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PubMed1985

Bond strength of cements to nickel-chromium and silver-palladium alloys.

The bonding of zinc phosphate, polycarboxylate, and reinforced ZOE cements to nickel-chromium and silver-palladium alloys was measured by cementing flat surfaces of the metals together. Polycarboxylate cement produced higher bond strengths than the other two cements to both metals. Polycarboxylate cement bonded better to nickel-chromium alloys than to a silver-palladium alloy. Zinc phosphate and reinforced ZOE cements had similar bond strengths except for Biobond, to which zinc phosphate cement provided higher bond strength. Polycarboxylate cement failed cohesively to both types of metals, and zinc phosphate and reinforced ZOE cements failed adhesively.

Chromium Alloys↗
PubMed1989

Flexural strength of a high-temperature soldered cobalt-chromium alloy.

The flexural strength of a high-temperature soldered cobalt-chromium alloy was compared with that of the intact alloy. In one test group the specimens were soldered by Vitallium welding rods and in the other group Bego cobalt-chromium solder was used. The cylindrical portion of all specimens was mounted equally in an Instron testing machine. No statistically significant differences were found in flexural strength between the groups.

Chromium Alloys↗
PubMed1983

Chromium supplementation of human subjects: effects on glucose, insulin, and lipid variables.

Seventy-six normal, free-living subjects were given supplements of 200 micrograms chromium (Cr) in the form of chromic chloride or a placebo in a double-blind crossover study with 3-month experimental periods. Twenty of the 76 subjects had serum glucose concentrations greater than or equal to 100 mg/dL 90 minutes after a glucose challenge (1 g glucose per kilogram of body weight). Chromium supplementation significantly decreased (P less than 0.05) the 90-minute glucose concentration of these subjects from 135 +/- 9 to 116 +/- 11 mg/dL; fasting glucose concentrations also decreased significantly. The 90-minute serum glucose levels of the 35 subjects with glucose concentrations less than the fasting serum glucose level were increased significantly by Cr supplementation, from 71 +/- 1 to 81 +/- 4 mg/dL. Fasting and 90-minute serum glucose concentrations of the remaining subjects who displayed 90-minute glucose concentrations greater than fasting levels but less than 100 mg/dL were not affected by Cr supplementation. In this study, immunoreactive serum insulin concentration, body weight, lipids, and other selected clinical variables did not change significantly during Cr supplementation. These data demonstrate that Cr supplementation decreases the serum glucose levels of subjects with 90-minute glucose concentrations greater than or equal to 100 mg/dL following a glucose challenge, increases serum glucose levels of subjects with 90-minute glucose concentrations less than fasting levels, and has no effect on the serum glucose levels of subjects with 90-minute glucose values similar to but greater than fasting levels.

Adult↗
PubMed1987

Effects of supplemental chromium on patients with symptoms of reactive hypoglycemia.

To determine if chromium (Cr) is involved in hypoglycemia, eight female patients with symptoms of hypoglycemia were supplemented with 200 micrograms of Cr as chromic chloride for three months in a double-blind crossover experimental design study. Chromium supplementation alleviated the hypoglycemic symptoms and significantly raised the minimum serum glucose values observed two to four hours following a glucose load. Insulin binding to red blood cells and insulin receptor number also improved significantly during Cr supplementation. These data suggest that impaired Cr nutrition and/or metabolism may be a factor in the etiology of hypoglycemia.

Adult↗
PubMed1995

Chromium improves insulin response to glucose in rats.

The effects of chromium (Cr) supplementation on insulin secretion and glucose clearance (KG) during intravenous glucose tolerance tests (IVGTTS) were assessed in rats with impaired glucose tolerance due to dietary Cr deficiency. Male Wistar rats were maintained after weaning on a basal low-Cr diet containing 55% sucrose, 15% lard, 25% casein. American Institute of Nutrition (AIN)-recommended levels of vitamins, no added Cr, and an altered mineral content as required to produce Cr deficiency and impaired glucose tolerance. The Cr-supplemented group ([+Cr] n = 6) were provided with 5 ppm Cr as CrCl3 in the drinking water, and the Cr-deficient group ([-Cr]n = 5) received purified drinking water. At 12 weeks on the diet, both groups of rats were hyperinsulinemic (+Cr, 103 +/- 13; -Cr, 59 +/- 12 microU/mL) and normoglycemic (+Cr, 127 +/- 7; -Cr, 130 +/- 4 mg/dL), indicating insulin resistance. After 24 weeks, insulin levels were normal (+Cr, 19 +/- 5; -Cr, 21 +/- 3 microU/mL) and all rats remained normoglycemic (+Cr, 124 +/- 8; -Cr, 131 +/- 6 mg/dL). KG values during IVGTTS were lower in -Cr rats (KG = 3.58%/min) than in +Cr rats (KG = 5.29%/min), correlating with significantly greater 40-minute glucose areas in the -Cr group (P < .01). Comparisons of 40-minute insulin areas indicated marked insulin hyperresponsiveness in the -Cr group, with insulin-secretory responses increased nearly twofold in -Cr animals (P < .05). Chromium deficiency also led to significant decreases in cyclic adenosine monophosphate (cAMP)-dependent phosphodiesterase (PDE) activity in spleen and testis (P < .01). In these studies, Cr deficiency was characterized by both beta-cell hypersecretion of insulin and tissue insulin resistance that were associated with decreased tissue levels of cAMP PDE activity.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1988

Metabolic reduction of chromium as a threshold mechanism limiting its in vivo activity.

Various mechanisms tend to reduce hexavalent chromium (Cr(VI] in the organism, both outside and inside target cells. A reducing activity has been demonstrated in the blood (mainly in erythrocytes), in secretions of the alimentary tract (saliva, gastric juice) and in the lumen of terminal airways (epithelial-lining fluid and alveolar macrophages). Preparations of several types of cells from various animal species--including human liver, lung parenchyma and bronchial tree cells--are capable of metabolically reducing Cr(VI) to a variable extent. This process can be ascribed to different cytoplasmic components, e.g. to mitochondria, microsomal fractions and especially to cytosolic fractions, where reduction is partly due to electron donors (e.g. glutathione) and mainly to NADPH-dependent enzyme activities, such as DT-diaphorase. Reduction is not only selectively stimulated by enzyme inducers but also, in rat lung cells, by the repeated intra-tracheal administration of Cr(VI) itself. All these reducing reactions are interpreted as detoxifying mechanisms, which constitute a threshold phenomenon in chromium carcinogenesis.

Biotransformation↗
PubMed1989

Kinetics of chromium transformations in the environment.

Kinetics of chromium transformations under typical environmental conditions were systematically investigated using batch, microcosm and column experiments. Oxidation and reduction rates were evaluated in single phase water systems and in two phase water-solid systems. Natural and reference waters, sediments and soils representing a broad range of characteristics were used. Some of the investigated reactions, such as the reduction of Cr(VI) by S2- or Fe2+ ions under anaerobic conditions, were instantaneous and the experimental results exactly followed the stoichiometric and equilibrium calculations. Other reactions, such as the reduction of Cr(VI) by organics in sediments and soils, or the oxidation of Cr(III) by MnO2, were much slower and clearly exhibited kinetic controls. Reduction of Cr(VI) by organics was dependent on both the type and amount of organic material. Dissolved oxygen by itself did not induce measurable oxidation of Cr(III), spiked to the experimental waters, after 128 days. Slow Cr(III) oxidation to Cr(VI) was only noted in one of the natural waters and sediments with half-lives ranging from 2 to 9 years. In all cases the extent of Cr(III) oxidation did not exceed 15% of the initial Cr(III) present. The overall results indicate that the transport and transformation of chromium can be predicted using kinetics data derived from a simplified laboratory experiment, the Eh-pH data and the aquatic system characteristics. Results of the microcosm and laboratory experiments were in good agreement with the predicted concentrations.

Chemical Phenomena↗
PubMed1986

Delayed anaphylactoid reaction in a worker exposed to chromium.

A 29-year-old male welder reported systemic reactions after exposure to chromium. Inhalation challenge testing to 29 micrograms/m3 of sodium chromate aerosol resulted in late appearing systemic urticaria, angioedema, and severe bronchospasm that occurred at the same time as a threefold rise in plasma histamine. A direct leukocyte inhibitory factor test to 5.5 X 10(-6)mol/L Na2CrO4 was positive. Although the mechanism of this reaction is unknown, the positive leukocyte inhibitory factor and the general acceptance of hexavalent chromium as a contact skin sensitizer suggest that cell-mediated mechanisms could be involved.

Adult↗
PubMed1992

In vitro vibrational wear under small displacements of dental materials opposed to annealed chromium-steel counterbodies.

In vitro vibrational wear tests were performed on 17 composites and one amalgam with human enamel as a reference. The specimens were fixed on a computer-controlled X-Y translation table that generated an oscillatory movement under small displacements. The dental material specimens were in permanent contact with an annealed chromium-steel counterbody. The tests were performed in ambient air of normal humidity at room temperature under non-lubricated sliding conditions. The friction between the counterbody and each of the various materials was measured on-line. After completion of the tests, the wear volumes were determined by contactless profilometry, and the wear pattern was studied with SEM. The simple vibrational test used in this study allowed a fast classification of different dental materials in terms of the relative wear on either the specimen or the counterbody material. The ratio of the wear volume of the counterbody versus the wear volume of the dental material specimen was used to accurately classify the materials according to their in vitro wear behavior, especially when this ratio was related to the total wear volume of the dental material specimen and the counterbody. From an analysis of the wear behavior of the both contacting materials, it became obvious that neither the wear of the dental materials nor of the chromium-steel counterbody appears to correlate with either the inorganic filler hardness, the intrinsic surface roughness, the surface hardness or the Young's modulus of the dental materials.

Chromium Alloys↗
PubMed1983

The action of cobalt, nickel and chromium on phagocytosis and bacterial killing by human polymorphonuclear leucocytes; its relevance to infection after total joint arthroplasty.

Infection after total joint arthroplasty is a serious clinical complication. The accumulation of metallic wear and corrosion products may cause a localized reduction in the defense process, which may be particularly relevant in the cause of late infections. This hypothesis has been tested by exposing human polymorphonuclear leucocytes (PMN) in vitro to cobalt, nickel and chromium at various concentrations. The ability of PMNs to phagocytose and kill Staphylococcus epidermidis was measured. Nickel and cobalt reduced the number of bacteria phagocytosed by about 50% at a concentration of 0.05 and 0.01 mumol ml-1 respectively over an 18 h incubation period. Neither metal affected the rate at which S. epidermidis was killed. Chromium had no effect. All metals were used at sub-toxic levels.

Blood Bactericidal Activity↗
PubMed1987

Reduction of hexavalent chromium by mitochondria: methodological implications and possible mechanisms.

The reduction of hexavalent chromium by rat liver mitochondria was studied under various experimental conditions. The occurrence of possible artifacts arising from inadequate methods for Cr(VI) detection was also tested. Erroneous results due to the presence of NAD(P)H (above 0.1 mM) could be demonstrated when the diphenylcarbazide method is employed. Modifications of this colorimetric procedure are proposed, in order to minimize artifacts occurring when Cr(VI) is detected in NAD(P)H-added mixtures. Although no interfering substances that can affect colorimetric methods are normally present in mitochondrial preparations, some methodological precautions are recommended. Mitochondria can reduce hexavalent chromium using either succinate or glutamate as electron donors. The succinate-supported reduction of Cr(VI) is active especially in the presence of ADP or an uncoupler, while reduction induced by glutamate occurs only in the presence of respiratory-chain inhibitors. In mitochondria supplemented by NAD-linked or FAD-linked substrates, different mechanisms in Cr(VI) reduction can therefore take place.

Animals↗
PubMed1989

Impact of chromium and tin on a nitrogen-fixing cyanobacterium Anabaena doliolum: interaction with bivalent cations.

The toxicity of chromium and tin on growth, uptake of NO3- and NH4+, nitrate reductase and glutamine synthetase activity of Anabaena doliolum, and its interaction with bivalent cations, viz. Ca2+, Mg2+, Mn2+, Ni2+, Co2+, and Zn2+, has been studied. Some interacting cations, viz. Ca, Mg, and Mn, substantially antagonized the toxic effects of chromium and tin with reference to growth and nutrient (NO3- and NH4+) uptake in the hierarchical sequence Ca greater than Mg greater than Mn, whereas the sequence of hierarchy was Mn greater than Mg greater than Ca for nitrate reductase and glutamine synthetase activity of A. doliolum. A synergistically inhibitory pattern of interaction was noted for all the parameters, viz. growth, uptake of NO3- and NH4+, nitrate reductase and glutamine synthetase activity of A. doliolum, when Ni, Co, and Zn were used in combination with test metals in the growth medium. These bivalent cations followed the synergistic inhibition sequence Ni greater than Co greater than Zn and potentiated the toxicity of test metals in the N2-fixing cyanobacterium under study.

Ammonia↗
PubMed1992

Nephrotoxic and hepatotoxic effects of trivalent and hexavalent chromium in a teleost fish Anabas scandens: enzymological and biochemical changes.

The effects of trivalent and hexavalent chromium (Cr3+ and Cr6+) compounds on renal and hepatic respiratory enzymes and metabolites of a freshwater fish, Anabas scandens, were studied. In a subchronic exposure of 30 days, both forms of chromium inhibited the activities of lactate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, and isocitrate dehydrogenase, whereas the hexavalent form induced greater effects. The levels of pyruvate and lactate are not exactly reflected in lactate dehydrogenase activity.

Animals↗
PubMed1989

Chromium(III)-insulin derivatives and their implication in glucose metabolism.

Insulin has been reacted with five chromium(III) complexes that are capable of relatively facile substitution of aquo ligands. The new Cr(III) insulin derivatives have been characterized by means of electronic and infrared spectra, and evidence for major changes in the protein structure, including the state of aggregation, has been presented. Supporting evidence for the arguments favoring the beneficiary role of chromium(III) in glucose metabolism has been obtained using in vivo studies, and it has been shown that insulin derived with Cr(salen) (H2O)2+ is capable of reversing the blood sugar, serum cholesterol, and phospholipids levels to those of normal rats. The results emphasize the dependence of biopotency on the structure of Cr(III) complexes used for derivation of insulin and discount the postulates that Cr(III) serves to assemble insulin and receptor units through metal-sulphur bonding. The influence of Cr(III) on the structural stability and state of aggregation of insulin and their possible role in glucose metabolism is discussed.

Animals↗
PubMed1994

Chromium toxicity in Neurospora crassa.

A comparative study has been made on the mechanisms of toxicities of trivalent and hexavalent forms of chromium in Neurospora crassa. Of the two forms, Cr6+ is more toxic than Cr3+. The toxicity of Cr3+ was found to be due to its specific antagonism with iron uptake. Fe3+ was found to be very effective in reversing the toxicity of Cr3+ by concomitantly suppressing its uptake. That the Cr3+ toxicity caused a conditional intracellular iron deficiency was indicated by the decrease in the activities of catalase and uricase and a progressive increase in the excretion of iron binding compound into the medium. The toxicity of Cr6+ (as Cr2O7(2-)) was found to be due to its specific antagonism of sulfate uptake. Methionine was found to be more effective in reversing dichromate toxicity than sulfate, probably by repressing the synthesis of sulfate permeases responsible for dichromate (Cr6+) uptake. Maximal uptake of Cr6+ was nearly tenfold lower and Vmax much higher than that of Cr3+. Evidence has been adduced to show that Cr6+ and Cr3+ were toxic by themselves and that interconversion between the tri- and hexavalent forms of chromium did not occur to any detectable extent.

Biological Transport↗
PubMed1979

The cytotoxic, mutagenic and clastogenic effects of chromium-containing compounds on mammalian cells in culture.

Examples of chromic and chromate salts have been examined for their effects on a cultured Chinese hamster cell line. The responses studied were cytotoxicity, mutagenesis and clastogenesis. Chromate (hexavalent chromium) salts of both high and medium water solubility were active in producing all three classes of response, whereas an insoluble chromate salt and a soluble chromic (trivalent chromium) salt were inactive. In addition to illustrating the value of using mammalian cells in culture for screening chemicals for biological activity, the results of this study reinforce current views regarding the genotoxic properties of chromates.

Animals↗
PubMed1992

An alternative to the USEPA's proposed inhalation reference concentrations for hexavalent and trivalent chromium.

The passage of the Clean Air Act Amendment of 1990 reflects a growing public concern over human exposure to air toxics. The EPA is currently identifying inhalation reference concentrations (RfCs) to be used as risk criteria for determining whether existing or predicted ambient levels of chemicals are above acceptable concentrations. This paper evaluates the risk assessment methods used by the EPA to develop the recently proposed RfC (0.002 micrograms/m3) for both trivalent chromium [Cr(III)] and hexavalent chromium [Cr(VI)]. Based on our evaluation, these RfC values do not appear to have been developed in accordance with standard Agency procedures or classic toxicology methods for setting RfCs. In particular, the "key" study used by the EPA [E. Lindberg and G. Hedenstierna (1983) Arch. Environ. Health 38, 367-374] as the basis for their proposal is not appropriate because it examined only the effects of exposure to chromic acid mist [Cr(VI)], even though most environmental exposure is to Cr(VI) and Cr(III) as a dust. The health hazards of Cr(VI) as an acid mist are significantly different from those associated with Cr(VI) as a dust. Further, the EPA's key study did not evaluate exposure to Cr(III), the toxicity of which is significantly different from both particulate Cr(VI) and chromic acid mist. Finally, the uncertainty factors used to account for data gaps were unusually high, thus providing RfC values equal to or below most naturally occurring environmental levels and standard analytical limits of detection. In this paper, we propose alternative RfCs for Cr(VI) as chromic acid mist and for Cr(VI) as a dust. Based on the Lindberg and Hedenstierna study, we derived an RfC of approximately 0.12 micrograms/m3 for chromic acid mist. An RfC of 1.2 micrograms/m3 is recommended for particulate Cr(VI) based on animal studies that evaluate long-term inhalation exposure to Cr(VI) dust. Due to its low toxicity, an RfC for Cr(III) is not warranted.

Administration, Inhalation↗
PubMed1980

Mechanisms of chromium toxicity in mammalian cell cultures.

Our observations about the cytotoxic and cytogenetic effects of hexavalent and trivalent chromium compounds in mammalian cells cultured in vitro are reviewed. Additional data concerning the induction of chromosomal aberrations and sister chromatid exchanges, the inhibition of nucleic acid and protein synthesis, the interference with nucleotide metabolism, and the modification of membrane-linked enzyme activity are reported. A possible mechanism of chromium action is proposed.

Animals↗