Effects Of Lanthanum Chloride Research Articles

The effect of lanthanum chloride on the electrocrystallization behavior of cobalt and grain refinement in deposition layers

The effect of lanthanum chloride on the electrocrystallization behavior of cobalt and grain refinement in deposition layers

Effects of lanthanum on the antioxidant capacity of chloroplasts and chlorophyll fluorescence parameters of maize seedlings under chromium stress

Effects of lanthanum chloride (LaCl3) on chromium tolerance of maize were investigated at chloroplast level. The results showed that Cr stress significantly increased activities of ascorbate peroxidase, glutathione reductase, monodehydro-ascorbate reductase, dehydroascorbate reductase, superoxide dismutase, and glutathione peroxidase, nonphotochemical quenching, malondialdehyde (MDA) and hydrogen peroxide contents, but significantly reduced the ratios of reduced ascorbate to dehydroascorbate and reduced glutathione to oxidized glutathione, the contents of chlorophyll and carotenoids, maximum photochemical efficiency of PSII, photochemical quenching, quantum efficiency of PSII photochemistry, net photosynthetic rate, plant height and biomass, compared with control. Compared to Cr stress alone, LaCl3 significantly reduced MDA and H2O2 contents and increased other indicators under Cr stress. LaCl3 alone also enhanced above indicators except MDA and H2O2, compared with control. Our results suggested that LaCl3 improved the Cr tolerance of maize crops by upregulating the antioxidant capacity and the function of chloroplasts.

Lanthanum-containing bioparticles are associated with the influence of lanthanum on high phosphate mediated bone marrow stromal cells viability.

Lanthanum (La)-based binder appears effective in reducing serum inorganic phosphate (Pi) levels among chronic dialysis patients, yet concern remains about La accumulation in bone during long-term oral administration. In this study, the effect of lanthanum chloride (LaCl3) on bone marrow stromal cells (BMSCs) viability was investigated under high Pi situation. We found low concentration (10-9M) of LaCl3 increased BMSCs viability, while high concentration (10-5M) of LaCl3 not only inhibited BMSCs viability but also stimulated high Pi induced cell apoptosis. In addition, La-containing calcium phosphate (CaP) particles can be detected on cell surfaces and inside cells. We also found that inhibition of CaP formation by adding sodium pyrophosphate, a recognized inhibitor of hydroxyapatite formation, abrogated LaCl3 induced the BMSCs viability. For isolated La-containing CaP particles, the particle size increased and crystal phase switched with elevated concentration of LaCl3. These results demonstrated that La-containing CaP particles were associated with the process of LaCl3 mediated BMSCs viability and the physicochemical properties of these particles played an important role in modulating BMSCs function.

Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models

Ovarian cancer is the leading cause of mortality resulting from gynecologic cancer. A common anti-ovarian tumor drug is cisplatin; however, repeated use of cisplatin causes severe resistance and leads to poor long-term survival rate in ovarian cancer patients. Recently, it was reported that lanthanum chloride (LaCl3) may inhibit tumor growth and induce apoptosis in certain cancer cells. In the present study, the effect of LaCl3 on ovarian cancer was determined in vivo and in vitro. A cisplatin-sensitive human ovarian cancer cell line, COC1, was used in the current study. A xenograft animal model of ovarian cancer was established injecting COC1 or cisplatin-resistant COC1 cells (COC1/DDP) cells into mice. A TUNEL assay was used to determine the apoptosis of the COC1 or COC1/DDP cells and a immunohistochemical assay was conducted to measure the expression of B-cell lymphoma-2, Ki67, breast cancer 1 (BRCA)1, BRCA2 and excision repair cross-complementation group 1 in COC1 or COC1/DDP cells. It was observed that LaCl3 promoted apoptosis in COC1 and COC1/DDP cells. In addition, LaCl3 plus cisplatin led to further increase in the expression levels of tumor suppressor genes and decrease in the expression of oncogenes. Furthermore, application of LaCl3 and cisplatin inhibited tumor growth in vivo in a xenograft animal model. These results indicated the synergistic role of LaCl3 on cisplatin-induced inhibition of cancer cell proliferation and tumor growth, providing a potential and effective candidate for the treatment of ovarian tumors.

The effects of lanthanum chloride on proliferation and apoptosis of cervical cancer cells: involvement of let-7a and miR-34a microRNAs.

Lanthanide elements have been documented to possess various biologic effects, and their compounds have been studied intensely for their anti-cancer potential. However, the underlying mechanisms remain largely unknown. In the present study, we propose that the levels of proliferation and apoptosis related microRNAs (miRNAs), let-7a and miR-34a, which mediate the apoptosis of cervical cancer cells, can be affected by the lanthanum ion. Our data showed that LaCl3 inhibited the proliferation and induced the apoptosis of cervical cancer cells both in vivo and in vitro by regulating let-7a, miR-34a and their downstream genes. This study provides novel evidence demonstrating that the anticancer mechanism of lanthanum chloride is partially attributed to miRNAs regulation and establishes an experimental basis for the clinical application of lanthanum chloride as an anti-cancer drug.

Inhibitory effect of lanthanum chloride on migration and invasion of cervical cancer cells

Tumor metastasis remains the main reason for treatment failure and death of patients with cervical cancer. The present study was designed to explore the effects of lanthanum chloride (LaCl3) on the invasion and migration of cervical cancer cells and the underlying mechanisms. The migration and invasion of tumor cells was evaluated by a modified Transwell/Boyden chamber assays. It is well known that MMPs (Matrix metalloproteinases) and NF-κB (Nuclear factor-κB) pathway play important roles in migration and invasion of tumor cells, and also the expression of MMPs were regulated by NF-κB signaling. The expression of MMP-1 and MMP-9 was detected by reverse transcription polymerase chain reaction (RT-PCR); Western blot and the NF-κB-DNA-binding activity assay were used to analyze the NF-κB activity. The results indicated that LaCl3 was capable of inhibiting the cell invasion and migration of human cervical cancer Hela cells by decreasing the expression of MMP-1 and MMP-9 via blocking NF-κB pathway.

Effects of lanthanum chloride on glutamate level, intracellular calcium concentration and caspases expression in the rat hippocampus

Lanthanum chloride (LaCl(3)) can affect neurobehavioral development and impair cognitive abilities. The mechanism underlying LaCl(3)-induced neurotoxic effects is still unknown. The purpose of this research was to investigate the neuronal impairment induced by LaCl(3) and discuss the possible mechanism from the aspects of the alteration of glutamate level, intracellular calcium concentration ([Ca(2+)](i)), Bax, Bcl-2 and caspases expression in the hippocampus. Lactational rats were exposed to 0, 0.25, 0.50 and 1.0% LaCl(3) in drinking water, respectively. Their offspring were exposed to LaCl(3) by parental lactation and then administrated with 0, 0.25, 0.50 and 1.0% LaCl(3) in drinking water for 1month. The results showed that 0.25, 0.50 and 1.0% LaCl(3) exposure induced neuronal impairment in the hippocampus of young rat. Hippocampal glutamate level, [Ca(2+)](i) and ratio of Bax and Bcl-2 expression increased significantly after LaCl(3) exposure. Besides, LaCl(3) exposure increased GRP78, GRP94, GADD153 and p-JNK expression, promoted the activation of caspase-3, caspase-9 and caspase-12, induced PARP cleavage and caused excessive apoptosis. These results indicate that LaCl(3) increases glutamate level, [Ca(2+)](i) and ratio of Bax and Bcl-2 expression, which cause excessive apoptosis by the mitochondrial and endoplasmic reticulum stress-induced pathway, and thus neuronal damages in the hippocampus.

Effects of lanthanum chloride on the expression of immediate early genes in the hippocampus of rats

To study influence of lanthanum chloride (LaCl(3)) on the expression of immediate early genes (IEGs) including c-jun, early growth response gene 1 (Egr1) and activity-regulated cytoskeletal gene (Arc) in the hippocampus of rats, and discuss the mechanism of LaCl(3) undermining learning and memory capability. Forty female Wistar adult rats were divided into control group, low LaCl(3)-contaminated group (0.25%), medium LaCl(3)-contaminated group (0.50%), and high LaCl(3)-contaminated group (1.00%) by randomized design. Each group had ten female rats along with five male rats and mated by the ratio of 2:1. The amounts of pups in the above four groups were 80, 83, 78 and 75 separately. The pups in respective group were La-dyed by lactation, and then the pups in LaCl(3)-contaminated groups drank 0.25%, 0.50% and 1.00% LaCl(3) separately for one month. Learning and memory capability of pups were measured in jumping stairs experiment. Hippocampal lanthanum content was determined by inductively coupled plasma mass spectrometry (ICP-MS). Hippocampal c-jun, Egr1 and Arc mRNA expression was detected by RT-PCR, and corresponding protein expression was measured by Western blotting method. In the jumping stairs experiment, pups in 0.25%, 0.50% and 1.00% LaCl(3)-contaminated groups respectively made (1.75 ± 0.71), (2.38 ± 0.92) and (3.00 ± 0.76) mistakes; significantly higher than control group (1.25 ± 0.46) (q values were 4.386, 6.793, P < 0.05). However, the incubation period of 0.25%, 0.50% and 1.00% LaCl(3)-contaminated groups were (174.13 ± 33.72), (139.25 ± 45.83) and (75.50 ± 18.56) respectively, which were all significantly lower than that of control group (206.75 ± 20.47) (q values were 2.958, 6.121, 11.902, P < 0.05). Hippocampal c-jun mRNA expression were (0.89 ± 0.08), (0.77 ± 0.12), (0.58 ± 0.14) and (0.29 ± 0.10); while the c-jun protein expression were (0.72 ± 0.13), (0.64 ± 0.11), (0.43 ± 0.11) and (0.31 ± 0.14), and the Egr1 mRNA expression were (0.78 ± 0.09), (0.61 ± 0.13), (0.53 ± 0.10) and (0.22 ± 0.08), Egr1 protein expression were (0.65 ± 0.18), (0.40 ± 0.15), (0.32 ± 0.13) and (0.14 ± 0.09) in 0.25%, 0.50% and 1.00% LaCl(3)-contaminated groups; and all of which presented a dose-effect relationship that the correlation coefficients of these parameters with dose were -0.900 (t = 11.309, P = 0.000), -0.969 (t = 7.058, P = 0.000), -0.898 (t = 11.179, P = 0.000) and -0.962 (t = 6.739, P = 0.000). LaCl(3) undermines the learning and memory capability of rats, which is possibly related to lower expression of c-jun and Egr1 gene and protein induced by lanthanum in hippocampus.

Effect of lanthanum chloride on growth of breast cancer cells and regulation of c-met transcription

Lanthanum salt is a prescription drug, but its underlying functions and mechanisms are not fully understood currently. To explore the potential therapeutic value of lanthanum chloride, cytotoxicity test was applied to investigate its effects on cell proliferation. Furthermore, we observed its influence on pro-oncogene c-met by reverse transcription polymerase chain reaction (RT-PCR). In MCF-7 cell line, lanthanum chloride repressed cell proliferation at high concentrations but had no significant inhibition effect on cell growth at low concentrations. However, we observed that lanthanum chloride repressed c-met transcription at a low concentration. This may suggest that lanthanum chloride is a potent drug to inhibit the high expression of c-met in carcinoma cells and play a clue for inhibiting the growth and invasion of tumor.

Effect of LaCl3 on the Structure and Properties of Magnesium Alloys

By use of the Zwick electronic universal material testing machine, X-ray diffractometer, SEM, EDX, image analyzer and corrosion test, the effects of LaCl3 on the mechanical properties, structure, fractography and corrosion behavior of magnesium alloy have been studied. The results show that minute nodular Al10La2Mn7 phases can be formed in Mg melts after fluxes containing LaCl3 are added to Mg melt. The Al10La2Mn7 phases can act as the nucleating site of γ phases, and the γ phases can be refined. With the flux containing 5% LaCl3, the σb and δ of the Mg alloy can be improved from 161MPa and 2.1% to 203MPa and 4.0% by 26% and 100%, respectively. The corrosion rate of magnesium alloys can decrease from 1.10 mg/(cm2.d) to 0.17 mg/(cm2.d) by 84% with the use of flux containing 5% LaCl3. Rare earth (RE) elements are often added to the magnesium alloy to improve the alloy structure and the room or elevated temperature mechanical properties. But up to present, the RE elements added to Mg melt is often in the form of pure RE alloy or RE master alloy [1]. Because RE is the oxidizable material, this kind of adding process often leads to low RE utilization ratio and high use-cost. Besides, this process can easily induce segregation of RE and the appeared coarse RE phases will lower the Mg alloy mechanical properties. By far, there is few research reports about RE contained compound added to Mg alloy melt. In this paper, the effects of Lanthanum chloride (LaCl3) on the structure and mechanical properties of Mg alloy are studied for the first time. The aim is to explore a new way to improve the Mg alloy properties.

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

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. (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. 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. (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.

Changes in gene expression during programmed cell death in tomato cell suspensions.

To identify genes involved in plant programmed cell death (PCD), changes in gene expression during PCD in a model system of suspension-cultured tomato cells were studied. In this system, cell death is triggered by treatment with camptothecin, an inhibitor of topoisomerase 1. Cell death was accompanied by internucleosomal DNA degradation, indicating that the cell death process shares similarities with apoptosis in animals. Tomato homologues of DAD1 and HSR203, two genes that have been implicated in PCD, were isolated. During camptothecin-induced PCD tomato DAD1 mRNA levels roughly halve, while tomato HSR203 mRNA levels increase 5-fold. A differential display approach was used to identify novel genes that show changes in expression levels during camptothecin-induced PCD. This resulted in isolation of two up-regulated (CTU1 and CTU2) and four down-regulated (CTD1, CTD2, CTD4, and CTD5) cDNA clones. CTU1 shows high homology to various gluthatione S-transferases, whereas CTU2 is as yet unidentified. CTD1 is highly similar to Aux/IAA early-auxin-responsive genes. CTD2 corresponds to the tomato RSI-I gene, CTD4 is an unknown clone, and CTD5 shows limited homology with a proline-rich protein from maize. Addition of the calcium channel blocker lanthanum chloride prevented camptothecin-induced cell death. The effect of lanthanum chloride on camptothecin-induced gene expression was studied to discriminate between putative cell death genes and general stress genes. The possible role of the various predicted gene products in plant PCD is discussed.

Changes in lipid peroxidation, the redox system and ATPase activities in plasma membranes of rice seedling roots caused by lanthanum chloride.

Highly purified plasma membranes were isolated by aqueous two-phase partitioning from rice (Oryza sativa) seedling roots. The effects of lanthanum chloride (LaCl3) on the activities of lipid peroxidation, the redox system and H+-ATPase, Ca2+-ATPase of plasma membranes were studied. The lipid peroxidation of plasma membranes could be depressed by certain low concentrations of LaCl3 and enhanced by high concentrations of LaCl3, while the lipid peroxidation was also dependent on the plasma membrane protein and incubation time. The relative activity of O2 uptake of plasma membranes was inhibited by all tested LaCl3 concentrations. In contrast, the reduction rate of Fe(CN)6(3-) by plasma membranes was stimulated below 40 microM of LaCl3, but was reduced above 60 microM of LaCl3. The relative activities of both H+-ATPase and Ca2+-ATPase increased constantly from control to LaCl3 of concentration 60 microM where the activities of both enzymes were the maximum. but decreased remarkably at 80 microM LaCl3 concentrations various LaCl3 were added to culture solutions. In the other measurement case in which various LaCl3 concentrations were added directly to reaction medium and the plasma membrane vesicles only came from the control cultured rice seedling roots, the response of H+-ATPase activity to La3+ was similar to the response in culture solution. However, the La3+ concentration was only 20 microM when the activity of H+-ATPase was the maximum. In contrast to the case of LaCl3 addition to culture solution, Ca2+-ATPase activity was inhibited by all concentrations of La3+ which were added directly to the reaction medium. The above results revealed that REEs inhibited electron transfer from NADH to oxygen in plant plasma membranes, depressed the production of active oxygen radicals, and reduced the formation of lipid peroxides through plasma membrane lipid peroxidation. REEs ions also enhanced the H+ extrusion by both standard redox system and H+-ATPase in plasma membranes at certain concentrations. A possible role for the plant cell wall in REEs effects on plasma membranes was also suggested.

Effect of lanthanum chloride on established atherosclerosis in the cholesterol-fed rabbit. Mitral valve as a site for assessment of treatment effects.

The ability of lanthanum chloride (LaCl3) to retard the progression of established atherosclerosis was investigated in cholesterol-fed rabbits. Rabbits were initially maintained on a high-fat plus cholesterol-supplemented diet for 10 weeks to induce lesions and were then changed to a low-fat diet or a low-fat diet supplemented with LaCl3 for an additional 24 weeks to permit their serum cholesterol levels to normalize. LaCl3 did not affect the rate at which serum cholesterol levels returned to normal. The dose of LaCl3 was approximately 30 mg/kg body weight/day. In comparison with controls, LaCl3-treated rabbits exhibited histologically less severe coronary artery and mitral valve atherosclerosis. Lesion severity in the carotid arteries was unaffected by LaCl3 treatment. Although statistically significant, the salutary effects of LaCl3 were relatively small. The data support the hypothesis that calcium antagonists can retard the progression of established atherosclerotic lesions. The data also illustrate the value of the mitral valve as a site to assess treatment effects on monocyte/macrophages in vivo.

The effects of lanthanum chloride on pregnancy in mice and on preimplantation mouse embryos in vitro

A single intraperitoneal injection of 10 −6.5 mol lanthanum chloride/g body wt (44 mg metal/kg body wt) into pregnant mice reduced the number of successful pregnancies and the average litter size. The most susceptible periods of pregnancy were peri-implantation (days 4 and 6) and near-term period (days 14 and 16). Injection of lanthanum during the peri-implantation period resulted in a cessation of pregnancy in 24–43% of females, and injection during near-term period produced the cessation of pregnancy in 36–46% of the females. The average litter size after injection of lanthanum during peri-implantation or near-term periods was reduced to about 75% of the average litter size in the control animals. No external malformations were observed among fetuses. Paradoxically, the exposure of 1-cell stage embryos to 10 −3.0 M and 10 −3.5 M lanthanum chloride in vitro resulted in a significant improvement of the proportion of embryos developing into blastocysts.

Calcium Inhibitors and the Hatching of Globodera Rostochiensis

The effects of lanthanum chloride and ruthenium red on hatching of Globodera rostochiensis do not show that free calcium ions are essential for the initiation of hatching. Lanthanum chloride is not an effective inhibitor of hatching but is a moderately effective hatching agent. It partially inhibits the hatch-stimulating activity of potato-root exudate, possibly by complex formation. Ruthenium red effectively inhibits exudate-initiated hatching by inactivating the hatching factor and inhibiting nematode movement.