Endogenous excretion and true absorption of cobalt as affected by the oral supply of cobalt

At the end of a 49-d experiment with 32 growing male rats, a period of 8 d was used to determine endogenous excretion and true absorption as well as apparent absorption and retention of cobalt with the aid of the isotope dilution technique. For this purpose, a single im dose of⁵⁸Co was applied at d 35 of the experiment. After that, urine and feces were collected separately from d 8 to 15 after injection of the isotope. The specific cobalt activity of the liver was used as an endogenous reference source. The basal diet provided 5.9 ppb cobalt, the different treatment groups were obtained by supplementing the diet with 0, 10, 50, 250, or 1250 ppb cobalt. The different diets were offered from the beginning of the experiment. In the balance period, apparent and true absorption as well as fecal excretion behaved similar to cobalt intake, whereas urinary excretion increased more rapidly with increasing cobalt supply. Endogenous fecal excretion accounted for 3.5 ng Co/d in the groups fed the diets without and with 10 ppb cobalt. An increase was not observed until supplementing the diet with 50 ppb cobalt. This increase between 250 and 1250 ppb cobalt was higher than the corresponding increase in the dietary cobalt supply. This indicates that endogenous fecal excretion might be more important for homeostatic regulation at a higher dietary cobalt concentration. Endogenous renal excretion as calculated from the results of the isotope dilution technique showed a similar kind of response to increasing cobalt supply as endogenous fecal loss. Nevertheless, the elimination of excessive cobalt mainly took place by adjusting urinary excretion, whereas the variations in true absorption and endogenous fecal excretion had no quantitative importance. Apparent and true absorption were on average 28.0 and 29.8%, respectively, of the cobalt intake. In the case of retention, a marked decline was observed from 19% in the depletion group to 3% with 1250 ppb cobalt, again demonstrating the importance of urinary excretion for controlling the cobalt content of the organism.     

Intestinal absorption of cobalt and iron: mode of interaction and subcellular distribution.

1. The absorption kinetic of 59Fe-(FeCl3) and 60CO-(CoCl2) 10 min after administration of increasing doses (0.5--1,000 nmoles metal) into tied-off duodenal segments of normal and iron-deficient rats shows saturation characteristic for both metals; in iron-deficient rats the absorption of both metals was enhanced. 2. The addition of increasing amounts of cobalt to the 59Fe-containing test solutions caused a decrease of the absorption of iron. 3. The study of the time dependence of this interaction in iron-deficient rats revealed, that cobalt inhibits the release of iron from mucosal cells into the blood, whereas the uptake of iron from the lumen into the mucosal cells did not differ from the controls without administration of cobalt. 4. The subcellular distribution of 59Fe and 60 Co in mucosal cell homogenates of iron-deficient rats after ultracentrifugation on a polyvinylpyrrolidone-CsCl solution shows a similar pattern for both metals; in the presence of cobalt the subcellular distribution of 59Fe is not changed. 5. From these results the conclusion is drawn that cobalt inhibits iron absorption not by an interference with iron binding sites on or in the luminal membranes of the mucosal cells but by an interaction with the releasing process at the contraluminal side.     

Determination of cobalt in water samples using solidified floating organic drop microextraction coupled with graphite furnace atomic absorption spectrometry

Abstract

A simple, rapid and inexpensive method of the solidified floating organic drop extraction (SFODME) technique coupled with graphite furnace atomic absorption spectrometry (GFAAS) has been developed for the determination of cobalt in water samples. 8-Hydroxyquinoline was used as a complex agent and 1-undecanol was used as the extraction solvent. The factors, including solvent types, solution pH, extractant volume and interfering ions, were investigated and optimised. Under the optimum conditions, the calibration graphs were linear in the range 0.05–10.0 ng mL^-1 cobalt, the limit of detection was 0.02 ng mL^-1, the limit of quantification was 0.05 ng mL^-1 and the relative standard deviation for 10 replicate measurements of 3 ng mL^-1 cobalt was 2.8%. The proposed method was successfully applied for the determination of cobalt in different water samples and the results were satisfactory.     

Mutagenicity, carcinogenicity and teratogenicity of cobalt metal and cobalt compounds

Cobalt metal and cobalt compounds are extensively used for the production of high-temperature alloys, diamond tools, cemented carbides and hard metals, for the production of various salts used in electroplating and as catalysts, drying agents in paints, additives in animal feeds and pigments. Cobalt oxides are used not only in the enameling industry and for pigments, but also in catalytic applications. There is no indication that cobalt metal and cobalt compounds constitute a health risk for the general population. Allergic reactions (asthma, contact dermatitis) can be induced by certain cobalt compounds. Interstitial fibrosis has also been observed in workers exposed to high concentrations of dust containing cobalt, tungsten, iron, etc., mainly in the cemented carbides and the diamond-polishing industries. Several experiments have demonstrated that single or repeated injections of cobalt metal powder or some forms of cobalt salt and cobalt oxide may give rise to injection site sarcoma in rats and in rabbits but the human health significance of such data is questionable. Intratracheal administration of a high dose of one type of cobalt oxide induces lung tumors in rats but not in hamsters. In the latter long-term inhalation of cobalt oxide (10 mg/m3) did not increase the incidence of lung cancer. The human data are too limited to assess the potential carcinogenic risk for workers. Co2+ interacts with protein and nucleic acid synthesis and displays only weak mutagenic activity in microorganisms. Some cobalt salts have been reported to enhance morphological transformation of Syrian hamster embryo cells. Cobalt chloride displays some limited mutagenic activity in yeast and some cobalt compounds are able to produce numerical and structural chromosome aberrations in plant cells. Cobalt and its salts appear to be devoid of mutagenic and clastogenic activity in mammalian cells. Cobaltous acetate and cobaltous chloride have not been found to be teratogenic in hamsters and rats respectively.     

Human serum transferrin cobalt complex: stability and cellular uptake of cobalt

Transferrin (Tf) receptor expression is up-regulated on tumour cells. The human serum iron transport protein transferrin (Tf) can bind to many metals including gallium and cobalt. Cobalt has a positron-emitting isotope with a half-life of 18 h and would thus be a useful isotope for imaging purposes. This study has examined the stability of the Co-Tf in the presence of serum and albumin and the uptake of radioactive Co from Co-Tf by tumour cells. Dialysis of 57Co-Tf with serum or with apo-Tf resulted in loss of most 57Co from the complex. The time course of Co uptake from cells incubated with Co-Tf showed an initial rapid association with cells, then a slower rate of accumulation, that is, a similar uptake profile to that of iron. Competition and displacement experiments showed that uptake specifically occurred by interaction with Tf receptors.     

The mechanism of cobalt biosorption

Nonliving biomass of the common seaweed Ascophyllum nodosum is capable of accumulating cobalt from aqueous solutions to the extent of 160 mg Co(2+)/g. Successful desorption of cobalt from the biomass by acidic CaCl(2) solutions revealed that the metal uptake phenomenon is reversible, implying physical sorption of cobalt. Chemical and instrumental analysis including electron microscopy, infrared (IR) spectroscopy, X-ray dispersion and diffraction analysis provided supporting evidence that the biosorption mechanism involves predominantly ion exchange. Alginates of the cell wall (-COOH groups) play an important role in cobalt binding. Coordination and sorption in the cell wall structure occur simultaneously and rapidly whereas penetration of cobalt into the cell occurs at a lower rate.     

Effects of cobalt on plants

Cobalt, a transition element, is an essential component of several enzymes and co-enzymes. It has been shown to affect growth and metabolism of plants, in different degrees, depending on the concentration and status of cobalt in rhizosphere and soil. Cobalt interacts with other elements to form complexes. The cytotoxic and phytotoxic activities of cobalt and its compounds depend on the physico-chemical properties of these complexes, including their electronic structure, ion parameters (charge-size relations) and coordination. Thus, the competitive absorption and mutual activation of associated metals influence the action of cobalt on various phytochemical reactions. The distribution of cobalt in plants is entirely species-dependent. The uptake is controlled by different mechanisms in different species. Biosorption involves ion-exchange mechanism in algae, but in fungi both metabolism-independent and -dependent processes are operative. Physical conditions like salinity, temperature, pH of the medium, and presence of other metals influence the process of uptake and accumulation in algae, fungi, and mosses.