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At least 19 recordsLinked to original sources
PubMed2005

Localization of lanthanum in bone of chronic renal failure rats after oral dosing with lanthanum carbonate.

BACKGROUND: Lanthanum carbonate has been shown to be a safe, effective phosphate-binding agent. We have shown that an impaired mineralization in chronic renal failure rats treated with high doses of lanthanum carbonate develops secondary to phosphate depletion and is therefore pharmacologically mediated rather than a direct effect of lanthanum on bone. Although bulk bone lanthanum concentrations are low, it is important to consider the localization within a given tissue. METHODS: Using the scanning x-ray micro-fluorescence set-up at beamline ID21 of the European Synchrotron Radiation Facility, calcium and lanthanum distributions in bone samples were mapped. RESULTS: In chronic renal failure rats loaded orally with lanthanum carbonate (12 weeks) (2000 mg/kg/day), bulk bone lanthanum concentrations reached values up to 5 microg/g wet weight. Lanthanum could be demonstrated at the edge of the mineralized bone, at both actively mineralizing and quiescent sites, independent of the type of bone turnover. In the presence of hyperparathyroid bone disease, lanthanum was also distributed throughout the mineralized trabecular bone. No correlation with the presence of osteoid, or the underlying bone pathology could be demonstrated. After a 2- or 4-week washout period before sacrifice, lanthanum localization did not change significantly. CONCLUSION: The comparable localization of lanthanum in different types of bone turnover, and the unchanged localization after washout and consequent disappearance of the mineralization defect, indicates no relationship between the localization of lanthanum in bone and the presence of a mineralization defect.

Administration, Oral↗
PubMed2006

Absolute bioavailability and disposition of lanthanum in healthy human subjects administered lanthanum carbonate.

Lanthanum carbonate [La2(CO3)3] is a noncalcium, non-aluminum phosphate binder indicated for hyperphosphatemia treatment in end-stage renal disease. A randomized, open-label, parallel-group, phase I study was conducted to determine absolute bioavailability and investigate excretory routes for systemic lanthanum in healthy subjects. Twenty-four male subjects were randomized to a single lanthanum chloride (LaCl3) intravenous infusion (120 microg elemental lanthanum over a 4-hour period), a single 1-g oral dose [chewable La2(CO3)3 tablets; 4 x 250 mg elemental lanthanum], or no treatment (control). Serial blood, urine, and fecal samples were collected for 7 days postdosing. The absolute bioavailability of lanthanum [administered as La2(CO3)3] was extremely low (0.00127% +/- 0.00080%), with individual values in the range of 0.00015% to 0.00224%. Renal clearance was negligible following oral administration (1.36 +/- 1.43 mL/min). Intravenous administration confirmed low renal clearance (0.95 +/- 0.60 mL/min), just 1.7% of total plasma clearance. Fecal lanthanum excretion was not quantifiable after intravenous administration owing to high and variable background fecal lanthanum and constraints on the size of the intravenous dose. These findings demonstrate that lanthanum absorption from the intestinal tract into the systemic circulation is extremely low and that absorbed drug is cleared predominantly by nonrenal mechanisms.

Administration, Oral↗
PubMed2006

Evolution of bone and plasma concentration of lanthanum in dialysis patients before, during 1 year of treatment with lanthanum carbonate and after 2 years of follow-up.

BACKGROUND: Lanthanum carbonate (LC) has been proposed as a new phosphate binder. Presented here are the results from one centre that participated in a multicentre trial to assess the effect of treatment with LC and calcium carbonate (CC) on the evolution of renal osteodystrophy in dialysis patients. Bone biopsies were performed at baseline, after 1 year of treatment and after a further 2-year follow-up period to assess the lanthanum concentration in bone and plasma. METHODS: Twenty new dialysis patients were randomized to receive LC (median dose 1250 mg) for 1 year (n = 10), followed by 2 years of CC treatment or CC (n = 10) during the whole study period (3 years). RESULTS: After 36 weeks of treatment, steady state was reached with plasma lanthanum levels varying around 0.6 ng/ml. Six weeks after cessation of 1 year of treatment, the plasma lanthanum levels declined to a value of 0.17 +/- 0.12 ng/ml (P < 0.05) and after 2 years to 0.09 +/- 0.03 ng/ml. Plasma and bone lanthanum levels did not correlate with the average lanthanum dose at any time point. The mean bone concentration in patients receiving LC increased from 0.05 +/- 0.03 to 2.3 +/- 1.6 microg/g (P < 0.05) after 1 year and slightly decreased at the end of the study to 1.9 +/- 1.6 microg/g (P < 0.05). CONCLUSIONS: Bone deposition after 1 year of treatment with LC is low (highest concentration: 5.5 microg/g). There is a slow release of lanthanum from its bone deposits 2 years after the discontinuation of the treatment and no association with aluminium-like bone toxicity.

Aged↗
PubMed2004

[Rheological phase synthesis and characterization of lanthanum salicylate and luminescence properties of Tb3+ -doped lanthanum salicylate].

Lanthanum salicylate and Tb3+ -doped lanthanum salicylate were synthesized with the rheological phase reaction method. Elemental analysis, IR, TG, DTA and powder X-ray diffraction were investigated to determine the composition, crystal structure and coordination manner between the COO- and ion La3+ of lanthanum salicylate. The emission and excitation spectra of Tb3+ -doped lanthanum salicylate were also discussed. Powder X-ray diffraction suggests that the compound has a layered monoclinic structure, and the lattice parameters are a = 21.6010 A, b = 13.8015 A , c = 3.8103 A, beta = 97.11 degrees, V = 1127.2 A3, Z = 2, rhocal = 1.621 g x cm(-3) and rhoexp = 1.653 g x cm(-3). The Tb3+ -doped lanthanum salicylate exhibits very strong green luminescence of Tb3+ under the excitation of UV light. And the transition from 5D4 to 7F5 is the strongest one.

Carbon Dioxide↗
PubMed1984

The effects of lanthanum on the ultrastructure of hypertrophic chondrocytes and the localization of lanthanum precipitates in condylar cartilages of rats fed on normal and rachitogenic diets.

Ionic lanthanum was used to examine the distribution of calcium-binding sites in the condylar cartilages of rats that had been fed on normal and/or vitamin D-deficient rachitogenic diets for 4 weeks. Certain specific changes in the ultrastructure of the cartilage were attributed to the presence of the trivalent cation in the fixation medium. Cartilages from the rachitic animals showed a marked reduction in the quantity of lanthanum deposition on the outer surface of the chondrocytes and in the extracellular matrix. Returning rachitic rats to the control diet resulted in a corresponding return to a normal ultrastructural distribution of lanthanum in the condylar cartilages. No intracellular lanthanum deposits were observed. The results suggest that a vitamin D-dependent calcium-binding component may be an integral part of the chondrocyte plasma membrane structure.

Animals↗
PubMed2005

Anticancer activity of the lanthanum compound [tris(1,10-phenanthroline)lanthanum(III)]trithiocyanate (KP772; FFC24).

Aim of this study was to investigate the anticancer properties of the new lanthanum compound [tris(1,10-phenanthroline)lanthanum(III)]trithiocyanate (KP772; FFC24). In vitro, growth inhibition by KP772 was comparable for >60 tumour cell models with IC50 values generally in the low microM range. KP772 induced tumour cell apoptosis indicated by chromatin condensation, caspase substrate cleavage and mitochondrial membrane depolarisation. DNA is unlikely to represent the primary molecular target of KP772, as no significant interaction or damage of DNA was detectable both in vitro and in living cells. Moreover, we found no evidence for induction of radical species. In contrast, KP772 potently inhibited DNA synthesis paralleled by a massive block of cell cycle in G0/G1 phase and a selective decrease of cyclin B1. Although treatment with KP772 induced expression of p53 and p21Waf1, transfection of wild-type p53 into knock-out cells only marginally enhanced the cytostatic activity of KP772. In vivo, the anticancer activity of KP772 against human DLD-1 colon carcinoma xenografts was comparable to that of cisplatin and methotrexate at doses not causing significant adverse effects. With regard to toxicity, the LD50 and no-observed-adverse-effect levels (NOAEL) of KP772 in Sprague-Dawley rats were 21.6 and 7.5 mg/kg, in outbred albino mice 62 and 10 mg/kg, respectively. In summary, KP772 exerts anticancer activity via potent induction of cell cycle arrest and/or apoptosis and has promising in vivo anticancer activity against a human colon cancer xenograft. Together, these data suggest further development of KP772 as a new anticancer metal-drug.

Animals↗
PubMed2002

Accumulation and elimination of lanthanum by duckweed (Lemna minor L.) as influenced by organism growth and lanthanum sorption to glass.

Lanthanide emissions to the environment increase as a result of the growing industrial applications of these elements. However, robust data to evaluate the environmental fate of lanthanides are scarce. This article describes the accumulation and elimination of lanthanum (La) by common duckweed (Lemna minor L.). Speciation modeling was performed to assure that solubility products were not exceeded. It also showed that La was predominantly associated with ethylenediaminetetraacetic acid (EDTA). Lanthanum concentrations in plants and medium and the amounts sorbed to glass vessels were quantified by using the radioisotope 140La. The amount of La adsorbed on the glass reached values of 25% of the total La present. A model was formulated to describe La uptake in exponentially growing duckweed in the presence of an adsorptive surface. Growth-induced dilution appeared more efficient in lowering plant La concentrations than actual elimination. An elimination study revealed two compartments, of which the smallest eliminated 50 times faster than the bigger compartment, which eliminated mainly by growth dilution. The average bioconcentration factor was 2,000 L/kg fresh weight and 30,000 L/kg dry weight, comparable with those of other higher plants. At the applied concentration of 10 nM, no effects were observed on duckweed growth. However, the high bioconcentration factor warrants monitoring of lanthanide emissions.

Adsorption↗
PubMed2004

[Anti-endotoxin effect of lanthanum chloride in vivo: an experimental study of mice].

OBJECTIVE: Lanthanum is one of rare earth with extremely active chemical property and has been evidenced to possess antibacterial effect as well as the function of blocking calcium flux and regulating cellular immunity. Our previous studies showed that lanthanum could affect the biological activity of LPS and inhibit the activity in vitro. In this study, we explored the anti-LPS effects of lanthanum chloride in vivo so as to provide evidence in searching for new anti-endotoxic agents for the prevention and treatment of endotoxemia. METHODS: (1) 96 BALB/c mice were divided into 2 groups: experimental group including 84 mice injected intraperitoneally with 17.5 mg/kg, LD(50) dose, of LPS mixed with lanthanum chloride of the dosages of 1 mg/kg, 2 mg/kg, 5 mg/kg, 10 mg/kg, 20 mg/kg, 40 mg/kg, and 80 mg/kg respectively; and control group including 12 mice injected intraperitoneally with 17.5 mg/kg of LPS. The mortality rates of different mice within 7 days were observed so as to observe the protective effect of lanthanum chloride. (2) 40 BALB/c mice were randomly divided into 2 group 2: experimental group injected intraperitoneally with lanthanum chloride of the dosages 10 mg/kg for 3 days and then injected with 1 LD(50) dosage of LPS 30 minutes after the last injection of lanthanum chloride of the dosages 10 mg/kg; and control group injected intraperitoneally with normal saline for 3 days and then with 1 LD(50) dosage of LPS 30 minutes after the last injection of normal saline. The mortality rates of different mice within 7 days were observed. (3) 40 BALB/c mice were randomly divided into 4 groups: LPS group, injected intraperitoneally with LPS of sublethal dosage (12.5 mg/kg), lanthanum chloride treatment group, injected intraperitoneally with LPS of sublethal dosage 1 hour after the venous injection of 10 mg/kg lanthanum chloride, lanthanum chloride control group, injected intravenously with 10 mg/kg lanthanum chloride, and NS control group, injected intraperitoneally with NS. Four hours after the intraperitoneal injection blood sample were collected to detect the plasma tumor necrosis factor-alpha (TNFalpha) and liver and thymus tissues were collected to examine the expression of TNFalpha mRNA and apoptosis of thymocytes by Rt-PCR and flow cytometry so as to observe the effects of lanthanum chloride on LPS-induced reaction in vivo. RESULTS: The mortality rates of the mice administrated with LD(50) dosage of LPS combined with 5, 10, and 20 mg/kg lanthanum chloride were 0, 0, and 8% respectively, all significantly lower than that of the control group (67%, all P < 0.01). The mortality rate of the LPS-challenged mice that were pretreated with 10 mg/kg of lanthanum chloride was 20%, significantly lower than that of the control group (55%, P < 0.05). (2) In the mice with endotoxemia that were pretreated with lanthanum chloride the plasma TNFalpha level was 0.44 +/- 0.22 ng/ml and the TNFalpha mRNA expression in liver was (3.93 +/- 0.62) x 10(5) copies/ micro g RNA, both significantly lower than those of the mice with endotoxemia without pretreatment of lanthanum chloride, 0.99 +/- 0.24 ng/ml and (1.9 +/- 0.33) x 10(7) copies/ micro g RNA (both P < 0.001). The percentage of DNA fragmentation of thymocytes in the mice challenged with LPS and pretreated with lanthanum chloride was 14.77% +/- 1.0%, significantly lower than that of the untreated mice (55.38% +/- 3.88%, P < 0.001), the percentage of hypodiploidy in thymocytes of the mice challenged with LPS was 15.56% +/- 0.59%, significantly higher than that of the lanthanum chloride treated mice (6.05% +/- 0.71%, P < 0.001). (3) Morphologic observation showed that pathological changes of the thymocytes and liver and lung tissues were remarkably milder in the lanthanum chloride-treated mice than in the mice challenged only by LPS. CONCLUSIONS: (1) Lanthanum chloride can bind LPS and reduce its toxicity, which shows protective effects on mice challenged by lethal dose LPS. (2) Lanthanum chloride can greatly decrease the secretion of TNFalpha and TNFalpha mRNA expression in the mice the secretion of TNFalpha and TNFalpha mRNA expression in the mice challenged with LPS. Furthermore, LPS-induced apoptosis of thymocyte and damage of liver and lungs are inhibited by lanthanum chloride.

Animals↗
PubMed1997

Contrasting actions of lanthanum on different recombinant gamma-aminobutyric acid receptor isoforms expressed in L929 fibroblasts.

Functional studies have indicated that, unlike most divalent cations, lanthanum increases both native and recombinant gamma-aminobutyric acid (GABA) receptor (GABAR) currents. In the present study, we have examined whether lanthanum shows subunit-dependent selectivity for modification of currents from different GABAR isoforms. The effects of lanthanum on three different GABAR isoforms, alpha1beta3gamma2L, alpha6beta3gamma2L, and alpha6beta3delta, were determined by transient expression of combinations of alpha1, alpha6, beta3, gamma2L, and delta subunit cDNAs in L929 fibroblasts. Whole-cell recording was used to determine the concentration-response curves for lanthanum for the three different isoforms at submaximal concentrations of GABA. Lanthanum displayed strong potentiation of alpha1beta3gamma2L GABAR currents consistent with earlier reports of potentiation of GABAR currents by lanthanum in neurons and recombinant GABAR isoforms. However, in contrast to the potentiation of alpha1beta3gamma2L GABAR currents by lanthanum, alpha6beta3delta GABAR currents were strongly inhibited and alpha6beta3gamma2L GABAR currents were weakly inhibited by lanthanum. Interaction of lanthanum with GABAR isoforms was competitive, with lanthanum decreasing the EC50 value for GABA of alpha1beta3gamma2L GABARs without changing the maximum current and increasing the EC50 value for GABA of alpha6beta3delta and alpha6beta3gamma2L GABAR currents (greater shift in EC50 value in the alpha6beta3delta compared with the alpha6beta3gamma2L GABARs) without changing the maximum GABAR current. Neither potentiation nor inhibition of GABAR currents by lanthanum showed any voltage dependence. These results suggest that 1) changing the alpha-subunit subtype from alpha1 to alpha6 altered the effect of lanthanum from potentiation to inhibition, 2) changing the gamma2L subunit to the delta-subunit changed the level of maximal inhibition of alpha6 subtype-containing GABAR currents by lanthanum, and 3) the site for interaction with lanthanum probably was on the extracellular surface of GABARs.

Animals↗
PubMed1984

Effect of lanthanum on urinary acidification and sodium transport by the turtle and toad bladder.

Lanthanum has been extensively used to evaluate the role of extracellular and membrane-bound calcium on several aspects of cell function. In the present study we evaluated the effect of mucosal or serosal addition of lanthanum on Na and H+ transport by the turtle bladder, in vitro, to gain insight concerning the role of calcium on these processes. Mucosal addition of lanthanum was associated with a decrease in Na transport and H+ secretion. The inhibition was of rapid onset, achieving a maximal inhibition at 10(-3) M for H+ secretion and 5 X 10(-4) for Na transport. The effect was rapidly and totally reversible with the removal of lanthanum. The mucosal effect of lanthanum addition was observed only at pH 7.4 for H+ secretion and at pH 7.4, 6.4, and 5.4 for Na transport. Agents capable of 'screening' the negative change of membrane proteins, such as cadmium or zinc, could neither elicit nor prevent the effect of lanthanum on H+ secretion. The effect of serosal addition of lanthanum on H+ or Na transport was different from that observed with mucosal addition; it was of slow onset, smaller magnitude, partially reversible, and only elicited by high concentrations (10 mM) of lanthanum. Serosal addition of lanthanum caused an early increase and a late decrease in radioactive calcium efflux. Mucosal addition of lanthanum caused an increase in calcium efflux. The data demonstrate that lanthanum inhibits Na and H+ transport in the turtle bladder and suggest that the mechanism of action of lanthanum is the result of either displacement of membrane-bound calcium or altered cell membrane permeability to calcium.

Animals↗
PubMed1978

Effects of lanthanum on calcium-dependent phenomena in human red cells.

Lanthanum (0.25 mM) does not penetrate into fresh or Mg2+-depleted cells, whereas it does into ATP-depleted or ATP + 2,3-diphosphoglycerate-depleted cells, into cells containing more than 3 mM calcium, or cells stored for more than 4 weeks in acid/citrate/dextrose solution. In fresh cells loaded with calcium, extracellular lanthanum blocks the active Ca2+-efflux completely and inhibits (Ca2+ + Mg2+)-ATPase (ATP phosphohydrolase, EC 3.6.1.3) activity to about 50%. In Mg2+-depleted cells Ca2+-Ca2+ exchange is inhibited by lanthanum. Ca2+-leak is unaffected by lanthanum up to 0.25 mM concentration; higher lanthanum concentrations reduce leak rate. In NaCl medium Ca2+-leak +/ S.D. amounts to 0.28 +/ 0.08 mumol/1 of cells per min, whereas in KC1 medium to 0.15 +/ 0.04 mumol/1 of cells per min at 2.5 mM [Ca2+]e and 0.25 mM [La3+]e pH 7.1. Lanthanum inhibits Ca2+-dependent rapid K+ transport in ATP-depleted and propranolol-treated red cells, i.e. whenever intracellular calcium is below a critical level. The inhibition of the rapid K+ transport can be attributed to protein-lanthanum interactions on the cell surface, since lanthanum is effectively detached from the membrane lipids by propranolol. Lanthanum at 0.2--0.25 mM concentration has no direct effect on the morphology of red cells. The shape regeneration of Ca2+-loaded cells, however, is blocked by lanthanum owing to Ca2+-pump inhibition. Using lanthanum the transition in cell shape can be quantitatively correlated to intracellular Ca2+ concentrations.

Biological Transport, Active↗
PubMed2004

Lanthanum carbonate.

Lanthanum carbonate is a novel, non-aluminium, non-calcium phosphate binding agent that forms a water-insoluble compound, lanthanum phosphate, in the gut. Lanthanum carbonate (elemental lanthanum 375-3000 mg/day) reduced serum phosphorus levels compared with placebo in two randomised, double-blind, multicentre 4-week trials in patients with chronic renal failure receiving regular haemodialysis. In two large, randomised trials in patients with chronic renal failure requiring haemodialysis, lanthanum carbonate (elemental lanthanum 375-3000 mg/day) was as effective as calcium carbonate and/or other conventional phosphate binders in reducing and maintaining serum phosphorus levels (< or =5.6 mg/dL over 6 months and < or =5.9 mg/dL over 2 years). Lanthanum carbonate was generally well tolerated. Most adverse events were mild-to-moderate in severity, with gastrointestinal events being the most common. The tolerability profile of lanthanum carbonate was similar to those of conventional phosphate binders; however, hypercalcaemic episodes occurred significantly less frequently over 6 months with lanthanum carbonate than with calcium carbonate. In a randomised 1-year trial, numerically fewer lanthanum carbonate (elemental lanthanum < or =3750 mg/day) recipients had renal bone disease at study end than at baseline; however, in the calcium carbonate < or =9000 mg/day group, numerically more patients had renal bone disease at study end compared with baseline.

Animals↗