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PubMed1997

Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes.

Chromium is an essential nutrient involved in normal carbohydrate and lipid metabolism. The chromium requirement is postulated to increase with increased glucose intolerance and diabetes. The objective of this study was to test the hypothesis that the elevated intake of supplemental chromium is involved in the control of type 2 diabetes. Individuals being treated for type 2 diabetes (180 men and women) were divided randomly into three groups and supplemented with: 1) placebo, 2) 1.92 micromol (100 microg) Cr as chromium picolinate two times per day, or 3) 9.6 micromol (500 microg) Cr two times per day. Subjects continued to take their normal medications and were instructed not to change their normal eating and living habits. HbA1c values improved significantly after 2 months in the group receiving 19.2 pmol (1,000 microg) Cr per day and was lower in both chromium groups after 4 months (placebo, 8.5 +/- 0.2%; 3.85 micromol Cr, 7.5 +/- 0.2%; 19.2 micromol Cr, 6.6 +/- 0.1%). Fasting glucose was lower in the 19.2-micromol group after 2 and 4 months (4-month values: placebo, 8.8 +/- 0.3 mmol/l; 19.2 micromol Cr, 7.1 +/- 0.2 mmol/l). Two-hour glucose values were also significantly lower for the subjects consuming 19.2 micromol supplemental Cr after both 2 and 4 months (4-month values: placebo, 12.3 +/- 0.4 mmo/l; 19.2 micromol Cr, 10.5 +/- 0.2 mmol/l). Fasting and 2-h insulin values decreased significantly in both groups receiving supplemental chromium after 2 and 4 months. Plasma total cholesterol also decreased after 4 months in the subjects receiving 19.2 micromol/day Cr. These data demonstrate that supplemental chromium had significant beneficial effects on HbA1c, glucose, insulin, and cholesterol variables in subjects with type 2 diabetes. The beneficial effects of chromium in individuals with diabetes were observed at levels higher than the upper limit of the Estimated Safe and Adequate Daily Dietary Intake.

Adult↗
PubMed1998

Occupational exposure to chromium--an assessment of environmental pollution levels and biological monitoring of exposed workers.

In an aircraft construction factory where adhesives containing Cr(VI) compounds were used, the risk of chromium exposure was studied by assessing airborne chromium levels and urinary levels of chromium excretion. Chromium exposure was evaluated by personal sampling over a period of 4 hr in a group of 16 occupational workers selected from a group of 55. Chromium absorption was determined by collecting urine samples from all subjects (n = 55) at 3 different times: prior to the work-shift at the beginning of the working week and prior to and after the workshift at the end of the working week. Each urine sample was tested for chromium and creatinine concentration. Results showed very low exposure to airborne chromium, since values obtained (0.02-1.5 micrograms/m3, GM: 0.17, GSD: 5.34 micrograms/m3) were significantly lower than the ACGIH Hygiene Standard (50 micrograms/m3). Likewise, urinary chromium excretion (0.16-7.74 micrograms/g creat.) was higher than excretion in the general population (0.07-0.17 microgram/g creat.) but lower than BEI-ACGIH (30 micrograms/g creat.). The greatest difference between excretion levels measured before and after the workshift was 2.44 micrograms/g creat, i.e. 4 times lower than the difference proposed by ACGIH (10 micrograms/g creat.).

Adult↗
PubMed1981

Effect of supplemental dietary chromium or nicotinic acid on carbohydrate metabolism during basal, starvation, and refeeding periods in poults.

A series of experiments were conducted with turkey poults to ascertain the effects of supplemental chromium or excess of nicotinic acid on growth and carbohydrate metabolism. A 23% protein starter diet was selected to emphasize the effect of chromium under basal, starvation for 48 hr, and refeeding periods. Thirty percent protein diets were also used to determine if the effects were compounded by protein levels. Supplemental chromium (20 ppm) significantly increased (P less than .05) weight at 3 weeks of age of poults consuming 23% protein diets, while an additional 250 ppm of nicotinic acid had little effect on poult weight at 3 weeks (P greater than .05). Supplemental chromium did not increase (P greater than .05) feed consumption of poults consuming both 23 and 30% protein diets. Supplemental chromium increased liver glycogen at 3 weeks of age and following refeeding after the 48 hr fast (P less than .05). Blood glucose was significantly affected by starvation-refeeding (P less than .05) but was not affected by either chromium or nicotinic acid. Supplemental chromium increased (P less than .01) active glycogen synthetase, while nicotinic acid increased (P less than .01) active phosphorylase at both protein levels. Synthetase was not decreased by starvation but was increased (P less than .01) by refeeding regardless of protein level fed. Phosphorylase was not affected by a starvation-refeeding regimen. Chromium supplementation increased in the vitro incorporation of (14C) glucose into glycogen during basal, starvation and refeeding periods (P less than .01), again, regardless of protein level.

Animal Feed↗
PubMed1987

Chromium and vanadium effects on glucose metabolism and lipid synthesis in the chick.

The effects of 20 ppm chromium (CrCl3.6H2O) and/or 20 ppm vanadium (NaVO3.nH2O) on growth, glucose metabolism, and lipid synthesis in chicks were studied in a 2 X 2 factorial experiment. Chicks were fed experimental diets from day-old to 3 weeks of age. At 3 weeks, four chicks per treatment were injected intraperitoneally (i.p.) with 250 mu Ci 3H2O and 4 mu Ci [U-14C]glucose. Chicks were bled by cardiac puncture and killed 30 min postinjection. Dietary vanadium reduced body and liver weights and liver cholesterol while serum cholesterol was increased. Chromium had no effect on these parameters and there was no significant interaction of chromium with vanadium. Chromium and vanadium each increased 14C incorporation into liver fatty acids over that of controls. However, the combination of chromium and vanadium was without effect so that the interaction was significant. Incorporation of 3H from H2O into liver fatty acids paralleled that of 14C from glucose for all treatments. In vitro studies on the uptake and oxidation of glucose by liver slices from chicks fed the basal diet were conducted. Chromium increased the rate of glucose utilization 16% over control and vanadium increased the rate by 33%. The combination of chromium and vanadium was no different from vanadium alone. A chromium vanadium antagonism was observed in some metabolic processes but not on body or organ weight.

Animals↗
PubMed1996

[Mortality of chromium plating workers in Japan--a 16-year follow-up study].

Health hazards due to exposure to chromium in the chromium plating industry has been documented in only a few epidemiological studies. A prospective cohort study was conducted to examine the health hazards of chromium plating with a follow-up period of over sixteen years. Subjects were 1193 male metal platers in the small-scale chromium plating plants in Tokyo. They were divided into a chromium plater subgroup (n = 623) and non-chromium plater subgroup (n = 567) and were followed up from October 1976 through December 1992. The 95% confidence interval (95%CI) of the standardized mortality ratio (SMR) was used to evaluate statistical significance. In the chromium plating subgroup, the risk of chronic hepatitis or liver cirrhosis was significantly elevated (SMR 2.34; 95%CI 1.17-4.19) and a trend toward statistical significance was seen for the risk of lung cancer (SMR 1.18; 95%CI 0.99-3.04). No significantly elevated risk was seen in the non-chromium plating subgroup. We concluded that, as the number of disease-specific deaths was small, further follow-up is necessary.

Adult↗
PubMed1999

[Chromium carcinogenicity].

Chromium belongs to the group of trace elements hich are essential in numerous functions of the human body. Chromium deficiency may be responsible for various dysfunctions, whereas exposure to chromium at higher concentrations is toxic and may lead to the occurrence of neoplastic diseases. Epidemiological studies of chromium exposure proved its carcinogenity, and thus the IARC recognised Cr(VI) and its compounds as one of ascertained carcinogens. Some findings of these studies were reviewed in the first part of this work. The second part presents some molecular aspects of chromium carcinogenity which are still the subject of medical research. The direct and indirect effects of chromium and its compounds on DNA are analysed as are the relationships between the level of chromium oxidation and carcinogenity, and between the presence of reductants and the kind of DNA damage. Methods for the assessment of chromium mutagenity and genotoxicity are also discussed, and special attention is paid to tests of mutation in bacteria and yeast as well as to sister chromatid exchange (SCE) test.

Antimutagenic Agents↗
PubMed2002

[Study on the influencing factor of cultivating mungbean sprouts rich in chromium].

Getting organic chromium by cultivating chromium-enriched mungbean sprouts was studied. Chromium content in mung-bean sprouts was determined and the growth performance was observed under different conditions. The result showed that the optimal condition of cultivating chromium-enriched mungbean sprouts was soaking mungbean seeds in 40 mg/kg chromium solution about 24 hours, then cultivating under 25 degrees C for 5 days. The supernatant of chromium-enriched mungbean sprouts and normal mungbean sprouts were tested by scanning with ultraviolet spectrometry within the range of 200-320 nm wavelength. It is found that a characteristic ultraviolet absorption peak appears at 257 nm, and its optical density is descended with the increasing of chromium in the chromium-enriched mung-bean sprouts.

Chromium↗
PubMed2005

Effect of chromium on the insulin resistance in patients with type II diabetes mellitus.

INTRODUCTION: Chromium deficiency in diabetic patients is a debatable problem. The prevailing opinion suggests the presence of low serum concentrations in such patients and therefore an early, long-term addition of chromium to the standard therapy is recommended. PURPOSE: The aim of the present study was to evaluate the effect of chromium on the insulin resistance in diabetic patients with type II diabetes mellitus. MATERIAL AND METHODS: We have studied a total of 34 overweight patients with type II diabetes mellitus, who were distributed in two study sub-groups--patients with very good metabolic control and patients with bad control. For sixty days the patients of both groups received 30 microg of chromium picolinate as food additive. We measured the serum concentration of chromium (using atom-absorption methods), immune-reactive insulin and the insulin resistance index at baseline and at the end of the two-month period. RESULTS: The serum concentrations of chromium was significantly lower in diabetic patients than in the healthy individuals used as controls (2.18 +/- 0.87 nmol/l versus 4.03 +/- 0.96 nmol/l; p < 0.001). We found a significant decrease of the immune-reactive insulin and the insulin resistance index after a two-month application of chromium 30 microg daily (1 tablet of chrome picolinate). The effects of this trace element are analysed in the light of an improved first phase of secretion of insulin or facilitated post-receptor insulin sensibility as a way of potentiating the insulin action. CONCLUSION: Chromium included early in the complex therapy of diabetes is beneficial in the reduction of the degree of insulin resistance.

Adult↗
PubMed1999

Chromium induced contact dermatitis and indices for diagnosis.

Chromium exposure plays an important role in development of contact dermatitis. The prevalence of contact dermatitis among tannery workers and cement-exposed workers is high. This study was designed to determine the prevalence of contact dermatitis among some Egyptian workers exposed to chromium and to investigate the role of patch test and IgE immunoassay in diagnosis of contact dermatitis. Eighty-three male workers who were exposed to chromium were selected after application of certain exclusion criteria to be the target population of this study. Forty male workers away from exposure to chromium were taken to be the controls. All the exposed and non exposed workers were investigated through an interview questionnaire, clinical examination, patch test and determination of blood and urine chromium levels, absolute eosinophilic count and total IgE level. The results showed that there was no significant difference between exposed workers with clinically diagnosed contact dermatitis and the clinically free exposed workers regarding age and work duration. 7.7% of exposed workers with positive patch test suffered from contact dermatitis while 31.6% of exposed workers with negative patch test suffered from contact dermatitis. There was no statistically significant difference between clinically diagnosed contact dermatitis workers and clinically free workers regarding blood and urine chromium levels. IgE level and absolute eosinophilic count were statistically higher among exposed workers with contact dermatitis than among clinically free exposed workers. According to the results of this study, it is concluded that the diagnosis of skin hypersensitivity to chromium should depend upon the history of chromium exposure, clinical examination and a battery of investigations including IgE level, eosinophilic count and patch test.

Air Pollutants, Occupational↗
PubMedDate not supplied

[Nose disease caused by occupational exposure to chromium in the electroplating industry: cytomorphological aspects].

Twenty-six workers were studied (9 chrome-platers exposed to chromium dioxide and 17 workers exposed to metallic chromium dust) in order to investigate the macroscopic and cytological changes of the nasal mucosa due to exposure to water-soluble hexavalent chromium or to metallic chromium dust in the electroplating industry and the role of different valencies in the onset of nasal disease. Experimental and epidemiological data have shown that hexavalent chromium, which has strong oxidative power, induces more noticeable toxic effects on tissues and mucous membranes than other compounds. The correlation between the degree of local toxic effects and the chemical state of chromium was demonstrated in both the macro- and the microscopic investigations and in particular in the cytological examinations: cases of atypia were found only in workers exposed to hexavalent chromium. Evidence of atypia raises the question of whether hexavalent chromium may act as a carcinogenic agent on the rhinosinusal mucosa. For this reason, the introduction of cytological nasal examination in health surveillance programmes for this category of workers acquires considerable importance. Sample collection from the nasal mucosa by brushing is the method of choice since it is simple, non-invasive and gives good diagnostic results.

Adult↗
PubMed1985

Chromium: a review of environmental and occupational toxicology.

The following topics are covered in this brief review on the environmental and occupational toxicology of chromium: occurrence, production and uses of chromium and chromium compounds; experimental toxicology; chromium toxicity for man; hygienic and ecologic aspects of chromium contamination of the environment. The review provides a conclusive evidence which suggests that chromium, especially its hexavalent form, is both toxic and carcinogenic, but its trivalent form is physiologically essential in the metabolism of insulin. It is also emphasized that among the major sources of environmental chromium today are the cement industry and the increasingly widespread use of chromium compounds added as an anticorrosion admixture to a variety of cooling systems, e.g. in large power plants, which may greatly contribute to the overall pollution of outdoor air at the sites.

Aging↗
PubMed1985

Specificity and inducibility of the metabolic reduction of chromium(VI) mutagenicity by subcellular fractions of rat tissues.

The mutagenicity of sodium dichromate in the Ames test was decreased as a consequence of chromium(VI) reduction by tissue postmitochondrial (S-9 or S-12) fractions from untreated rats with the following rank of efficiency: liver; kidney; and lung. The effects of lung preparations were significantly enhanced following the intratracheal administration of high doses (0.25 mg/kg) of dichromate itself, 5 times per week for 4 weeks (i.e., 20 fractionated instillations). No changes were conversely detected following single weekly doses of 1.25 mg/kg for the same period (i.e., four cumulative instillations). The local stimulation of chromium(VI) metabolism was also confirmed by testing the mutagenicity of calcium chromate and chromium trioxide, whereas the metabolism of a number of other activatable or deactivatable mutagens was not significantly affected by intratracheal treatment with chromium(VI). Of three enzyme inducers injected i.p. which modified the spectral properties and/or concentration of cytochromes P-450 in liver and lung microsomes, only Aroclor 1254 proved to stimulate chromium(VI) metabolism in lung cells. In liver cells, Aroclor 1254 and to a lower extent phenobarbital induced chromium(VI) reduction, while 3-methylcholanthrene was ineffective. Pretreatment of rats with these three compounds resulted in a selective induction of the metabolic activation of promutagens [benzo(a)pyrene and its trans-7,8-diol, 2-aminofluorene, aflatoxin B1] and of the metabolic deactivation of direct-acting mutagens [2-methoxy-6-chloro-9-[3-(2-chloroethyl)-aminopropylamino] acridine X 2HCl, epichlorohydrin, 4-nitroquinolino-N-oxide] by S-12 and microsomal fractions. These findings indicate that, in addition to already recognized detoxification mechanisms operating outside target cells (26), specific and inducible chromium-reducing pathways, mediating threshold phenomena in chromium carcinogenesis, do also occur in the intracellular environment.

Animals↗
PubMed1984

A comparison of chromium-51 and iron-59 for estimating erythrocyte survival in the cat.

Erythrocyte survival studies were conducted on eight, normal, healthy, 1-year-old male specific-pathogen-free cats using both chromium-51 and iron-59 simultaneously. The chromium-51 procedure gave a half-life value of 11.1 +/- 0.9 days. This was considerably lower than would be expected on the basis of the experimentally determined iron-59 erythrocyte survival time of 51.2 +/- 14.9 days. The results of this study indicated that there was considerable loss of the chromium-51 label in the cat other than that from senescence alone. An analysis of the chromium-51 disappearance curve indicated that there were two exponential disappearance rates for the chromium-51 label and, in the absence of cell death, approximately 67% of the label was lost with a rate constant of 0.02 per day and 33% was lost with a rate constant of 0.1 per day. An equation is presented which models the loss of chromium-51 label which could be used to calculate erythrocyte survival from a chromium-51 disappearance curve. Blood volume measurements, hemograms, bone marrow differential results, and iron kinetic values also were determined and the results presented. While a reasonable approximation of the erythrocyte life span could be made by correcting the chromium-51 values for losses other than senescence, the iron-59 procedure would be the preferred method in cats.

Animals↗
PubMed1995

[Concentration of chromium in blood serum of patients with chronic renal failure].

UNLABELLED: A group of 66 patients with chronic renal failure (CRF) was studied. 42 of them (21 to 63 years old) were treated with haemodialysis and 24 of them (20 to 63 years old) were treated without dialysis. A group of 16 healthy subjects, 19 to 73 years old, were also studied. The blood samples in non-hemodialyzed patients and healthy subjects were taken only once after cannula had been inserted into the antebrachial vein. The blood samples in hemodialyzed patients were withdrawn four times: just before dialysis, during haemodialysis after the first hour of dialysis (from the arterial and from venous line of the dialyser) and after haemodialysis. Chromium concentrations in serum in all examined groups and chromium concentrations in the dialysis fluid as well as in the demineralized water used for dialysis were measured by flame atomic absorption spectrophotometry. In all patients with CRF serum chromium concentration was significantly higher than in the controls. During haemodialysis a decrease of serum chromium concentration was observed. Significant correlations between chromium concentration and creatinine concentration, haemoglobin concentration, haematocrit value, erythrocytes were observed. CONCLUSIONS: 1. Serum chromium concentration in patients with CRF was significantly higher than in normals. 2. No significant differences were found in serum chromium concentration between subgroups of patients with chronic renal failure. 3. Haemodialysis decreases significantly serum chromium concentration.

Adult↗
PubMed1996

Chromium induces a persistent activation of mitogen-activated protein kinases by a redox-sensitive mechanism in H4 rat hepatoma cells.

Chromium is an important industrial metal, an environmental pollutant, and a human carcinogen. To investigate the mechanisms of chromium-induced carcinogenesis, activation of mitogen-activated protein (MAP) kinases ERK1 and ERK2 was examined in rat hepatoma cells following exposure to hexavalent chromium (Cr(VI)). Cr(VI) was found to activate both forms of MAP kinase in a dose- and time-dependent manner. In contrast to the protein kinase C (PKC) agonist, phorbol 12-myristate 13-acetate, which induced a transient activation of MAP kinases, Cr(VI) caused persistent activation of these enzymes. Furthermore, unlike phorbol 12-myristate 13-acetate, the ability of chromium to activate MAP kinases was found to be independent of PKC since chromium-induced MAP kinase activation occurred in PKC-depleted cells. Stimulation of ERK1 and ERK2 was associated with the ability of Cr(VI) to increase cellular peroxide levels as determined using the H2O2-sensitive fluorescent probe 2',7'-dichlorofluorescein diacetate and flow cytometry. Furthermore, the activation of these kinases by chromium was enhanced in cells treated with the glutathione-depleting agent, L-buthionine-[S,R]-sulfoximine, and attenuated in cells pretreated with an agent that elevates cellular levels of glutathione (i.e., N-acetyl-L-cysteine). The ability of chromium to modulate MAP kinase activity in this manner suggests a mechanism of chromium-induced carcinogenesis that involves the persistent stimulation of cellular regulatory pathways.

Animals↗
PubMed1984

Renal excretion of chromium-51 chloride in the dog.

To examine the renal handling of the trace element chromium, clearance studies were performed in pentobarbital sodium-anesthetized mongrel dogs following either gavage or intravenous administration of chromium-51(III) chloride. Ultrafilterable plasma chromium-51 comprised as much as 9-19% of the total plasma chromium-51 when the isotope was given by gavage but only 2-3% when given by intravenous infusion. The mean ratio of the clearance of ultrafilterable plasma chromium-51 to that of endogenous creatinine was approximately unity in all dogs [0.97 +/- 0.11 to 1.14 +/- 0.10 by gavage (n = 5); 0.84 +/- 0.05 to 0.97 +/- 0.05 intravenously (n = 4)]. Regardless of the route of administration, ultrafilterable plasma chromium-51 concentration and glomerular filtration rate appeared to be the primary determinants of renal chromium-51 excretion.

Animals↗
PubMed2004

Determining the safety of chromium tripicolinate for addition to foods as a nutrient supplement.

Trivalent chromium is an essential element required for normal carbohydrate, lipid, and protein metabolism in humans and animals. This article describes how one particular form of trivalent chromium, chromium tripicolinate (Chromax), a stable complex of trivalent chromium and picolinic acid, was determined to be safe for use as a nutrient supplement in foods (i.e., nutritional bars and beverages). A safety assessment of a nutrient supplement for use in food requires an evaluation of the safety of the product (Chromax), as well as an evaluation of the safety of the intended dietary ingredient (chromium tripicolinate). In this assessment, the production process, final product specifications, and product analysis results for Chromax were evaluated to determine the safety of the final product. Then, the Estimated Daily Intakes (EDIs) of trivalent chromium and picolinic acid from the proposed use of Chromax were calculated using data from the USDA's most recent Continuing Survey of Food Intakes by Individuals. The EDI for trivalent chromium was compared to the Acceptable Daily Intake (ADI) for this compound derived from animal studies, corroborated with human data, while the EDI for picolinic acid was compared to existing in vivo exposure to this compound that occurs naturally in the body. As long as the EDI of trivalent chromium is less than the ADI for this compound and the EDI of picolinic acid is less than its estimated in vivo exposure, Chromax can be considered safe for its intended use. Employing this approach, it was determined that Chromax is safe, as well as generally recognized as safe (GRAS), for use in nutritional bars and beverages as a nutrient supplement at a maximum use level of 2.4 mg of Chromax per product serving.

Adolescent↗
PubMed1985

Modification of chromium(VI)-induced DNA damage by glutathione and cytochromes P-450 in chicken embryo hepatocytes.

The role of glutathione and cytochrome P-450 in the production of DNA damage by chromium(VI) was examined in chicken embryo hepatocytes by the alkaline elution technique. Cellular levels of glutathione and cytochrome P-450 were altered by treating the hepatocytes with N-acetyl-L-cysteine, buthionine sulfoximine, isopentanol, or beta-naphthoflavone. A dramatic increase in chromium(VI)-induced DNA strand breaks was observed after increasing glutathione levels in the cells. Chromium(VI)-induced DNA strand breaks were even more numerous when the level of cytochrome P-450 was also increased. Upon depletion of glutathione levels and induction of cytochrome P-450 or cytochrome P-448, little or no DNA strand breaks or DNA interstrand cross-links were observed after chromium(VI) treatment. Chromium(VI)-induced DNA-protein cross-links generally decreased after either increases or decreases in cellular levels of glutathione or cytochrome P-450 or P-448. These results suggest that glutathione enhances chromium(VI)-induced DNA damage through metabolic activation of chromium(VI). The possible production of reactive chromium species upon metabolism by glutathione and cytochrome P-450 or P-448 and their involvement in DNA damage is discussed.

Animals↗