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PubMedDate not supplied

[Chromosome aberrations in a lymphocyte culture from persons in contact with chromium].

A detailed analysis was carried out of chromosome aberrations induced by chromium compounds in a lymphocyte culture of persons which were in contact with the compounds. It is shown that the frequency of cells with chromosome aberrations depends on the age and duration of contact with chromium and does not depend on the sex. It was marked that hexavalent chromium compounds have a higher cytogenetic activity. Mechanisms of mutagenic action of heavy metal ions are discussed (taking chromium as an example).

Adult↗
PubMed1995

[Preconcentration of trace chromium in natural water with activated carbon and its determination by colorimetry].

The adsorption and desorption behavior of chromium was studied. Trace chromium in water could be adsorbed on activated carbon at pH 9-10, then eluted with 0.5% sulfuric acid and determined by colorimetry. The content of chromium could be concentrated by 100 times. For sample, the coefficient of variation of 8 parallel determinations was 7.7%. The proposed method has been applied to the determination of trace chromium in natural waters with the recovery of 71.4%-90.0%, and with the detection limit of 0.04 microgram/L.

Carbon↗
PubMed1995

Effects of chromium on basal and insulin-induced tyrosine phosphorylation in H4 hepatoma cells: comparison with phorbol-12-myristate-13-acetate and sodium orthovanadate.

Chromium, in its various forms, is recognized both as a human carcinogen and as a nutrient essential in glucose homeostasis. Although the genotoxicity of this element is associated with its carcinogenic properties, the manner in which chromium mediates its epigenetic effects on cells, including its ability to potentiate insulin action, is not known. In the current studies, Western blotting with antiphosphotyrosine antibodies was used to study the effects of chromium on protein tyrosine phosphorylation in intact H4 rat hepatoma cells. Treatment of cells with hexavalent chromium [Cr(VI)] was found to induce the tyrosine phosphorylation of three prominent sets of proteins, having median molecular masses of 210, 125, and 87 kDa. Cr(VI) pretreatment also inhibited the insulin-induced tyrosine phosphorylation of the major substrate of the insulin receptor kinase, insulin receptor substrate-1, and its subsequent association with the 85-kDa regulatory subunit (p85) of phosphatidylinositol 3'-kinase. Furthermore, Cr(VI) was found to alter the pattern of other p85-binding (insulin-induced) phosphoproteins that were distributed throughout the soluble and particulate fractions of cells. Virtually all of the alterations in basal and insulin-induced phosphorylations associated with Cr(VI) treatment were also observed in cells treated with the protein kinase C (PKC) agonist phorbol-12-myristate-13-acetate. However, the effects of Cr(VI) were determined to be independent of PKC activity, because they were sustained in PKC-depleted cells. The pattern of phosphoproteins induced by Cr(VI) also had similarities to the pattern generated in response to the phosphatase inhibitor sodium orthovanadate. However, several specific differences, including the ability of vanadate to increase insulin receptor beta subunit autophosphorylation [i.e., an effect not observed with Cr(VI)], indicated that these agents modulate phosphorylation by distinct mechanisms. The ability of Cr(VI) to alter the phosphorylation state of key regulatory proteins in a manner similar to that of other biologically active agents suggests a mechanism by which this element can modulate the growth and metabolism of cells.

Animals↗
PubMed1993

A simple method of chromium coating using a ferrotype plate for scanning electron microscopy.

A simple method of chromium coating was developed. A chromium ferrotype plate for drying photoprints was used as a target of a planar magnetron ion-sputter coater. As a result, a high quality chromium film was obtained on dried specimens at room temperature without cooling. The grain size, measuring 1-2 nm in diameter, was small enough for observations of ultrastructures such as F1 particles on the inner mitochondrial membrane. In routine studies under x 100,000, however, chromium coating was not recommended because of its low emission of secondary electrons.

Chromium↗
PubMed1993

Recent advances in the clinical and biochemical effects of chromium deficiency.

Signs and symptoms of Cr deficiency in the general population appear widespread due not only to suboptimal intake of dietary Cr but also the elevated consumption of simple sugars that increase Cr losses. A large percentage of the subjects with marginally impaired glucose tolerance or elevated circulating insulin respond to supplemental Cr. The mechanism of action of Cr in the potentiation of insulin activity as well as the exact structure of biologically active chromium is unclear but significant progress is being made. In summary, recent advances in chromium nutrition research strengthen the association of insufficient dietary chromium and risk factors maturity-onset diabetes and cardiovascular diseases and further document the role of chromium in the maintenance of optimal health.

Animals↗
PubMed1995

[Does multiple use of a cuprophan dialyser influence levels of chromium and cadmium during hemodialysis in patients with chronic kidney failure?].

UNLABELLED: 42 patients between 21 and 63 years of age with chronic renal failure (CRF) treated with haemodialysis and 16 healthy subjects between 19 and 72 years of age were observed. All patients were divided in two groups: 15 patients treated with haemodialysis with cuprophan dialyser used first time and 27 patients treated with haemodialysis with cuprophan dialyser used more than three times. The blood samples in haemodialyzed patients were withdrawn four times: just before dialysis, during haemodialysis (after one hour of dialysis at both ends of the dialyzer) and after haemodialysis. Chromium and cadmium concentration in all examined groups, in dialysis fluid and in demineralized water were measured by flame atomic absorption spectrophotometry. During haemodialysis a decrease of serum chromium concentration and an increase of serum cadmium concentration in two groups of haemodialyzed patients were observed. No significant differences in serum chromium and cadmium concentration before dialysis, during dialysis and after dialysis were observed between two groups of haemodialyzed patients. CONCLUSION: The multiple use of cuprophan dialser did not influence significantly serum chromium and cadmium concentration in haemodialyzed patients.

Adult↗
PubMed1996

Chromium picolinate.

Chromium picolinate is a dietary supplement gaining in popularity among Americans, especially those seeking a weight-reduction program. Although the mechanism(s) responsible for the purported actions of chromium picolinate have not been thoroughly investigated, studies suggest that the biochemical, physiological, and behavioral actions of chromium picolinate may be a consequence of the effects of picolinic acid on the central nervous system. Analogues of picolinic acid have been shown to induce profound alterations in the metabolism of serotonin, dopamine, and norepnephrine in brain. Thus, caution should be used with chromium picolinate supplements especially by individuals prone to behavioral disorders.

Adult↗
PubMed1977

Effects of heavy metals (cadmium, copper, chromium and lead) on a freshwater snail: Biomphalaria glabrata Say (Gastropoda, Prosobranchia).

This study concerns the effects of heavy metals (cadmium, copper and chromium) on the mortality and fecundity of the adults of Biomphalaria glabrata and the viability of their embryos. Embryos were also tested for lead. The concentrations used ranged from 0 ppm to 4.0 ppm for Cd2+ and Cu2+ and from 0 to 1.4 ppm for Cr6+. Cadmium and copper were far more toxic than chromium. Fertility was abolished by 0.1 ppm of cadmium and copper and fecundity was severely affected by chromium. Some evident sublethal effects were observed. Survival of the hatchlings treated with chromium was of the same order of magnitude as that of the controls and sexual maturity did not show any delay. Forty-one percent of the embryos kept at concentrations of 0.1 ppm Pb2+ completed their development in 51 days, that is, with a delay of 37 days. The hatchlings at 0.1 ppm died after 15 days. The advantages of using freshwater pulmonates as a toxicity test are discussed.

Animals↗
PubMedDate not supplied

Effects of cobalt-chromium alloy surface casting on resistance to deflection fatigue and surface hardness of titanium.

This study investigated the resistance to deflection fatigue and surface hardness of grade 2 titanium bar samples to a portion of which a layer of cobalt-chromium alloy was cast under standard dental laboratory conditions. The uncovered part of the titanium bar was deflected, and the number of loading cycles required to cause a fatigue fracture in the titanium bar was recorded. The Vickers hardness of the titanium bar was measured, and the fracture surface was examined by scanning electron microscope and energy-dispersive spectroscopy. The number of loading cycles was considerably lower in bars with the cobalt-chromium surface cast (83 vs. 13.770 cycles) (P < .001), while the surface hardness of the titanium bar with the cobalt-chromium surface cast was higher than that without the surface cast (Vickers hardness number 329 vs. 178) (P < .001). These findings suggest that the cobalt-chromium surface cast dramatically affects the fatigue resistance of pure titanium, which should be considered when novel implant-supported prostheses made from premanufactured titanium parts are planned.

Analysis of Variance↗
PubMed1998

Investigations on the nephrotoxicity and hepatotoxicity of trivalent and hexavalent chromium compounds.

In contrast to trivalent chromium (Cr(III)) compounds, hexavalent chromium ((Cr(VI)) compounds are oxidizing agents capable of directly inducing tissue damage and possessing carcinogenic, mutagenic and teratogenic potency. After oral or dermal absorption of Cr(VI), the kidney is the main target organ for chromium accumulation, which might result in acute tubular necrosis in humans. In contrast, an acute toxic effect of Cr(VI) on the liver has not yet been described. Therefore, we used two established epithelial cell lines from the kidney (Opossum kidney cells) and the liver (Hep G2 cells) to design an in vitro-assay which is able to examine acute toxic effects of chromium compounds. Cells of both cell lines were treated with various concentrations of Cr(III) and Cr(VI) ranging from 0.01 micromol/l to 1 mmol/l for 24 h. Thereafter, cell morphology, organization of the intracellular cytoskeleton, number of viable cells and mean cell volume were examined. The results show that Cr(VI), but not Cr(III), has an acute cytotoxic effect and causes a dose-dependent loss in cell viability. The effective dose that caused 50% of cell death was 5 micromol/l for kidney epithelial cells and 50 micromol/l for liver epithelial cells. This means that kidney epithelial cells are 10 times more sensitive towards Cr(VI) treatment than liver epithelial cells and this might explain the known nephrotoxicity in vivo. The loss in cell viability was accompanied by a rounding and detachment of the cells and a marked reduction of intracellular F-actin-containing stress fibers. Microtubules and intermediate-sized filaments were observed to be unaffected. Only in the case of kidney epithelial cells, a dose-dependent cell volume increase was observed after Cr(VI) treatment at concentrations up to 50 micromol/l. At higher concentrations, the cell volume decreased due to the high number of cells undergoing lysis and the appearance of cellular fragments. Various chloride channel blockers with different specificities, molecular structures and inhibitory potentials were tested for their ability to prevent Cr(VI)-induced cell damage. None of the channel blockers was able to inhibit cell damage, suggesting that the uptake of Cr(VI) through the general anion transport system of the cell membrane might be only one facet of cellular uptake and toxification. The data presented here not only confirm the different organ-specific effects of Cr(III) and Cr(VI), but also provide a basis for future experiments on the understanding of acute toxicity of Cr(VI) compounds. Moreover, the results demonstrate that the designed in vitro-assay might be a useful tool to prove whether non-toxic Cr(III) can be oxidized to Cr(VI) under specific industrial conditions (for example, in the leather or chrome industry).

Animals↗
PubMed2002

Adsorption and oxidation of aniline and anisidine by chromium ferrocyanide.

The interaction of aniline and p-anisidine with chromium ferrocyanide has been studied. Maximum uptake of both anilines was observed around pH 7. The adsorption data obtained at neutral pH were found to follow Langmuir adsorption. Anisidine was a better adsorbate because of its higher basicity. In alkaline medium (pH>8) both aniline and anisidine reacted with chromium ferrocyanide to give colored products. Analysis of the products by GC-MS showed benzoquinone and azobenzene as the reaction products of aniline while p-anisidine afforded a dimer. IR analysis of the amine-chromium ferrocyanide adduct suggests that the outer metal ion of chromium ferrocyanide and amino group of amines are responsible for the interaction. A possible reaction mechanism for the product formation in alkaline medium has been proposed. The present study suggests that metal ferrocyanides might have played an important role in the stabilization of organic molecules through their surface activity in the prebiotic condensation reactions.

Journal Article↗
PubMed1996

Protective effect of vitamin E on chromium (VI)-induced cytotoxicity and lipid peroxidation in primary cultures of rat hepatocytes.

Pretreatment of primary cultures of rat hepatocytes with alpha-tocopherol succinate (vitamin E) for 20 h prior to exposure to K2Cr2O7 resulted in a marked decrease of chromium (VI)-induced cytotoxicity, as evaluated by the leakage of lactate dehydrogenase, without affecting cellular uptake and the subcellular distribution of chromium. The levels of chromium (VI)-induced lipid peroxidation, as monitored by malondialdehyde formation, were also inhibited by pretreatment with the vitamin. Pretreatment with vitamin E normalized the levels of nonenzymatic antioxidants such as glutathione and vitamin C suppressed by dichromate, and caused a distinct accumulation of vitamin E in hepatocytes. However, vitamin E pretreatment did not affect the activities of enzymatic antioxidants including glutathione reductase, superoxide dismutase, and catalase suppressed by dichromate. These results indicate that the protective effect of vitamin E against chromium (VI)-induced cytotoxicity as well as lipid peroxidation, may be associated more with the level of nonenzymatic antioxidants than the activity of enzymatic antioxidants.

Animals↗
PubMed2006

Effect of culture conditions and mother's age on the sensitivity of Daphnia magna Straus 1820 (Cladocera) neonates to hexavalent chromium.

Daphnia magna is a freshwater cladoceran used worldwide as test organism in aquatic toxicity assays. In Mexico there is a test protocol for this species; nevertheless, some aspects of the controlled neonate production, as well as the possible consequences of the reproducers' culture conditions on the response of neonates to the toxic substance, are not completely known. In the present study, we evaluated the effect of temperature and photoperiod on the acute toxicity of CrVI in D. magna neonates, aimed at providing useful information on the Median Lethal Concentration (LC50) to this heavy metal, which is used as reference toxicant in some laboratories. D. magna was cultured at 20 and 25 degrees C, in combination with two photoperiod values: 16:8 and 12:12 (light:dark) during 40 days; the green microalga Ankistrodesmus falcatus (4x10(5) cells ml(-1)) was supplied as food. Once the reproduction began, the neonates were removed and acute toxicity bioassays at 20 and 25 degrees C were performed, by exposing them to hexavalent chromium. We also determined changes in neonates' size at 20 and 25 degrees C. Chromium toxicity increased along with increasing temperatures, and LC50 values were slightly lower for the first and last clutches in the observed period, but these findings are not conclusive because of the large variability recorded. The average LC50's were 0.2076+/-0.0164 mg l(-1) (at 20 degrees C) and 0.1544+/-0.0175 mg l(-1) (at 25 degrees C). The reproducers' culture temperature had no effect on neonates' sensitivity to chromium, in spite of performing the tests at temperatures either lower or higher than those at which the neonates had been obtained. The length of neonates produced during the first two clutches (<1.25 mm) was significantly lower than that measured in neonates of following reproductions (>1.3 mm), and were smaller at 25 degrees C; however, this did not seem to affect their sensitivity to chromium.

Animals↗
PubMed1987

Evidence for the presence of mutagenic compounds other than chromium in particles from mild steel welding.

A modified Salmonella/microsome liquid culture assay was used to investigate the mutagenicity of the particulate fraction from mild steel welding. Previous reports have implicated compounds of chromium VI as the mutagenic and toxic agents in welding fumes, since only the particles from welding on stainless steel, which contains 15-25% chromium, were mutagenic, whereas particles from welding on mild steel, which contain less than 0.1% chromium, were not mutagenic or toxic. In this investigation, mild steel particles were shown to contain direct-acting and promutagenic compounds that induced frameshift mutations. The mutagenic agents, which were insoluble in sodium phosphate buffer, did not include chromium VI or organic compounds. Further, the expression of mutation appears to require a cell-particle interaction for the release of the mutagenic species from the particles.

Aerobiosis↗
PubMed1993

Homologous physiological effects of phenformin and chromium picolinate.

The insulin-sensitizing drug phenformin, in addition to its clinical utility in type II diabetes, has been reported to lower blood lipids, reduce body fat, enhance cellular immunity, and--in rodents--to increase mean lifespan and retard the development of growth of cancer. Initial studies with the insulin-sensitizing nutrient chromium picolinate indicate that it aids glucose tolerance in type II diabetes, lowers elevated LDL cholesterol, reduces body fat while increasing lean mass, and--in rats--increases median lifespan. These effects are thus analogous to those reported for phenformin; chromium picolinate should be tested to determine whether it likewise has a favorable impact on cellular immunity and cancer risk. The ability of both phenformin and chromium picolinate to increase lifespan suggests that age-related insulin resistance may play a profound role in the aging process. It may not be coincidental that caloric restriction--the best documented technique for increasing lifespan--markedly increases insulin sensitivity. Safe, appropriate measures for promoting lifelong insulin sensitivity include a low-fat diet, exercise training, and supplemental chromium picolinate.

Adipose Tissue↗
PubMed1994

Longevity effect of chromium picolinate--'rejuvenation' of hypothalamic function?

The first rodent longevity study with the insulin-sensitizing nutrient chromium picolinate has reported a dramatic increase in both median and maximal lifespan. Although the observed moderate reductions in serum glucose imply a decreased rate of tissue glycation reactions, it is unlikely that this alone can account for the substantial impact on lifespan; an effect on central neurohormonal regulation can reasonably be suspected. Recent studies highlight the physiological role of insulin as a modulator of brain function. I postulate that aging is associated with a reduction of effective insulin activity in the brain, and this contributes to age-related alterations of hypothalamic functions that result in an 'older' neurohormonal milieu; consistent with this possibility, diabetes leads to changes of hypothalamic regulation analogous to those seen in normal aging. Conversely, promoting brain insulin activity with chromium picolinate may help to maintain the hypothalamus in a more functionally youthful state; increased hypothalamic catecholamine activity, sensitization of insulin-responsive central mechanisms regulating appetite and thermogenesis, and perhaps trophic effects on brain neurons may play a role in this regard. Since both the pineal gland and thymus are dependent on insulin activity, chromium may aid their function as well. Thus, the longevity effect of chromium picolinate may depend primarily on delay or reversal of various age-related changes in the body's hormonal and neural milieu. A more general strategy of hypothalamic 'rejuvenation' is proposed for extending healthful lifespan.

Aging↗
PubMed2004

Effect of different doses of chromium picolinate on protein metabolism in infant rats.

This 12-day study was conducted to evaluate the effects of three different levels of dietary chromium (100, 200, and 500 microg/day) in the form of chromium picolinate (CrPic) on growth and protein use in weaned rats. No significant effect of CrPic on body weight gain, food intake, or food conversion rate was observed. Elevated doses of CrPic seemed to increase muscle mass, either by stimulating protein anabolism by activation of insulin by chromium or by lowering protein degradation. However, these effects had no repercussions on overall growth, suggesting that any anabolic effect of chromium due to the action of insulin was probably marginal.

Animals↗
PubMed1998

Electron paramagnetic resonance, kinetics of formation and decomposition studies of (bis(hydroxyethyl)amino-tris(hydroxymethyl)-methane)oxochromate(V): a model chromium(V) complex for DNA damage studies.

A new chromium complex, (bis(hydroxyethyl)amino-tris(hydroxymethyl)methane)oxochromate(V), has been characterized by epr spectroscopy. The chromium(V) complex was formed by the ligand displacement reaction of bis(2-ethyl-2-hydroxybutanato) oxochromate(V) with bis(hydroxyethyl)amino-tris(hydroxy-methyl)methane (BT). Both epr and kinetic data indicate that the reaction proceeds through a chromium(V) intermediate. Kinetics of formation of the intermediate exhibit a rate saturation at higher [BT] (> 30 mM) indicating a rate law constituting an equilibrium between the parent Cr(V) complex and the bis-tris ligand followed by a pure first order process. The g-value of the intermediate is consistent with a Cr(V) complex in which the BT is coordinated in a bidentate fashion replacing a coordinated hydroxy butanoic acid ligand, affording a mixed ligand complex. The equilibrium step (K = 36 M-1) consists of monodentate coordination by the BT ligand and the limiting first order rate constant (1.9 x 10(-2) s-1) manifests the rate of chelation by the polydentate ligand. The intermediate is converted to the product upon further chelation through the complete displacement of the remaining 2-ethyl-2-hydroxy butanoic acid by a first order process (k = 0.023 s-1). The epr data support a pair of products that are in rapid equilibrium. In these products, BT functions either as a tetra or a penta-dentate ligand coordinating through four or five alkoxy sites. The enthalpy and entropy of activations related to the two chelation steps were found to be 32 +/- 2 kJ/mol and -(1.7 +/- 0.2) x 10(2) J/mol K for the intermediate, and 36 +/- 1 kJ/mol and -(1.5 +/- 0.2) x 10(2) J/mol K for the product. Our data support an associative mechanism for the chelation steps. The Cr(V)-BT product is more stable than the parent complex. The second order disproportionation rate constant for the Cr(V)-BT complex was evaluated to be 0.1 M-1 s-1 compared to 8.0 M-1 s-1 for the parent complex. This is the first example of a chromium(V) complex with a non-macrocyclic ligand coordinating through oxygen donor atoms which is stable in aqueous solution at neutral pH over a long period of time.

DNA Damage↗