chromium-DNA adduct formation was detected. Thus, the nature of chromium(VI)-induced DNA damage appears to be dependent on the reactive intermediates, i.e. chromium(V) or hydroxyl radical, produced during the reduction of chromium(VI).

Animals↗
PubMed1978

Relative chromium response as an indicator of chromium status.

Twenty-seven women ages 40 to 75 were divided into normal (n = 15) and hyperglycemic (n = 12) groups on the basis of 3-hr glucose tolerance tests. Each subject received 5 g of brewer's yeast extract containing 4 microgram of chromium daily for 3 months. Glucose, insulin, and chromium levels were analyzed by oxidase, radioimmunoassay, and radiochemical neutron activation analysis methods, respectively. The fasting and 1-hr serum chromium levels (ng/ml) changed from 1.67 and 1.43 to 1.46 and 1.86 in the normal group, and from 1.89 and 1.03 to 0.94 and 1.03 in the hyperglycemic group. Considerable changes occurred in the relative chromium response (RCR) at the 1-hr point. RCR is defined as (1-hr serum chromium level/fasting serum chromium level) X 100. Among the normal subjects, 73% showed an improved RCR after the supplementation: mean RCR was 107% before and 140% after. Among the hyperglycemic subjects, 75% showed an improved RCR: mean RCR was 81% before and 149% after the supplementation. The increased RCR was associated with decreased serum insulin and glucose levels. This is interpreted as reflecting an improved chromium status for the majority of individuals in both groups after the supplementation. The observations suggest that 1) in response to a glucose load, serum chromium levels drop in subjects with presumably inadequate chromium storage; 2) a low value of relative chromium response at the 1-hr point indicates a suboptimal chromium nutritional status.

Aged↗
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↗
PubMed1977

Evaluation of chromium exposure based on a simplified method for urinary chromium determination.

The urine chromium levels for unexposed and chromium exposed persons were determined by a simplified method which is well suited for routine, large-scale use. A group of welders working on chromium alloyed steel were investigated. For these welders a high degree of correlation was found between the concentration of inhaled chromium and the chromium concentration in the urine immediately after work. At an exposure level of 0.05 mg/m3, measured as chromium, a urinary chromium concentration of approximately 40 microng/l was measured after work. This urinary chromium level is suggested as a guideline indicating the need for a thorough investigation of chromium exposure.

Air Pollutants↗
PubMed1978

[Chromium concentrations in urine of persons non-occupationally exposed to chromium and its compounds].

The investigation on 316 samples of urine from persons that are not professionally subject to the action of chromium or its compounds, demonstrated the following: - chromium is absent in the 8% of tested people; - average chromium concentration is 6.6 micrograms/l; - maximum chromium concentration is 36.6 micrograms/l. The average chromium concentration with regard to tested people living in the districts of Bergamo, Bolzano and La Spezia (4.21 - 4.16 - and 5.32 micrograms/l respectively) is 40% lower than chromium concentration observed in people living in the districts of Agrigento and Milan. The high rate of chromium elimination in people living in Milan (10,39 micrograms/l) depend upon the high chromium concentration in drinking water of this city (10.40 micrograms/l). In the 78% of urine samples a chromium concentration was found corresponding to or lower than 10 micrograms/l.

Chromium↗
PubMed1975

[Studies on the behavior of chromium in serum and urine in polytraumatized patients as well as on the chromium concentration of various infusion solutions].

Determinations of the oligoelement chromium were carried out by flameless atomic absorption spectroscopy in serum, whole blood, and urine of patients, undergoing intensive care, as well as in a great part of the solutions used for parenteral nutrition. With rising amino acid and protein content, respectively, the chromium content of the infusion solutions increased due to contamination. Pure nonglucose-carbohydrate-electrolyte solutions contained 16.5-49.0 mug chromium/litre, amino acid-carbohydrate solutions 36.5-105.0 mug chromium/litre and human albumin solutions, depending on concentration, 86.9-394.2 mug chromium/litre. The average chromium concentration in the patients' serum was 11.3 +/- 0.26 mug/litre, which is twenty times more than the normal values determined by this method, and increased from 8.3 to 16.4 mug/litre within the first seven days. The urinary chromium concentrations were 37.7 +/- 4.1 mug/litre, being three times higher than the average serum values, but remained constant from day to day. The approximate chromium administration by parenteral infusion therapy was 160-250 mug chromium/day, the urinary chromium excretion was 111 +/- 20.5 mug/day. Consequently, great amounts of parenterally supplied chromium seem to be stored in the patients' tissues. Effects and risks for the organism caused by these unphysiological chromium concentrations are discussed.

Accidents, Traffic↗
PubMed1992

Simultaneous determination of chromium(III) and chromium(VI) in aqueous solutions by ion chromatography and chemiluminescence detection.

A method for the simultaneous determination of chromium(iii) and chromium(vi) in a flow system based on chemiluminescence was developed. A Dionex cation-exchange guard column was used to separate chromium(iii) from chromium(vi), and chromium(vi) was reduced by potassium sulfite, whereupon both species were detected by use of the luminol-hydrogen peroxide chemiluminescence system. Linear calibration for both species was established over the concentration range 1-1000 micrograms l-1. The precision at the 20 micrograms l-1 level was 3.5% for chromium(iii) and 3.3% for chromium(vi), respectively. The detection limit was 0.5 micrograms l-1 for both species. Data were in agreement with Zeeman-effect background corrected atomic absorption spectrometry measurements.

Chromatography, High Pressure Liquid↗
PubMed1978

Whole blood chromium level and chromium excretion in the rat after zinc chromate inhalation.

Studies on absorption and excretion of chromium in the rat exposed to known atmospheric concentrations of zinc chromate in an inhalation chamber and the influence of diurnal variations in physical activity have been carried out. Chromium analyses were performed on samples of blood, urine and faeces using a method for determining chromium in small samples of biological material based on flameless atomic absorption spectrometry. Zinc chromate is absorbed quickly during exposure and excreted mainly via urine. An accumulation of chromium in blood was observed, followed by a slow elimination. It is suggested that chromium from zinc chromate enters the blood in the hexavalent state.

Animals↗
PubMed1977

[Chromium exposure biological indices and clinical findings in chromium plating industry (author's transl)].

According to the investigations carried out on workers of two chromium plating plants, the authors believe that chromium urinary excretion allows to determine the degree of its acute absorption. Moreover, the renal clearance of diffusible chromium allows the evaluation of chromium body burden and is related to the duration as well as to the severity of exposure. This interpretation is supported by the relation between the exposure biological indexes and the clinical and instrumental investigations which make possible the evaluation of lesions caused by chromium exposure, mostly concerning the respiratory system.

Body Burden↗
PubMed1976

Renal chromium accumulation and its relationship to chromium-induced nephrotoxicity.

This report is an attempt to study the renal handling of chromium under in vitro conditions and to relate this to the actions of the ion in the production of nephrotoxicity. Renal slice techniques were employed in these studies and were used to examine the effects of chromium on various renal transport processes. In addition, the accumulation of chromium by the renal tissue has also been studied. Marked accumulation by renal cortical slices of the rat was observed when 51Cr-labeled chromate or dichromate was added to the bathing solution. Some metabolic inhibitors interfered with this uptake process; in addition, some substrates metabolized by renal tissue reduced the accumulation of 51Cr. The use of [51Cr] dichromate and [51Cr]-chromate, as well as alterations in the bathing solution pH, indicated that in the rat chromium can interfere with renal transport processes, but that the oxidation state of this metal is not important. On the other hand, in the rabbit a greater interference with 51Cr uptake was noted at lower bathing solution pHs. This is interpreted to mean that chromate is the effective inhibitor in this species.

Animals↗
PubMed1978

Measurement of chromium VI and chromium III in stainless steel welding fumes with electrom spectroscopy for chemical analysis and neutron activation analysis.

Electron Spectroscopy for Chemical Analysis (ESCA) was explored as a means of studying the oxidation state of chromium in SMAC (coated electrode) stainless steel welding fume collected on Nucleopore filters in the laboratory. Chromuim VI and III (as a percent of the total chromium) obtained from ESCA analysis was applied to results from Neutron Activation Analysis (NAA) to yield an average of 69 microgram chromium VI per sample. Diphenylcarbazide/atomic absorption (DPC/AA) results are reported for samples submitted to an industrial laboratory. Possible chemical species and solubility of chromium VI in stainless steel fumes is discussed in light of analogy between the SMAC process and the manufacturing process for chromates.

Air Pollutants↗
PubMed1977

Chromium deficiency, glucose intolerance, and neuropathy reversed by chromium supplementation, in a patient receiving long-term total parenteral nutrition.

A white female, now age 40 and receiving total parenteral nutrition for more than 5 years, developed unexpected 15% weight loss after 3 1/2 years of regimen, together with peripheral neuropathy confirmed by nerve conduction measurements. An intravenous glucose tolerance test showed that the fractional rate (K) had decreased to 0.89%/min (normal greater than 1.2). There was observed during this glucose infusion a borderline normal insulin response with a fall in plasma free fatty acids and in plasma leucine. During daily infusion of well over 400 g of glucose, the respiratory quotient was 0.66. Chromium balance was negative. Chromium levels were, in blood 0.55 ng/ml (normal 4.9 to 9.5) and in hair 154 to 175 ng/g (normal greater than 500). Regular insulin daily (45 micron) in the infusate nearly maintained euglycemia but despite this, and even with further glucose intake to restore weight loss, intravenous glucose tolerance test (K) and respiratory quotient were unchanged. Administration of insulin was then stopped and 250 microng of Cr added to the daily total parenteral nutrition infusate for 2 weeks. After this the intravenous glucose tolerance test (K) and respiratory quotient became normal (1.35 and 0.78, respectively). Over the next 5 months insulin was not needed and glucose intake had to be reduced substantially to avoid overweight. In this period nerve conduction and well-being returned to normal. With a maintenance addition of chromium to the total parenteral nutrition infusate (tentatively this addition is 20 microng/day) the patient has remained well for 18 months (to July 1976). These results suggest that relatively isolated chromium deficiency in man, hitherto poorly documented, causes 1) glucose intolerance, 2) inability to utilize glucose for energy, 3) neuropathy with normal insulin levels, 4) high free fatty acid levels and low respiratory quotient and, 5) abnormalities of nitrogen metabolism.

Adult↗
PubMed1992

Production of 8-hydroxydeoxyguanosine in isolated DNA by chromium(VI) and chromium(V).

Chromium(VI) and Cr(V) compounds increased the concentration of 8-hydroxydeoxyguanosine (oh8dG) in isolated DNA, whereas no such increase was seen with Cr(III). Furthermore, incubating DNA with H2O2 and Cr(VI) or Cr(V) potentiated the formation of oh8dG above levels observed with either chromium compound alone. In the presence of catalase, the increase in DNA oxidation observed with Cr(VI) was inhibited, the base oxidation observed being equivalent to background levels, and this indicated involvement of H2O2 in the mechanism. Glutathione did not enhance chromium-induced formation of this oxidized base. These results help to explain a mechanism of chromium-induced DNA oxidation involving H2O2 via a Fenton-type reaction.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1991

In vivo nephrotoxicity induced in mice by chromium(VI). Involvement of glutathione and chromium(V).

The role of glutathione (GSH) and chromium (V) in chromium (VI)-induced nephrotoxicity in mice was investigated at 24 h after K2Cr(VI)2O7 ip injection. Nephrotoxicity was assessed by measurements of relative kidney weight and serum urea nitrogen. Cr(VI) nephrotoxicity was accompanied by decreased renal GSH and glutathione reductase (GSSG-R) levels. Pretreatment with buthionine sulfoximine, an inhibitor of GSH biosynthesis, enhanced Cr(VI)-induced nephrotoxicity, and remarkably diminished kidney GSH and GSSG-R levels. In contrast, pretreatment with glutathione methyl ester, a GSH-supplying agent, prevented Cr(VI) from exerting a harmful effect on mouse kidney and restored kidney GSH level. Administration of a Cr(V) compound, K3Cr(V)O8, induced much higher toxicity in mouse kidney than Cr(VI), but it failed to diminish renal GSH level. Another Cr(V) compound, Cr(V)-GSH complex, and Cr(III) nitrate did not cause a nephrotoxic effect in mice. The mechanism of Cr(VI)-induced nephrotoxicity was explained using GSH and Cr(V).

Animals↗
PubMed1992

Differential determination of chromium(VI) and total chromium in natural waters using flow injection on-line separation and preconcentration electrothermal atomic absorption spectrometry.

A rapid, sensitive and selective method for the differential determination of CrIII and CrVI in natural waters is described. Chromium(vi) can be determined directly by flow injection on-line sorbent extraction preconcentration coupled with electrothermal atomic absorption spectrometry using sodium diethyldithiocarbamate as the complexing agent and C18 bonded silica reversed-phase sorbent as the column material. Total Cr can be determined after oxidation of CrIII to CrVI by potassium peroxydisulfate. Chromium(III) can be calculated by difference. The optimum conditions for sorbent extraction of CrVI and oxidation of CrIII to CrVI are evaluated. A 12-fold enhancement in sensitivity compared with direct introduction of 40 microliters samples was achieved after preconcentration for 60 s, giving detection limits of 16 ng l-1 for CrVI and 18 ng l-1 for total Cr (based on 3 sigma). Results obtained for sea-water and river water reference materials were all within the certified range for total Cr with a precision of better than 10% relative standard deviation in the range 100-200 ng l-1. The selectivity of the determination of CrVI was evaluated by analysing spiked reference materials in the presence of CrIII, resulting in quantitative recovery of CrVI.

Chromium↗