OBJECTIVETo evaluate the effect of lanthanum chloride on expressions of collagen protein and find a way to prevent and treat scar.

METHODSFour linear incisions were made on the dorsal skin of an adult, female Sprague-Dawley rat as an animal model. One was non-manipulated as a control; the second was injected with distilled water as a sham-control; the third was injected with 50 mmol/L of lanthanum chloride, and the fourth was injected with 50 micrograms neutralizing antibody of TGF-beta 1 as a positive control. All of the wound tissues were harvested and assayed with ABC method in 14 days and 28 days after the surgery.

RESULTSThe expressions of type I, III and IV of collagen protein in the third group significantly reduced in 14 and 28 days after the operation, compared with the control or sham-control group. Its values wen as similar as the fourth group.

CONCLUSIONLanthanum chloride could inhibit the expressions of collagen protein, and it may be used to prevent and treat scars.

Animals ; Collagen ; biosynthesis ; drug effects ; Female ; Lanthanum ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Time Factors ; Wounds and Injuries ; metabolism

OBJECTIVETo probe the effects of long-term oral administration of lanthanum nitrate [La(NO(3))(3)] on morphological change in the liver, aftereffect of deposited La in the liver and their mechanism in rats.

METHODSYoung Wistar rats were divided into two groups, one fed with 0.1, 0.2, 2.0, 10.0 and 20.0 mg/kg of La(NO(3))(3) for six months and the other for the control. Changes in ratio of liver to body weight were observed after exposure to La(NO(3))(3) at varied doses for six months and one month after six-month exposure, as well as morphology of the liver in the rats with routine histochemistry and transmission electron microscopy (TEM) technique. Content of La in the liver was measured with inductively coupled plasma-mass spectrometry (ICP-MS).

RESULTSRatio of liver to body weight was significantly higher in the male rats exposed to 20.0 mg/kg of lanthanum for six months than that in the control group. Ratio of liver to body weight restored to normal in the rats exposed to 20.0 mg/kg of La one month after six-month exposure. Infiltration of inflammatory cells in the portal region of the liver, small amount of fat drops in hepatocytic cytoplasm, increased density of mitochondria stroma, lysosome containing highly-electronic-density bodies and dense granules, normal nucleus and slightly deformed nucleus of hepatocytes could be found in the rats exposed to 20.0 mg/kg. Areas of the liver deposited with glycogen after six-month exposure to 20.0 mg/kg of La accounted for (26.1 +/- 1.5)% and (4.1 +/- 1.4)%, respectively for male and female rats, significantly lower than those in the control group [(31.3 +/- 1.4)% and (39.4 +/- 0.9)%, respectively], with a statistical significance and very statistical significance, respectively. There was a little infiltration of inflammatory cells in the portal region of the liver one month after six-month exposure to 20.0 mg/kg of La, and amount of the dense bodies was lower in the rats exposed to La for six months. Liver contents of La in the rats of all experimental groups were lower one month after six-month exposure than those in the rats exposed for six months.

CONCLUSIONSExposure to a dose of 20.0 mg/kg La(NO(3))(3) for a long term could damage the liver structure to certain extent, but lanthanum deposited in the liver could be eliminated from the body gradually.

Administration, Oral ; Animals ; Female ; Lanthanum ; toxicity ; Liver ; drug effects ; metabolism ; pathology ; Male ; Organ Size ; Rats ; Rats, Wistar

BACKGROUND: The lipids of the stratum corneum, which originate from polar lipid precursors provided by the cells of the stratum granulosum via the exocytosis of lamellar bodies, with cornified cell envelope form competent epidermal barrier structurally and functionally. The ontogeny of the epidermal barrier is not clearly defined because of difficulty of sampling and methodology which defines epidermal lipids. OBJECT: From ultrastructural observation of skin samples obtained from human fetuses and newborn on serial developmental timings, we tried to clarify the sequential development of epidermal barrier. METHODS: Skin samples were obtained from 13 human fetuses from EGA(estimated gestational age) 10 to 23wks and 2 newborns. Specimens were observed by fluorescent confocal microscopy with nile red to identify the distribution of epidermal lipids, by transmission electron microscope with lanthanum to investigate the functional permeability barrier, with RuO4 to observe the intercellular lipid bilayer and morphology of lamellar bodies, with ion capture cytochemistry to investigate the formation of epidermal calcium gradient. RESULT: In nile red stain, the amount of epidermal lipid increased during fetal period. At EGA 23wks, the lipid distribution revealed linear and continuous pattern. In lanthanum tracer study, the electron dense tracer permeated all the intercellular space of the epidermis up to periderm and subepidermal space until EGA 21wks. At EGA 23wks, the tracer permeated intercellular space of epidermis weakly. It might be predicted that incomplete epidermal barrier is present at this time. In RuO4 stain, precursor of lamellar body was observed at EGA 15wks, and intercellular lipid bilayer was observed at EGA 16wks. As gestation increases, there was a steady increase in epidermal lipid bilayers. In ion capture cytochemistry, epidermal calcium gradient was first observed in follicular epidermis at EGA 20wks, and in interfollicular epidermis at EGA 23wks. From these results, it is concluded that the basic structures of epidermal barrier are formed at EGA 23wks, but it is not complete, and epidermal barrier arises first from follicular epidermis.
Calcium ; Epidermis ; Exocytosis ; Extracellular Space ; Fetus* ; Histocytochemistry ; Humans* ; Infant, Newborn* ; Lanthanum ; Lipid Bilayers ; Microscopy, Confocal ; Permeability ; Pregnancy ; Skin

The present study was intended to examine the effect of sodium vanadate on contractility of vascular smooth muscle. Aortic ring preparations were made from the rabbit thoracic aorta and endothelial cells were removed from the ring. The contractility of the aortic ring was measured under various conditions. The results were summarized as follows; 1) Sodium vanadate induced contraction of vascular smooth muscle in a dose-dependent fashion. 2) The contractile effects were not blocked by treatments with adrenergic blocking agent(phentolamine) and indomethacin, indicating the direct action of the drug on vascular smooth muscle. 3) In the presence of ouabain, Na(+)-K(+)-ATPase inhibitor, sodium vanadate still increased the contractility of vascular smooth muscle. 4) Treatment with 4.4'-diisothiocyanostilbene-2.2'-disulfonic acid(DIDS) blocked completely the contractile effects of sodium vanadate. 5) In the presence of verapamil, lanthanum and ryanodine, the contractility of the vascular smooth muscle by sodium vanadate was decreased. From the above results. it was suggested that sodium vanadate acts directly on vascular smooth muscle and causes contraction. It was probably due to inhibition of Ca(++)-ATPase in plasma membrane as well as increasing the release of Ca(++) from sarcoplasmic reticulum and Ca(++) influx across the plasma membrane, but not inhibition of Na(+)-K(+)-ATPase.
Aorta, Thoracic ; Cell Membrane ; Endothelial Cells ; Indomethacin ; Lanthanum ; Muscle, Smooth, Vascular* ; Ouabain ; Ryanodine ; Sarcoplasmic Reticulum ; Sodium* ; Vanadates* ; Verapamil

SO(4)(2-)/TiO(2)-La(2)O(3), a novel solid superacid, was prepared and its catalytic activities at different synthetic conditions are discussed with esterification of n-butanoic acid and n-butyl alcohol as probing reaction. The optimum conditions have also been found, mole ratio of n(La(3+)):n(Ti(4+)) is 1:34, the soaked consistency of H(2)SO(4) is 0.8 mol/L, the soaked time of H(2)SO(4) is 24 h, the calcining temperature is 480 degrees C, the calcining time is 3 h. Then it was applied in the catalytic synthesis of ten important ketals and acetals as catalyst and revealed high catalytic activity. Under these conditions on which the molar ratio of aldehyde/ketone to glycol is 1:1.5, the mass ratio of the catalyst used in the reactants is 0.5%, and the reaction time is 1.0 h, the yields of ketals and acetals can reach 41.4%-95.8%.
Acetylation ; Acids ; chemistry ; Catalysis ; Hydrogen-Ion Concentration ; Ketones ; chemistry ; Lanthanum ; chemistry ; Oxides ; chemistry ; Powders ; Sulfates ; chemistry ; Titanium ; chemistry

The present study were designed to characterize the action mechanisms of acetylcholine (ACh) -induced endothelium-dependent relaxation in arteries precontracted with high K (70 mM). For this, we simultaneously measured both muscle tension and cytosolic free Ca2 concentration ([Ca2 ]i), using fura-2, in endothelium-intact, rabbit carotid arterial strips. In the artery with endothelium, high K increased both [Ca2 ]i and muscle tension whereas ACh (10microM) significantly relaxed the muscle and increased [Ca2 ]i. In the presence of NG-nitro-L-arginine (L-NAME, 0.1 mM), ACh increased [Ca2 ]i without relaxing the muscle. In the artery without endothelium, high K increased both [Ca2 ]i and muscle tension although ACh was ineffective. 4-DAMP (10 nM) or atropine (0.1microM) abolished ACh-induced increase in [Ca2 ]i and relaxation. The increase of [Ca2 ]i and vasorelaxation by ACh was siginificantly reduced by either 3microM gadolinium, 10microM lanthanum, or by 10microM SKF 96365. These results suggest that in rabbit carotid artery, ACh-evoked relaxation of 70 mM K -induced contractions appears to be mediated by the release of NO. ACh-evoked vasorelaxation is mediated via the M3 subtype, and activation of the M3 subtype is suggested to stimulate nonselective cation channels, leading to increase of [Ca2 ]i in endothelial cells.
Acetylcholine ; Arteries ; Atropine ; Carotid Arteries* ; Cytosol ; Endothelial Cells ; Endothelium ; Fura-2 ; Gadolinium ; Lanthanum ; Muscle Tonus ; Nitric Oxide ; Nitroarginine ; Relaxation* ; Vasodilation

Wnk kinase maintains cell volume, regulating various transporters such as sodium-chloride cotransporter, potassium-chloride cotransporter, and sodium-potassium-chloride cotransporter 1 (NKCC1) through the phosphorylation of oxidative stress responsive kinase 1 (OSR1) and STE20/SPS1-related proline/alanine-rich kinase (SPAK). However, the activating mechanism of Wnk kinase in specific tissues and specific conditions is broadly unclear. In the present study, we used a human salivary gland (HSG) cell line as a model and showed that Ca2+ may have a role in regulating Wnk kinase in the HSG cell line. Through this study, we found that the HSG cell line expressed molecules participating in the WNK-OSR1-NKCC pathway, such as Wnk1, Wnk4, OSR1, SPAK, and NKCC1. The HSG cell line showed an intracellular Ca2+ concentration ([Ca2+]i) increase in response to hypotonic stimulation, and the response was synchronized with the phosphorylation of OSR1. Interestingly, when we inhibited the hypotonically induced [Ca2+]i increase with nonspecific Ca2+ channel blockers such as 2-aminoethoxydiphenyl borate, gadolinium, and lanthanum, the phosphorylated OSR1 level was also diminished. Moreover, a cyclopiazonic acid-induced passive [Ca2+]i elevation was evoked by the phosphorylation of OSR1, and the amount of phosphorylated OSR1 decreased when the cells were treated with BAPTA, a Ca2+ chelator. Finally, through that process, NKCC1 activity also decreased to maintain the cell volume in the HSG cell line. These results indicate that Ca2+ may regulate the WNK-OSR1 pathway and NKCC1 activity in the HSG cell line. This is the first demonstration that indicates upstream Ca2+ regulation of the WNK-OSR1 pathway in intact cells.
Cell Line* ; Cell Size ; Gadolinium ; Humans ; Lanthanum ; Oxidative Stress ; Phosphorylation ; Phosphotransferases ; Salivary Glands* ; Sodium Chloride Symporters ; Sodium-Potassium-Chloride Symporters

BACKGROUND: Water exposure is considered an important causative factor of irritant contact dermatitis. It is also known that water exposure can disrupt the stratum corneum (SC). However, there are only a few morphologic studies on the effect of water contact on the skin. OBJECTIVE: The aim of our study was to investigate the effects of prolonged water exposure on the permeability barrier and the ultrastructure of the SC intercellular lipids. METHODS: After prolonged water exposure of hairless mouse skin in vivo for 24, 36, 48, and 72 hrs respectively, the permeability barrier function was assessed by transepidermal water loss (TEWL) measurement, and the ultrastructure of SC by electron microscopy using osmium tetraoxide and ruthenium tetraoxide postfixation and calcium ion capture cytochemistry. Additionally, the lipid composition was evaluated using confocal microscopy with nile red stain and the integrity of the SC assessed using a lanthanum tracer. RESULTS: After prolonged water exposure, water caused a significant increase in TEWL with disappearance of the calcium gradient, but this did not significantly influence the recovery rate of TEWL. The intercellular lipids were disrupted, and multiple lacunae containing abnormal delaminated materials within the intercellular spaces were observed. Lanthanum tracer penetrated into the intercellular space of the SC. There was a progressive decrease in nile red staining with neutral lipid content. With increasing exposure to water, these results were more evident. CONCLUSION: Our results provide a better understanding of the disruptive effect of prolonged water exposure on barrier lipids, the penetration-enhancing effect of water and the increased susceptibility to irritants, with regard to duration of water exposure.
Animals ; Calcium ; Dermatitis, Contact ; Extracellular Space ; Histocytochemistry ; Irritants ; Lanthanum ; Mice ; Mice, Hairless ; Microscopy, Confocal ; Microscopy, Electron ; Osmium ; Permeability* ; Ruthenium ; Skin ; Water*

OBJECTIVETo study the effect of electromagnetic pulse (EMP) exposure on the permeability of blood-testicle barrier (BTB) in mice.

METHODSAdult male BALB/c mice were exposed to EMP at 200 kV/m for 200 pulses with 2 seconds interval. The mice were injected with 2% Evans Blue solution through caudal vein at different time points after exposure, and the permeability of BTB was monitored using a fluorescence microscope. The testis sample for the transmission electron microscopy was prepared at 2 h after EMP exposure. The permeability of BTB in mice was observed by using Evans Blue tracer and lanthanum nitrate tracer.

RESULTSAfter exposure, cloudy Evans Blue was found in the testicle convoluted seminiferous tubule of mice. Lanthanum nitrate was observed not only between testicle spermatogonia near seminiferous tubule wall and sertoli cells, but also between sertoli cells and primary spermatocyte or secondary spermatocyte. In contrast, lanthanum nitrate in control group was only found in the testicle sertoli cells between seminiferous tubule and near seminiferous tubule wall.

CONCLUSIONEMP exposure could increase the permeability of BTB in the mice.

Animals ; Blood-Testis Barrier ; metabolism ; radiation effects ; Coloring Agents ; Electromagnetic Fields ; Evans Blue ; Lanthanum ; Male ; Mice ; Mice, Inbred BALB C ; Permeability ; radiation effects ; Seminiferous Tubules ; metabolism ; radiation effects

OBJECTIVETo explore the effects of serum glucose and lipids by on chronically lanthanum exposure in rat.

METHODSThe Wistar rats were treated with oral exposure dose 0.1, 2 and 40 mg/kg of lanthanum chloride (LaCl(3)) respectively, after 90 days the rats were sacrificed and the blood was collected for measuring the glycosylated hemoglobin A (HbA1c), the serum was used for measuring glucose, total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) levels.

RESULTSThere were no any differences among the control and 3 dose LaCl(3) exposed rats on the blood HbA1c and serum Glu, TG and LDL-C levels (P > 0.05). The serum TC in 0.1 and 2 mg/kg LaCl(3) dose group rats were (1.38 +/- 0.14) mmol/L and (1.37 +/- 0.26) mmol/L respectively. It was lower than that of the controls (1.57 +/- 0.14) mmol/L significantly (P < 0.05), the serum HDL-C in 0.1 mg/kg dose group rats was (0.79 +/- 0.12) mmol/L and obviously lower than that of control group rats (0.93 +/- 0.10) mmol/L (P < 0.05).

CONCLUSION0.1 - 40 mg/kg LaCl(3) chronically exposed have not greater effect on serum glucose, TG and LDL-C levels in rats, but the lower dose LaCl(3) chronic exposure might cause serum TC and HLD-C level decreasing.

Animals ; Blood Glucose ; Cholesterol ; blood ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Environmental Exposure ; Glycated Hemoglobin A ; Lanthanum ; toxicity ; Lipids ; blood ; Male ; Rats ; Rats, Wistar ; Triglycerides ; blood