Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CHROMIUM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1993

Determination of chromium in blood and serum: evaluation of quality control procedures and estimation of reference values in Danish subjects.

This paper describes analytical methods to estimate environmental and occupational exposure levels of chromium in blood and serum by Zeeman atomic absorption spectrometry. Also reported is an internal quality control procedure involving a combination of an online quality control and subsequent statistical evaluation of the quality control results to evaluate the performance of the analytical methods. The solubilization of the blood by the proteinase Subtilisin A resulted in a recovery of chromium of 106 +/- 4.5%; the uncertainty was approximately 10% at a chromium level of 1 microgram l-1. The detection limit (LOD) for chromium in serum was 0.17 micrograms l-1 and 0.20 micrograms l-1 for chromium in blood. The LODs were sufficiently low for the determination of chromium in a large fraction of reference populations not occupationally exposed. The present study indicates that reference values for chromium in blood and serum are low but within the range in recent investigations, i.e. 0.04-0.35 micrograms l-1 in serum and 0.12-0.34 micrograms l-1 in human whole blood. The fraction of reference values below LOD was between 0.45 and 0.57 for chromium in serum and blood. Consequently, the reference populations were described by distribution free one-sided tolerance intervals and the precision of the estimation of the tolerance intervals was expressed as coverage intervals. The 95% one-sided tolerance limit calculated for chromium in serum was 0.60 micrograms l-1 with the coverage interval (95 +/- 4.8) percent at a probability of 0.95. Thus, the probability was 0.975 that the tolerance interval covers at least 90.2% of the distribution. In addition, the probability was 0.025 that the tolerance interval covers more than 99.8% of the population. It was only possible to calculate the 90% tolerance interval for chromium in blood with the coverage interval at 0.90 probability. The one-sided tolerance interval for chromium in blood was 0.37 micrograms l-1 with the coverage interval (90 +/- 9.9) percent at a probability of 0.90.

Chromium↗
PubMed1980

Carcinogenicity and mutagenicity of chromium.

Occupational exposure represents the main source of human contamination by chromium. For non-occupationally exposed people the major environmental exposure to chromium occurs as a consequence of its presence in food. Chromium must be considered as an essential element. Its deficiency impairs glucose metabolism. Trivalent chromium salts are poorly absorbed through the gastro-intestinal and respiratory tracts because they do not cross membranes easily. Hexavalent chromium can be absorbed by the oral and pulmonary routes and probably also through the skin. After its absorption, hexavalent chromium is rapidly reduced to the trivalent form which is probably the only form to be found in biological material. Epidemiological studies have shown that some chromium salts (mainly the slightly soluble hexavalent salts) are carcinogens. Lung cancers have, indeed, often been reported among workers in chromate-producing industry and, to a lesser extent, in workers from the chrome-pigment industry. The first attempts to produce cancers in experimental animals by inhalation or parenteral introduction gave negative or equivocal results but, from 1960, positive results have been obtained with various chromium compounds. As for the carcinogenic activity, the mutagenicity of chromium has mainly been found with hexavalent salts. In the majority of assay systems used, trivalent chromium appears inactive. It can be considered as evident, however, that the ultimate mutagen which binds to the genetic material is the trivalent form produced intracellularly from hexavalent chromium, the apparent lack of activity of the trivalent form being due to its poor cellular uptake.

Animals↗
PubMed1989

Generation of PM2 DNA breaks in the course of reduction of chromium(VI) by glutathione.

The carcinogen chromate is efficiently taken up and reduced to chromium(III) compounds by various biological systems. To test the possible DNA damage induced in the course of chromium(VI) reduction, we used a combination of chromate with the reductant glutathione (GSH) as well as a green complex of chromium(V), which is formed in the reaction of chromate with GSH. The combination of chromate and glutathione was found to cause single-strand breaks in supercoiled circular DNA of the bacteriophage PM2. The green chromium(V) complex Na4(GSH)4Cr(V).8H2O, prepared from chromate and glutathione, also cleaved supercoiled PM2 DNA. No DNA-degrading effects were observed with either chromate or the final product of the reaction with GSH, a purple anionic chromium(III) GSH complex. The nature of the buffering agents revealed a strong influence on the extent of DNA strand breaks produced by chromate and GSH. A variation of the GSH concentration in the reaction with chromate and PM2 DNA, performed in sodium phosphate-buffered solutions showed an initial increase in the number of strand breaks at GSH concentrations up to 1 mM followed by a decline at higher GSH concentrations. Since neither chromate, when administered individually, nor the final product of chromium(VI) reduction, the purple chromium(III) GSH complex, produced any detectable DNA cleavage, the critical steps leading to DNA strand breaks occur in the course of the conversion of chromium(VI) to chromium(III) by GSH, the most abundant intracellular low molecular thiol. Moreover, the demonstration that DNA cleavage is induced in the presence of the chromium(V) complex identifies chromium(V) as the oxidation state of the metal, which is involved in the steps leading to DNA-damaging effects of chromate.

Bacteriophages↗
PubMed2006

Chromium(VI) biosorption by dried Rhizopus arrhizus: effect of salt (NaCl) concentration on equilibrium and kinetic parameters.

Some industrial wastewaters contain high quantities of salts besides heavy metal ions. The presence of salt ions leads to high ionic strength, which may significantly affect the performance of the biosorption process so the effect of salts on the biosorption of heavy metal ions should be investigated. In this study the biosorption of chromium(VI) from saline solutions on dried Rhizopus arrhizus was studied as a function of pH, initial chromium(VI) and salt (NaCl) concentrations in a batch system. The biosorption capacity of R. arrhizus strongly depended on solution pH and maximum chromium(VI) sorption capacity of sorbent was obtained at pH 2.0 both in the absence and in the presence of increasing concentrations of salt. Chromium(VI)-salt biosorption studies were performed at this pH value. Equilibrium uptakes of chromium(VI) increased with increasing chromium(VI) concentration up to 250mgl(-1) and decreased considerably by the presence of increasing concentrations of salt. At 100mgl(-1), initial chromium(VI) concentration, dried R. arrhizus biosorbed 78.0mgg(-1) of chromium(VI) in 72h without salt medium. When salt concentration was raised to 50gl(-1), this value dropped to 64.0mgg(-1) of chromium(VI) at the same conditions resulting in 17.9% decrease of biosorption capacity. The equilibrium sorption data were analysed by using Freundlich, Langmuir, Redlich-Peterson and Langmuir-Freundlich (Sips), the two and three parameters adsorption models, using non-linear regression technique and isotherm constants were evaluated depending on salt concentration. The Langmuir-Freundlich (Sips) was the best suitable adsorption model for describing the biosorption of chromium(VI) individually and in salt-containing medium. Pseudo-first-order, pseudo-second-order and saturation type kinetic models described the biosorption kinetics accurately at all chromium(VI) concentrations in the absence and in the presence of changing concentrations of salt. Isotherm and saturation type kinetic constants varied due to the level of salt were expressed as a function of initial salt concentration.

Adsorption↗
PubMed2004

Estimation of diffusion coefficient of chromium in colloidal silica using digital photography.

In order to study the effectiveness of using colloidal silica, NYACOL DP5110, to stabilize chromium-contaminated soil, the diffusion of chromium in colloidal silica gel was estimated from laboratory experiments. To measure diffusion coefficients of chromium in the colloidal silica gel, a new measurement method based on digital photography was introduced. A series of experiments were designed and conducted to validate this new method and to estimate the diffusion coefficients of chromium in the colloidal silica gel. Accuracy of the proposed method was evaluated by several differentways. It was found that the apparent diffusion coefficient of chromium in colloidal silica gel ranged from 1.76 to 8.48 x 10(-10) m2/s depending mainly on the concentration of silica in the gel with chromium concentration less than 10(-2) M. Higher silica concentrations yielded lower diffusion coefficients due to the obstruction to the free movement of chromium. The adsorption isotherm of chromate to colloidal silica gel was found to be linear at pH 7; the partition coefficient was calculated to be 0.549 L/g. Mass balance calculations were performed to evaluate the accuracy of the proposed method and found that the measuring error was less than 6.5%. Based on the test data, the estimation of diffusion coefficients for chromium in colloidal silica gel using digital photography seems to be accurate and precise. This method is suitable for analyzing colored chemicals inside clear/white gels. From the results, it can be concluded that the gel behaves as a porous material with silica network forming continuous solid phase and its pore space saturated with water. The chromium ions diffuse in porous silica gel on a tortuous path. Therefore, the bulk diffusion dominates. Thus, the silica can be represented as a fix and impenetrable immersion in the solution. The presence of these motionless silica chains leads to an increase in the mean path of the diffusing molecules between two points in the system. On the basis of the test results, it can also be concluded that colloidal silica, NYACOL DP5110, for in-situ treatment of chromium-contaminated soils seems to be ineffective. Further research of more realistic simulation of diffusion and refined gel formulation with the capacity to convert the chromium to an immobile form is recommended.

Chromium↗
PubMed2004

Bioaccumulation of chromium from tannery wastewater: an approach for chrome recovery and reuse.

The presence of chromium in the effluent is a major concern for the tanning industry. Currently, chemical precipitation methods are practiced for the removal of chromium from the effluent, but that leads to the formation of chrome-bearing solid wastes. The other membrane separation and ion exchange methods available are unfeasible due to their cost. In this study, the removal of chromium from tannery effluent has been carried out using abundantly available brown seaweed Sargassum wightii. Simulated chrome tanning solution was used for the standardization of experimental trials. Various factors influencing the uptake of chromium, viz., quantity of seaweed, concentrations of chromium, pH of the chrome-bearing wastewater, and duration of treatment, have been studied. Chemical modification of the seaweed through pretreatment with sulfuric acid, magnesium chloride, and calcium chloride showed improved uptake of chromium. Langmuir and Freundlich isotherms have been fitted for various quantities of seaweed. The dynamic method of treatment of protonated seaweed with simulated chrome tanning solution at a pH of 3.5-3.8 for a duration of 6 h gave the maximum uptake of about 83%. A similar uptake has been established for commercial chrome tanning wastewater containing the same concentration of chromium. The Sargassum species exhibited a maximum uptake of 35 mg of chromium per gram of seaweed. Fourier transform infrared spectroscopy, energy-dispersive X-ray analysis, and flame photometry studies have been carried out to understand the mechanistic pathway for the removal of chromium. The potential reuse of chromium-containing seaweed for the preparation of basic chromium sulfate (tanning agent) has been demonstrated.

Animals↗
PubMed2004

Stereoselective synthesis of atropisomeric korupensamines A and B utilizing planar chiral arene chromium complex.

Naphthyl tetrahydroisoquinoline alkaloids, atropisomeric korupensamines A and B and ent-korupensamine B, were synthesized by syn-selective cross-coupling of a planar chiral arene chromium complex with naphthylboronic acid and subsequent axial isomerization or tricarbonylchromium migration to the inverted arene face as a key step. Palladium(0)-catalyzed cross-coupling of planar chiral arene chromium complex 12 with naphthylboronic acid 9 gave syn-biaryl coupling product 13. syn-Biaryl chromium complex 13 was heated in 1:1 mixture of di-n-butyl ether and 1,2-dichloroethane to give a face-inverted anti-biaryl chromium complex 14 without axial isomerization. Korupensamine A was synthesized from the syn-biaryl chromium complex 13 via o-formyl syn-biaryl chromium complex 10, and ent-korupensamine B was prepared from the face-inverted anti-biaryl chromium complex 14. On the other hand, difluoro-substituted syn-biaryl chromium complex 40 with a formyl group afforded anti-biaryl chromium complex 41 containing a rotated central bond by heating in xylene. The chromium-complexed fluorine atom was easily substituted with an isopropoxy group by nucleophilic substitution. Use of these reactions allowed (+)-2-bromo-3,5-difluorobenzaldehyde chromium complex (37) as a single chiral source to be converted to atropisomeric korupensamines A and B, respectively.

Chromium Compounds↗
PubMed2002

Role of different valence states of chromium in the elicitation of allergic contact dermatitis.

Chromium, a known contact sensitizer, is present at high levels in certain detergent bars (40-50 p.p.m.) sold in India. A concern was whether chromium present in such detergent bars could sensitize users or their use lead to the elicitation of allergic contact dermatitis. Chromium present in detergent bars was analyzed for its valence state. It was found to be trivalent [Cr (III)] and not hexavalent [Cr (VI)]. An elicitation test on normal volunteers, as well as on volunteers who were sensitive to chromium, was carried out to determine the elicitation potential of chromium (III) in the bars. Of the 48 volunteers who completed the study, 30 did not show any positive response to either potassium dichromate, the positive control, or the detergent bar containing chromium (III). 18 volunteers who were identified as chromium-sensitive showed a positive response to potassium dichromate but not to the detergent bar containing trivalent chromium. This study clearly showed that the detergent bar with 40-50 p.p.m. of trivalent chromium did not elicit any allergic contact dermatitis even in individuals known to be chromium-sensitive. Hexavalent chromium (potassium dichromate) did however, elicit allergic contact dermatitis in these subjects.

Chromium↗
PubMed2003

Chromium inhibits transcription from polycyclic aromatic hydrocarbon-inducible promoters by blocking the release of histone deacetylase and preventing the binding of p300 to chromatin.

Co-contamination with complex mixtures of carcinogenic metals, such as chromium, and polycyclic aromatic hydrocarbons is a common environmental problem with multiple biological consequences. Chromium exposure alters inducible gene expression, forms chromium-DNA adducts and chromium-DNA cross-links, and disrupts transcriptional activator-co-activator complexes. We have shown previously that exposure of mouse hepatoma Hepa-1 cells to chromate inhibits the induction of the Cyp1a1 and Nqo1 genes by dioxin. Here we have tested the hypothesis that chromium blocks gene expression by interfering with the assembly of productive transcriptional complexes at the promoter of inducible genes. To this end, we have studied the effects of chromium on the expression of genes induced by benzo[a]pyrene (B[a]P), another aryl hydrocarbon receptor agonist, and characterized the disruption of Cyp1a1 transcriptional induction by chromium. Gene expression profiling by using high density microarray analysis revealed that the inhibitory effect of chromium on B[a]P-dependent gene induction was generalized, affecting the induction of over 50 different genes involved in a variety of signaling transduction pathways. The inhibitory effect of chromium on Cyp1a1 transcription was found to depend on the presence of promoter-proximal sequences and not on the cis-acting enhancer sequences that bind the aryl hydrocarbon receptor-aryl hydrocarbon receptor nuclear translocator complex. By using transient reporter assays and chromatin immunoprecipitation analyses, we found that chromium prevented the B[a]P-dependent release of HDAC-1 from Cyp1a1 chromatin and blocked p300 recruitment. These results provide a mechanistic explanation for the observation that chromium inhibits inducible but not constitutive gene expression.

Animals↗
PubMed1998

Chromium research from a distance: from 1959 to 1980.

More than 50 years of work have led to the recognition of trivalent chromium as an essential element. Shortly after its identification as an essential element in 1959, its interaction with insulin in vitro and in vivo was established, and the site of action identified as the insulin-sensitive cell membrane. Despite other early clinical successes with chromium supplementation, four major problems have influenced the rate of progress since then: 1) chromium analysis; 2) interaction of chromium with other dietary factors; 3) diagnosis of chromium status; and 4) other controversies, such as the carcinogenic potential of chromium (since disproved) and the lack of an effect on glucose tolerance even in chromium deficient organisms (now explained). These controversies have mostly dissipated as new knowledge integrated seemingly irreconcilable facts and opinions. It is now known that chromium may potentiate the action of insulin either by an effect on insulin dependent functions, or by maintaining these functions with less insulin, or by a combination of both. Despite much progress in the last 30 years, major challenges in chromium research remain, such as the development of practical methods for diagnosing chromium deficiency. Of several approaches for solving this problem, the most feasible might be to standardize the urinary chromium response following an insulinogenic challenge, such as an oral load of glucose or of glucose plus fructose (for maximal stimulation) with urine collection before and during the 2-hour test.

Chromium↗
PubMed2006

Review of the evidence regarding the carcinogenicity of hexavalent chromium in drinking water.

Recent analyses have revealed that 38% of municipal sources of drinking water in California have detectable levels of hexavalent chromium. This observation provided new impetus to characterize the carcinogenic risk associated with oral exposure to hexavalent chromium in drinking water. Notwithstanding the well-characterized increases in cancer associated with inhalation exposure to this chemical, the marked reduction of hexavalent chromium to trivalent chromium in the stomach suggests that exposure to hexavalent chromium in drinking water may not pose a carcinogenic risk. A reevaluation of studies that investigated the toxicokinetics, the genotoxicity, and the mechanism of carcinogenicity of hexavalent chromium, as well as the available human and animal cancer studies, was undertaken to determine if there is evidence that exposure to this chemical in drinking water may pose a carcinogenic risk. Mechanistic studies suggest the potential for a carcinogenic response if hexavalent chromium enters cells. Both toxicokinetic and genotoxicity studies indicate that a portion of an orally administered dose of hexavalent chromium is absorbed and gets into cells of several tissues, causing DNA damage. The only lifetime oral study of hexavalent chromium in animals conducted thus far yielded a statistically significant increase in stomach tumors compared to controls. Also, in a limited-term cancer study, co-exposure to hexavalent chromium in drinking water and ultraviolet light produced skin tumors in mice. The only available cancer study of humans exposed to hexavalent chromium in drinking water revealed a statistically significant increase in stomach tumors. Moreover, a meta-analysis of occupational studies also revealed a statistically significant increase in stomach cancers. The increases in stomach tumors in both human and animal studies, along with the toxicokinetic, genotoxic, and mechanistic data, suggest that oral exposure to this agent appears to pose a carcinogenic risk.

Animals↗
PubMed1989

Chromium(V) is produced upon reduction of chromate by mitochondrial electron transport chain complexes.

Incubation of chromate with isolated rat liver submitochondrial particles under anaerobic conditions in vitro results in reduction of chromium(VI) and formation of chromium(V). In the presence of NADH, submitochondrial particles (SMPs) were active in reducing chromate as shown by UV-vis spectroscopic studies, and forming a chromium(V) species which was detectable by electron paramagnetic resonance spectroscopy. In the presence of succinate, SMPs were less effective in reducing chromate and forming chromium(V) relative to their NADH-dependent activity. However, SMPs showed a higher rate of oxygen depletion with NADH as compared to succinate as substrate, suggesting that differences in the NADH-dependent versus succinate-dependent chromate-reductase activity of SMPs is probably due to differences in efficiency of electron donation by succinate and NADH. The use of specific electron transport chain inhibitors allowed the sites of chromium(VI) reduction and chromium(V) formation in SMPs to be determined. Rotenone, antimycin and cyanide all produced approximately 40% inhibition of the NADH-dependent chromate-reductase activity. Thus, complex I (NADH:ubiquinone oxidoreductase) appears to be responsible for the inhibitor-insensitive, and complex IV (ferrocytochrome c:oxygen oxidoreductase) for the inhibitor-sensitive NADH-dependent chromium(VI) reduction and chromium(V) formation. Cyanide and antimycin produced approximately 50% inhibition of the succinate-dependent chromate-reductase activity of SMPs, while no detectable inhibition was observed with rotenone. These results confirm the chromate-reductase activity of complex IV, and suggest that complex II (succinate:ubiquinone oxidoreductase) is responsible for the inhibitor-insensitive succinate-dependent chromate-reductase activity of SMPs. Since chromium(VI) is effectively metabolized by electron transport chain complexes of the mitochondrial inner membrane in vitro, and chromium(V) is formed as an intermediate in the process, mitochondria may play a role in chromium(VI) carcinogenesis.

Animals↗
PubMed1994

Preferential formation and repair of chromium-induced DNA adducts and DNA--protein crosslinks in nuclear matrix DNA.

The distributions of chromium-DNA adducts and DNA-protein crosslinks induced by treatment of intact CHO cells with carcinogenic chromium were examined in distinct chromatin subfractions: a chromatin subfraction released by digestion of isolated nuclei with micrococcal nuclease (1SF, 14% of total nuclear DNA), bulk chromatin (74% of total DNA) and a nuclear matrix fraction (12% of total DNA). The identity of the matrix fraction was confirmed by hybridization of DNA from each subfraction with a cDNA probe prepared from total mRNA isolated from CHO cells, which showed that the 1SF and nuclear matrix fractions were 2.3- and 3.8-fold enriched in actively transcribed genes respectively, compared to total unfractionated DNA. Immediately following treatment of cells with 150 microM sodium chromate for 2 h the binding of chromium to each chromatin fraction was found to be non-uniform. Compared with total unfractionated nuclei, the nuclear matrix fractions were enriched in chromatin-bound chromium (3.4-fold), whereas the bulk chromatin fraction was relatively depleted (0.5-fold). Approximately 13% of nuclear chromium was associated with the detergent-soluble lipid component of nuclei. A similar distribution of chromatin-bound chromium was also apparent 24 h after the chromate treatment. Immediately after the 2 h chromate treatment, chromium-DNA adducts were detected in all the chromatin subfractions. Total nuclear and bulk chromatin DNA contained similar levels of this type of damage. The 1SF fraction was depleted approximately 3-fold in this type of damage compared with total nuclear DNA. In contrast, the nuclear matrix was markedly enriched in chromium-DNA adducts (approximately 4-fold compared with total nuclear DNA) at this time. As previously demonstrated, chromium-DNA adducts in total nuclear DNA decreased within the first 24 h, but thereafter persisted at a similar level. Chromium-DNA adducts in nuclear matrix DNA also reached maximum levels at the end of the 2 h treatment and decreased to 68% and 39% of this level by 24 and 48 h after treatment respectively. In contrast, the adduct levels in the 1SF and bulk chromatin fractions did not change up to 48 h after treatment. Chromium-induced DNA-protein crosslinks, which were stable to 8 M urea and 2% SDS, occurred almost exclusively in the nuclear matrix fraction. The crosslinks in this fraction reached a maximum level at the end of the 2 h treatment, but returned to control levels 24 h later.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Exercise training and dietary chromium effects on glycogen, glycogen synthase, phosphorylase and total protein in rats.

The effects of exercise training and dietary chromium intake on rat liver and muscle glycogen metabolism, tissue and body weight and feed consumption were examined. After 16 wk of training, liver, gastrocnemius and biceps femoris glycogen concentrations were higher in the trained compared to sedentary groups, independent of dietary chromium. There was a chromium x training interaction on glycogen synthase activities in the liver and gastrocnemius muscle. Liver glycogen phosphorylase activities (expressed per g liver) were lower in the chromium-supplemented rats as compared to the non-supplemented rats after 5 wk of dietary treatment, but were similar after 8 wk and higher after 18 wk. Gastrocnemius phosphorylase activity (expressed per mg protein) was lower in the trained rats as compared to the sedentary rats after 16 wk, independent of dietary chromium. Biceps femoris phosphorylase activities were not altered due to training or dietary chromium. Total protein concentration increased in the liver but decreased in the gastrocnemius due to dietary chromium. In summary, liver glycogen synthase and phosphorylase activities were dependent upon dietary chromium. Dietary chromium altered gastrocnemius synthase, but not phosphorylase activities. Changes in enzyme activities may be related to the chromium-dependent effects on liver protein and the chromium and training-dependent effects on gastrocnemius total protein.

Animals↗
PubMed1999

The role of chromium in nutrition and therapeutics and as a potential toxin.

Since the 1950s it has been known that chromium is important for the expression of glucose tolerance and that in chromium deficiency the use of glucose is impaired. Chromium has been recognized as an essential nutrient since the finding of low-molecular-weight chromium as a biological modifier of insulin action and the clinical demonstration of deficiency associated with glucose intolerance that responded to the administration of chromium. The major impediment to the use of orally administered chromium is poor absorption of trivalent chromium in its inorganic form. Trivalent chromium is more available in yeast and, more recently, as chromium picolinate for oral absorption. The widespread use of these supplements has resulted in controversy regarding chromium's role as a nutrient, its use for treatment of insulin resistance, and its potential toxicity. This report reviews the evidence for the potential toxicity of chromium supplements in contrast with its usefulness as a nutrient or therapeutic agent in the treatment or prevention of insulin resistance.

Chromium↗
PubMed1999

Exposure to hexavalent chromium does not increase 8-hydroxydeoxyguanosine levels in Korean chromate pigment workers.

This study was performed to determine whether chromium exposure increased 8-hydroxydeoxyguanosine levels in respiratory epithelial and white blood cells of chromate pigment workers. The subjects of this study were 22 chromium pigment workers and 16 controls in a chromate pigments factory. To estimate the level of exposure, hexavalent chromium concentrations in the factory air were measured. Chrominum concentrations of venous blood and spot urine, and 8-hydroxydeoxyguanosine levels in DNA extracted from sputum and white blood cells were determined. Correlation coefficients were calculated between them and their statistical significance was tested. Hexavalent chromium concentration in the factory air ranged from below limit of detection to 0.5150 mg/m3. Chromium levels in blood and 8-hydroxydeoxyguanosine levels in DNA extracted from venous blood and sputum were not statistically different between the two groups. Urine chromium level was significantly higher among workers. Among the correlation coefficients between blood chromium concentration, urine chromium concentration, blood 8-OH-dG level, and sputum 8-OH-dG level, none was statistically significant for workers, controls, and total subjects. Duration of employment did not show any significant correlation with those four variables, either. These results suggest that neither the hydroxyl radical nor 8-hydroxydeoxyguanosine is formed by the reduction of hexavalent chromium, or that one or both of these is formed and then effectively removed by oxygen free radical scavengers or 8-hydroxydeoxyguanosine repair enzymes. Since increased exposure to hexavalent chromium did not result in increased 8-hydroxydeoxyguanosine levels, it is unlikely that hexavalent chromium induces lung cancer through 8-hydroxydeoxyguanosine formation.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1990

The effect of chromium picolinate on serum cholesterol and apolipoprotein fractions in human subjects.

Chromium has been implicated as a cofactor in the maintenance of normal lipid and carbohydrate metabolism. A deficiency of chromium results from diets low in biologically available chromium. Picolinic acid, a metabolite of tryptophan, forms stable complexes with transitional metal ions, which results in an improved bioavailability of the metal ion chromium. To determine whether or not chromium picolinate is effective in humans, 28 volunteer subjects were given either chromium tripicolinate (3.8 micromol [200 micrograms] chromium) or a placebo daily for 42 days in a double-blind crossover study. A 14-day period off capsules was used between treatments. Levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, and apolipoprotein B, the principal protein of the LDL fraction, decreased significantly while the subjects were ingesting chromium picolinate. The concentration of apolipoprotein A-I, the principal protein of the high-density lipoprotein (HDL) fraction, increased substantially during treatment with chromium picolinate. The HDL-cholesterol level was elevated slightly but not significantly during ingestion of chromium picolinate. Only apolipoprotein B, of the variables measured, was altered significantly during supplementation with the placebo. These observations show that chromium picolinate is efficacious in lowering blood lipids in humans.

Adult↗
PubMedDate not supplied

Chromium (III) metabolism by the kidney.

The kidney is the principal route of excretion of the essential trace element chromium. Previous studies suggest that five to 40 percent of plasma chromium (III) is ultrafilterable and that 60 to 95 percent of filtered chromium is reabsorbed in the renal tubule. However, less than five percent of a stable Cr (III)-EDTA chelate is reabsorbed; therefore, this complex has been used to measure glomerular filtration. An increased fractional excretion of chromium may result from a glucose challenge or from a volume diuresis. These mechanisms have been postulated to cause an increased urinary excretion of chromium in patients with diabetes mellitus. Investigations of chromium metabolism and excretion must be interpreted with caution because chromium analysis is known to be subject to many sources of error and chromium (III) salts may not be physiologically equivalent to biological chromium complexes. Analytical refinements should permit further delineation of normal chromium homeostatic mechanisms and allow better identification of abnormalities in chromium metabolism.

Animals↗