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PubMed2000

Effects of chromium picolinate supplementation on insulin sensitivity, serum lipids, and body composition in healthy, nonobese, older men and women.

BACKGROUND: Chromium is an essential nutrient required for carbohydrate and lipid metabolism. Chromium supplementation in humans has been reported to improve glucose metabolism and improve serum lipid parameters and to reduce body fat; parameters that worsen with aging. As a result, chromium picolinate has been widely promoted as a health aid for the general population. The purpose of the study was to examine the effects of chromium supplementation on insulin sensitivity, serum lipids, and body composition in nonobese, healthy men and women of advanced age. METHODS: A randomized, double-blind, placebo-controlled study with 19 subjects (9 men and 10 women), aged 63-77, were given either chromium picolinate, 1,000 microg/d, or a placebo for 8 weeks. Serum lipids were measured at baseline and 8 weeks. Insulin sensitivity and body composition were measured with the minimal-model intravenous glucose tolerance test and dual-energy x-ray absorptiometry scan, respectively, at baseline and after 8 weeks of chromium or placebo supplementation. RESULTS: No significant change in serum lipids, insulin sensitivity, or body composition was observed in the chromium group compared with the placebo group. CONCLUSIONS: Chromium picolinate supplementation alone does not appear to improve insulin sensitivity, serum lipids, or change body composition in nonobese, healthy men and women of advanced age.

Absorptiometry, Photon↗
PubMed1992

Protective effects of thiol containing chelating agents against liver injury induced by hexavalent chromium in mice.

The effects of the chelating agents, L-cysteine ethyl ester (LCEE), L-cysteine methyl ester (LCME), N-acetyl-L-(+)-cysteine (NAC), 2,3-dimercapto-1-propanesulfonic acid (DMPS), N-(2-mercaptopropionyl)-glycine (MPG), and 2,3-dimercaptosuccinic acid (DMSA), on the distribution, excretion and hepatotoxicity of ip injected hexavalent chromium were studied in male mice. The chelating agents (500 mg/kg) were injected iv as single doses given immediately or 30 min after potassium dichromate (20 mg Cr/kg) as hexavalent chromium was administered. When the chelating agents were injected immediately after the metal compound was administered, LCEE, LCME, NAC, DMPS, and MPG reduced the chromium contents in the liver and kidney, and facilitated the urinary excretion of chromium. The liver injury induced by chromium, which was evaluated by serum ornithine carbamyl transferase (OCT) activity, was prevented significantly by LCEE, LCME, DMPS, and MPG. On the other hand, when these chelating agents were injected at 30 min after the chromium administration, only DMSA could prevent the liver injury induced by the metal, and decreased the chromium contents in the liver. However, when DMSA was given at 3 hr after the metal administration, there was no therapeutic effect on them. These results suggest that the chelating agents tested may be useful in the treatment of intoxications due to hexavalent chromium, but there is the difference in the therapeutic effects of the chelating agents owing to the time intervals after the administration of the metal.

Animals↗
PubMed1995

Long-term exposure to chromium(VI) oxide leads to defects in sulfate transport system in Chinese hamster ovary cells.

Chromium(VI) resistant Chinese hamster ovary (CHO) cell lines were established in this study by exposing parental CHO-K1 cells to sequential increases in CrO3 concentration. The final concentration of CrO3 used for selection was 7 microM for Cr7 and 16 microM for Cr16 cells. Cr16-1 was a subclone derived from Cr16 cells. Next, these resistant cells were cultured in media without CrO3 for more than 6 months. The resistance of these cells to CrO3 was determined by colony-forming ability following a 24-h treatment. The LD50 of CrO3 for chromium(VI) resistant cells was at least 25-fold higher than that of the parental cells. The cellular growth rate, chromosome number, and the hprt mutation frequency of these chromium(VI) resistant cells were quite similar to their parental cells. The glutathione level, glutathione S-transferase, catalase activity, and metallothionine mRNA level in Cr7 and Cr16-1 cells were not significantly different from their parental cells. Furthermore, Cr16-1 cells were as sensitive as CHO-K1 cells to free-radical generating agents, including hydrogen peroxide, nickel chloride, and methanesulfonate methyl ester, and emetine, i.e., a protein synthesis inhibitor. The uptake of chromium(VI) and the remaining amount of this metal in these resistant and the parental cell lines were assayed by atomic absorption spectrophotometry. Experimental results indicated that a vastly smaller amount of CrO3 entered the resistant cell lines than their parental cells did. A comparison was made of the sulfate uptake abilities of CHO-K1 and chromium(VI) resistant cell lines. These results revealed that the uptake of sulfate anion was substantially reduced in Cr7 and Cr16-1 cells. Extracellular chloride reduced sulfate uptake in CHO-K1 but not in Cr16-1 cells. Therefore, the major causative for chromium(VI) resistance in these resistant cells could possibly be due to the defects in SO4(2-)/C1- transport system for uptake chromium(VI).

Animals↗
PubMed2000

Differential effect of chromium compounds on the immune response of the African mouth breeder Oreochromis mossambicus (Peters).

The objective of this study was to investigate the effect of trivalent (chromic chloride) and hexavalent (potassium dichromate) forms of chromium in the African mouth breeder Oreochromis mossambicus (Peters), with reference to the humoral immune response and lymphoid cells/organs. The 96 h LD50 for hexavalent and trivalent chromium was found to be 75 and 1,000microg fish(-1), respectively. Groups of fishes were injected intraperitoneally with 10, 1, 0.1 and 0.01% LD50 hexavalent and trivalent forms of chromium and subsequently immunised with bovine serum albumin (5 mg in 0.2 ml physiological saline). Both forms of chromium suppressed the antibody response, with hexavalent chromium being more suppressive than trivalent chromium. Reduction in spleen weight, splenocyte number and the percentage of blood lymphocytes was observed following administration of both forms of chromium. The possible immunological mechanisms behind the differential suppression of the antibody response and the reduction in spleen weight, splenocyte and lymphocyte counts are discussed.

Animals↗
PubMed1998

Sexual maturation and fertility of male and female mice exposed prenatally and postnatally to trivalent and hexavalent chromium compounds.

The reproductive toxicity of trivalent and hexavalent chromium compounds was investigated in male and female mice exposed to 1000 ppm chromium chloride and potassium dichromate via their mother during gestational and lactational periods. Fertility was reduced in male offspring exposed to either trivalent or hexavalent chromium compounds. Body weights and weights of testes, seminal vesicles and preputial glands were reduced in trivalent-exposed male offspring. The exposure of female mice offspring to trivalent and hexavalent chromium compounds delayed sexual maturation. Fertility was reduced in female offspring exposed to either trivalent or hexavalent chromium compounds. The exposure of female mice to hexavalent chromium compound reduced the number of implantations and viable fetuses respectively. Body weight and weights of ovaries and uteri were reduced in trivalent-exposed female offspring. The results indicate that under our experimental conditions, the exposure of male and female mice offspring to either trivalent or hexavalent chromium compounds during gestational and lactational periods impair reproductive functions and fertility in adulthood.

Animals↗
PubMed1993

Carbohydrate utilization by tilapia (Oreochromis niloticus x O. aureus) as influenced by different chromium sources.

An experiment was conducted to study the influence of three different forms of chromium (CrCl3.6H2O, Na2CrO4.4H2O and Cr2O3) on the utilization of two carbohydrates (glucose and cornstarch) by juvenile hybrid tilapia (Oreochromis niloticus x O. aureus). Average initial body weight of the fish was 1.13 +/- 0.02 g. Fish were fed 5% body wt/d. Significantly (P < 0.05) greater body weight gain, food intake, protein retention, energy retention and body lipid concentration were observed in fish fed the starch diet than in those fed the glucose diet. Fish fed the glucose diet supplemented with any type of chromium had significantly greater weight gain than those fed the glucose diet without chromium supplementation. Fish fed the glucose diet supplemented with Cr2O3 had greater weight gain, food intake, protein retention, energy retention and body lipid concentration than those fed the unsupplemented glucose diet or the glucose diet supplemented with CrCl3.6H2O or Na2CrO4.4H2O. Delayed plasma glucose peak time was observed in tilapia fed the glucose diet supplemented with any type of chromium. Chromium supplementation generally lowered the glucose-6-phosphatase activity in tilapia. Phosphofructokinase activity was significantly higher in fish fed the glucose diet supplemented with Cr2O3 than in the other glucose-fed groups. These data suggest that chromium supplementation improved glucose utilization by tilapia and that Cr2O3 supplementation was markedly more effective than other chromium forms.

Animals↗
PubMed2005

Effects of dengue virus infection on peripheral blood cells of mice exposed to hexavalent chromium with drinking water.

BACKGROUND & OBJECTIVE: The occupational and non-occupational exposure to hexavalent chromium Cr (VI) is common. The effect of chromium compromises the immune response of the host. Dengue virus (DV) infection causes various changes in the peripheral blood cells. It is, therefore, possible that the chromium toxicity may affect the disease process during DV infection. The present study aims to study the effects of dengue virus infection on peripheral blood cells of mice fed Cr (VI) with drinking water. METHODS: One group of mice was given ad libitum drinking water containing Cr (VI) and the other group used as the normal control mice was given plain water to drink. At the 3, 6 and 9 wk of Cr (VI) drinking, a set of mice from each group was inoculated intracerebrally (ic) with DV and studied at the 4th and 8th day post inoculation. RESULTS: It was observed that Cr (VI) drinking led to reduction in lymphocytes, haemoglobin and the haematocrit values while the granulocyte, monocyte and platelet counts were increased. On the other hand, most of the parameters were decreased following inoculation of normal mice with DV. In Cr (VI)-fed mice the effects of DV infection were minimal. The most significant finding of these experiments was that the reduction in platelet counts following inoculation with DV was markedly less in Cr (VI)-fed mice than that in DV-inoculated normal control mice. INTERPRETATION & CONCLUSION: Cr(VI) compounds have been declared as a potent occupational carcinogen. On the contrary, Cr(III) salts such as chromium polynicotinate, chromium chloride and chromium picolinate, are used as micronutrients and nutritional supplements, and have been shown to exhibit health benefits in animals and humans. Whether therapeutic doses of chromium (III) compounds may be able to prevent the DV-induced fall in platelet counts, needs to be investigated.

Administration, Oral↗
PubMed1998

The effects of cobalt chromium upon macrophages.

The purpose of this study was to elucidate the mechanisms by which cobalt chromium particulate wear debris contribute to the aseptic loosening of total joint prostheses. Incubation of macrophages with cobalt chromium led to release of tumor necrosis factor-alpha (TNF-alpha) and prostaglandin E2 (PGE2), but did not lead to release of interleukin-1 beta (IL-1 beta) or interleukin 6 (IL-6). Exposure of macrophages cocultured with osteoblasts to cobalt chromium also led to significant release of TNF-alpha and PGE2, but did not lead to significant IL-6 or IL-1 beta production. The release of PGE2 in the coculture system was greater than that detected when macrophages were exposed to cobalt chromium without the osteoblast contribution. Exposure of radiolabeled calvaria to media from macrophages incubated with cobalt chromium in coculture with osteoblasts led to release of 45Ca. In contrast, exposure of radiolabeled calvaria to media from isolated macrophages incubated with these particles did not result in release of 45Ca. Exposure of macrophages to cobalt chromium was toxic, as reflected by release of the intracellular enzyme lactate dehydrogenase. Macrophages play a role in the initiation of bone resorption at the interface through the phagocytosis of cobalt chromium particles and subsequent release of TNF-alpha and PGE2. The presence of osteoblasts at the interface may be required for amplification of the inflammatory response and ultimately for bone resorption.

Animals↗
PubMed2000

Clinical findings of irritation among chromium chemical production workers.

BACKGROUND: Several reports of workers in chromate production and chromeplating have indicated that exposure to hexavalent chromium is associated with skin and nasal irritation. METHODS: A cohort of 2, 357 workers first employed between 1950 and 1974 at a chromate production plant was identified. Clinical findings of irritation were identified by a physician as a result of routine examinations or visits to the medical clinic by members of the cohort. Percentages of the cohort with various clinical findings, the time from hire to occurrence of the first finding, and the mean and median annual hexavalent chromium (measured as CrO(3)) concentration for the job title where the clinical finding first occurred were determined. A proportional hazards model was used to evaluate the relationship between hexavalent chromium exposure and first occurrence of each of the clinical findings. RESULTS: Nasal irritation and nasal ulceration were the most common clinical findings reported, occurring in more than 60% of the cohort. The average time to first occurrence of these findings was less than 3 months, whereas the time to first occurrence of the other findings ranged from 10 to 22 months. Median exposure to hexavalent chromium at the time of occurrence for most of the findings was about 20 microg/m(3). The proportional hazards model indicated that ulcerated nasal septum, irritated skin, and perforated eardrum were significantly associated with ambient hexavalent chromium exposure; all clinical findings with the exception of conjunctivitis and irritated skin were associated with the calendar year of hire, with the risk being lower as the calendar year of hire became more recent. Annual average ambient hexavalent chromium concentrations generally dropped in the plant over the period of the study. CONCLUSIONS: Workers in the chromate production plant in this study experienced a variety of nasal and skin irritations. Irritated and ulcerated nasal septa, in particular, were quite common clinical findings, occurring in over 60% of the cohort, and they occurred in relatively short periods of time-less than 3 months from date of hire. Annual average concentrations of chromium may not be a good predictor of clinical findings of irritation. Am. J. Ind. Med. 38:127-131, 2000. Published 2000 Wiley-Liss, Inc.

Chemical Industry↗
PubMedDate not supplied

Effects of trivalent chromium on hepatic CYP-linked monooxygenases in laying hens.

Chromium is an essential nutrient required for the metabolism of carbohydrates and lipids in humans and many animal species. We evaluated whether feeding laying hens with high levels of different chemical forms of trivalent chromium may affect hepatic metabolizing cytochrome P-450 (CYP)-linked enzymes. Modulation of CYP-dependent monooxygenases (which play a pivotal role in the endogenous metabolism) by Cr(III) was tested using either specific substrates as probes of different CYPs or testosterone as a multi-bioprobe. The CYP-supported oxidases were studied in liver microsomes from laying hens fed with diet supplemented with either 25 or 50 ppm chromium chloride as a yeast or as aminoniacinate. Although at 25 ppm no appreciable effects were observed, at 50 ppm a general inactivation of the recorded monooxygenases (ranging from 34% loss for ethoxycoumarin O-deethylase with chromium chloride to 85% loss for O-deethylation of ethoxyresorufin with either chromium yeast or aminoniacinate) were achieved in the supplemented groups vs controls. The only exception was the O-dealkylation of pentoxyresorufin, which was significantly boosted by both chromium yeast (up to 65% increase) and chromium aminoniacinate (up to 141%). Measurements of the regio- and stereoselective hydroxylation of testosterone used as a multi-bioprobe corroborated the inactivating properties of Cr(III) at the higher dose. Taken as a whole, these findings seem to indicate that high levels of Cr(III) supplementation can substantially impair CYP-catalysed drug metabolism in laying hens.

Animals↗
PubMed1994

Effects of the genotoxic carcinogen chromium(VI) on basal and hormone-inducible phosphoenolpyruvate carboxykinase gene expression in vivo: correlation with glucocorticoid- and developmentally regulated expression.

Previous studies have shown that a number of different genotoxic carcinogens that induce different types of DNA damage preferentially alter the expression of inducible genes in vivo. To investigate further the mechanistic basis for these effects, we examined the effects of the human lung carcinogen chromium(VI) on expression of the hormone-inducible cytosolic phosphoenolpyruvate carboxykinase (PEPCK) gene in chick embryo liver. Chromium(VI) pretreatment had significant effects on both basal and glucocorticoid-inducible PEPCK expression in 14-d-old embryo liver. These effects were principally a result of changes in PEPCK transcription. In contrast, treatment with chromium(VI) 1 h after treatment with glucocorticoid had no effect on PEPCK induction, suggesting that an early event in the induction process is the target for carcinogen effects. In 16-d-old liver, in which PEPCK expression is no longer responsive to glucocorticoid induction, both basal and inducible PEPCK expression were also refractory to chromium(VI) effects, indicating that carcinogen responsiveness is a phenotypic rather than an inherent property of inducible genes and is related to their competence for induction. Chromium(VI) had no effect on cAMP induction of PEPCK expression, demonstrating that carcinogens target their effects to specific regulatory pathways. Comparison of the effects of chromium(VI) with those of cycloheximide suggests that chromium(VI) targets its effects to a labile, constitutively expressed repressor involved in PEPCK gene regulation.

Animals↗
PubMed2000

Protein degradation by peroxide catalyzed by chromium (III): role of coordinated ligand.

In order to understand the role of coordinated ligands in controlling the biotoxicity of chromium (III), interactions of three types of chromium (III) complexes viz. trans-diaquo [1,2 bis (salicyledeneamino) ethane chromium (III) perchlorate, [(Cr(salen)(H(2)O)(2)](ClO(4)); tris (ethylenediamine) chromium (III) chloride, [Cr(en)(3)]Cl(3), and monosodium ethylene diamine tetraacetato monoaquo chromiate (III), [Cr(EDTA)(H(2)O)]Na with BSA has been investigated. Spectroscopic and equilibrium dialysis studies show that the two cationic complexes Cr(salen)(H(2)O)(+)(2) and Cr(en)(3+)(3) bind to the protein with a protein-metal ratio of 1:8 and 1:4. The anionic complex Cr(EDTA)(H(2)O)(-) binds to the protein with a protein-metal ratio of 1:2. The binding constant K(b) as estimated from the fluorescence quenching studies has been found to be 7.6 +/- 0.4 x 10(3) M(-1), 3.1 +/- 0.2 x 10(2) M(-1), and 1.8 +/- 0.2 x 10(2) M(-1) for Cr(salen)(H(2)O)(+)(2), Cr(en)(3+)(3), and Cr(EDTA)(H(2)O)(-) respectively indicating that the thermodynamic stability of protein-chromium complex is Cr(salen)(H(2)O)(+)(2) > Cr(en)(3+)(3) approximately Cr(EDTA)(H(2)O)(-). The complexes Cr(salen)(H(2)O)(+)(2) and Cr(EDTA)(H(2)O)(-) in the presence of hydrogen peroxide have been found to bring about protein degradation, whereas Cr(en)(3+)(3) does not bring about any protein damage. This clearly shows that the nature of the chromium (III) complex plays a major role in the biotoxicity of chromium (III).

Chromium↗
PubMed1999

Inhibition of protein synthesis by chromium(VI) differentially affects expression of urokinase and its receptor in human type II pneumocytes.

Exposure to chromium(VI) increases the incidence of cancer, respiratory distress, and pulmonary fibrosis. The latter is a pathological disorder characterized by decreased urokinase-type plasminogen activator (uPA) activity and fibrinolysis. In this study, treatment of alveolar type II cells (A549) with 1 to 5 microM chromium(VI) for 4 and 12 h decreased both the specific activity and the amount of uPA protein. Chromium reduced uPA protein levels by inhibiting protein synthesis and had no effect on uPA mRNA levels or the rate of uPA protein degradation. In contrast, both mRNA and protein levels for the uPA receptor (uPAR) were increased by treatment with concentrations of chromium(VI) that did not completely inhibit protein synthesis. The chromium-induced increase in uPAR resulted from increased message stability. These data indicate that chromium has differential effects on expression of the proteins in the pulmonary fibrinolytic cascade. The net loss of uPA activity may promote fibrosis following inhalation of chromium(VI).

Cells, Cultured↗
PubMed1990

A method for removal of toxic chromium using dialysis-sac cultures of a chromate-reducing strain of Enterobacter cloacae.

A method for removal of toxic hexavalent chromium (chromate: CrO2-4) was developed by use of dialysis-sac cultures of a chromate-reducing strain of Enterobacter cloacae (HO1). E. cloacae strain HO1 cells were put in dialysis (semipermeable membrane) sacs, and the sacs were submerged in water containing toxic CrO2-4. The dialysis sacs allowed CrO2-4 to diffuse into the culture, and CrO2-4 was reduced anaerobically in the dialysis sacs by the E. cloacae cells. Because reduced chromium readily formed insoluble chromium hydroxides in the dialysis sacs, the greater part of reduced chromium was unable to diffuse out through the semipermeable membrane. Thus the dialysis culture of E. cloacae strain HO1 could successfully remove toxic chromium from the surrounding water. If the initial concentration of CrO2-4 was less than 4 mM (208 ppm as chromium), about 90% of the total chromium could be removed from water by the described method.

Bacteriological Techniques↗
PubMed1988

Investigations on the quantitative determination of nickel and chromium in human lung tissue. Industrial medical, toxicological, and occupational medical expertise aspects.

Nickel (Ni) and some of its relatively insoluble compounds as well as chromates may be able to induce cancer in the region of the lungs, as well as in the nose and paranasal sinuses after occupational exposure. Latency periods may amount to 20 years and more. The results of recent investigations have shown that these metals cumulate in the lung tissue after inhalation of relatively insoluble chromium and nickel compounds. The quantitative detection of these heavy metals in samples of pulmonary tissue hence permits the amount of past exposure to be estimated. To establish the normal values, samples of pulmonary tissue from 30 normal subjects were investigated for chromium and nickel content. The samples were taken from different segments and lobes of the lungs, taking topographical anatomical criteria into consideration. In addition, 15 persons who had formerly been exposed to nickel and/or chromium (11 nickel refinery workers, of whom 10 had died of lung cancer, 2 stainless steel welders, 1 foundry worker, 1 electrical technician) were also investigated. From the results of 495 tissue samples from the normal group, median chromium concentrations between 130 and 280 ng/g were calculated, with median nickel concentrations of 20-40 ng/g (wet weight). If these values are related to the nickel concentrations measured in refinery workers, values 112-5,860 times higher were found. The concentrations were about 500 times higher than normal for nickel, and about 60 times higher than normal for chromium in the stainless steel welders. For the foundry workers who died of lung cancer, chromium and nickel concentrations in the normal range were calculated, with the exception of the nickel concentrations in the upper and lower lobes of the right lung. The very high nickel concentrations found in the samples of lung tissue from former nickel refinery workers should be regarded as a guideline with regard to the appraisal of the causal relationship between lung cancer and occupational exposure to relatively insoluble nickel compounds. This result is also supported by epidemiological investigations on this subgroup and must thus be considered etiologically conclusive. For the welders, chromium and nickel concentrations were found that were markedly above normal, but as yet there is no epidemiologically reliable verification for the increased occurrence of malignancies in this occupational group.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1990

Reduction of hexavalent chromium by ascorbic acid and glutathione with special reference to the rat lung.

The reduction of 20 microM hexavalent chromium [chromium(VI)] by L-ascorbic acid (AsA) (0.06-2 mM) and/or glutathione (GSH) (2-15 mM) in buffer solutions, cell-free bronchoalveolar lavage fluids or soluble fractions of rat lungs was investigated at physiological pH (37 degrees C). The reduction in AsA solution was pseudo-first-order in a single phase with respect to chromium(VI), but that in GSH solution showed a two-phase process. The half-life of chromium(IV) ranged from seconds to hours. The reducing ability of AsA was markedly higher than that of GSH. Coexistence of equimolar GSH with AsA accelerated the reduction rate slightly, in comparison with that in the corresponding AsA solution. Lavage fluids containing 0.06 mM AsA showed pH-dependent reactions similar to those of the corresponding AsA solutions. The lung-soluble fractions reduced chromium(VI) in a process composed of phase I and phase II, characterized by the reducing ability of AsA-GSH cooperation and of AsA alone, respectively. Reduction in the former was 30-40% more rapid than in the latter. The biological half-life of chromium(VI) in the lung was estimated to be 0.6 min, on the basis of the reducing activity in the first phase. However, the apparent biological half-life of chromium(VI) was about 2 min in rat lungs after intratracheal injection of chromate, involving depletion of AsA, but no significant changes in GSH. The difference is discussed in terms of AsA-induced initiative reduction in the alveolar lining fluid and subsequent obstructive effects of the resulting trivalent species on trans-membrane permeability of chromate anions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

The effect of chromium on parameters related to iron metabolism.

The effect of chromium on some parameters related to iron metabolism was investigated. Preliminary experiments showed that this metal ion was taken up by serum proteins and was dependent on the amount of chromium present in the medium. It was also shown that the uptake of iron was reduced significantly in the presence of chromium. In vivo study showed that the serum levels of iron and total iron binding capacity (TIBC) were reduced by 28 and 11%, respectively, following daily administration of chromium (1 mg/kg) for 45 d. Serum ferritin was reduced by 22% under this condition. Hematocrit and hemoglobin levels were also affected in chromium-treated animals and were both reduced by 17%. Spectrophotometric titration of each individual amino acid located in the iron binding site of transferrin revealed that tyrosine might be the most suitable ligand for the binding of chromium to transferrin. These results suggest that chromium may compete with iron in binding to apo-transferrin, and influence iron metabolism and its related biochemical parameters.

Amino Acids↗
PubMedDate not supplied

Chromium metabolism. A literature review.

The trivalent state of chromium (Cr3+) is that encountered in biological milieus and is responsible for its nutritional activity. The principal route by which trivalent chromium enters the body is the digestive system. Chromium in foods is present both in the inorganic form and as organic complexes. Intestinal absorption of chromium is low (0.5-2%), and the mechanism has not yet been fully elucidated. Absorbed chromium circulates as free Cr3+, as Cr3+ bound to transferrin or other plasma proteins, or as complexes, such as glucose tolerance factor (GTF)-Cr. Circulating trivalent chromium can be taken up by tissues, and its distribution in the body depends on the species, age, and chemical form. It is excreted primarily in the urine by glomerular filtration or bound to a low-mol-wt organic transporter. Chromium metabolism is still imperfectly understood. The use of 51Cr has nevertheless furnished valuable data concerning its transport and excretion.

Animals↗