Page last updated: 2024-11-06

gadolinium chloride

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

Gadolinium chloride (GdCl3) is an inorganic compound that finds applications in various scientific and industrial fields. It is a white hygroscopic solid, highly soluble in water. Its synthesis typically involves reacting gadolinium oxide with hydrochloric acid. Gadolinium chloride is of significant interest in magnetic resonance imaging (MRI) due to its paramagnetic properties. When administered as a contrast agent, it enhances the visibility of tissues and organs, aiding in the diagnosis of various medical conditions. Moreover, gadolinium chloride exhibits luminescent properties, making it a potential candidate for use in optical sensors and bioimaging applications. The compound also plays a role in the synthesis of other gadolinium-containing materials, such as gadolinium-doped nanoparticles. Research on gadolinium chloride focuses on understanding its physicochemical properties, exploring its applications in different fields, and assessing its safety and potential toxicity. Ongoing studies aim to improve its effectiveness as a contrast agent in MRI, develop novel applications, and minimize any associated risks.'

gadolinium chloride: a macrophage inhibitor; reduces pulmonary injury and inflammatory mediator production induced by inhaled ozone [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID61486
CHEBI ID37288
MeSH IDM0116932

Synonyms (26)

Synonym
[gdcl3]
gadolinium(3+) chloride
CHEBI:37288
einecs 233-386-6
nsc 174322
gadolinium chloride
gadolinium(iii) chloride, anhydrous, powder, 99.99% trace metals basis
nsc174322
10138-52-0
wln: gd g3
gadolinium trichloride
gadolinium chloride (gdcl3)
trichlorogadolinium
unii-p7082wy76d
SC11010
gadolinium(iii) chloride, anhydrous, gdcl3
gadolinium chloride;gadolinium trichloride;gadolinium(iii) chloride;gadolinium(iii) chloride, anhydrous, ?gdcl3
AKOS024458319
gadolinium(iii) chloride, ultra dry
gadolinium(iii) chloride, anhydrous, beads, -10 mesh, 99.99% trace metals basis
gadolinium(iii) chloride, anhydrous (99.9%-gd) (reo)
mfcd00011024
Q415113
HY-103314
gadolinium(iii) chloride hydrate (99.9%-gd) (reo)
CS-0027602

Research Excerpts

Overview

Gadolinium chloride is a specific inhibitor of Kupffer cells (KCs), which are important promoters of various liver injuries. It is a potent blocker of voltage-sensitive Ca2+ channels.

ExcerptReferenceRelevance
"Gadolinium chloride (GdCl(3)) is a specific inhibitor of Kupffer cells (KCs), which are important promoters of various liver injuries. "( GdCl3 abates hepatic ischemia-reperfusion injury by inhibiting apoptosis in rats.
Gu, X; Jia, S; Li, JY; Zhang, WH; Zhou, Y, 2009
)
1.8
"Gadolinium chloride is a potent blocker of voltage-sensitive Ca2+ channels. "( The use of gadolinium to investigate the relationship between Ca2+ influx and glutamate release in rat cerebrocortical synaptosomes.
Brammer, MJ; Gomez, MV; Romano-Silva, MA, 1994
)
1.73
"Gadolinium chloride (GdCl3) is a commonly used Kupffer cell inhibitor."( Effect of gadolinium chloride treatment on concanavalin A-induced cytokine mRNA expression in mouse liver.
Hara, K; Maeda, O; Okamoto, T; Tsuzuike, N, 1998
)
1.42

Effects

ExcerptReferenceRelevance
"Gadolinium chloride (GdCl3) has been reported to block Kupffer cell (KC) phagocytic activity in rats. "( Modulation of kupffer cell activity by gadolinium chloride in endotoxemic rats.
Leiderer, R; Menger, MD; Rüttinger, D; Vollmar, B; Wanner, GA, 1996
)
2.01

Treatment

Gadolinium chloride treatment significantly suppressed the increased ALT, which was accompanied by decreased hepatic mRNA expression related to innate immune responses and ERK/JNK phosphorylation. The treatment also attenuated superoxide anion release after a lipopolysaccharide or tumor necrosis factor-alpha (TNF-alpha) challenge.

ExcerptReferenceRelevance
"The gadolinium chloride treatment significantly suppressed the increased ALT, which was accompanied by decreased hepatic mRNA expression related to innate immune responses and ERK/JNK phosphorylation."( Kupffer cell-mediated exacerbation of methimazole-induced acute liver injury in rats.
Akai, S; Oda, S; Tsuneyama, K; Uematsu, Y; Yokoi, T, 2016
)
0.92
"Gadolinium chloride pretreatment (-3 days) of the Splex group significantly reduced both their febrile responses to LPS (8 microg/kg ip) and their KC uptake of FITC-LPS 7 days postsurgery."( The spleen modulates the febrile response of guinea pigs to LPS.
Blatteis, CM; Evans, A; Feleder, C; Li, Z; Perlik, V, 2003
)
1.04
"Gadolinium chloride treatment fully depleted ED2-positive cells from the liver and significantly attenuated superoxide anion release after a lipopolysaccharide or tumor necrosis factor-alpha (TNF-alpha) challenge. "( Kupffer cell depletion attenuates superoxide anion release into the hepatic sinusoids after lipopolysaccharide treatment.
Fukuda, M; Horie, Y; Ishii, H; Kamegaya, Y; Kato, S; Mizukami, T; Ohgo, H; Okamura, Y; Yokoyama, H, 2004
)
1.77
"Gadolinium chloride pretreatment to ablate Kupffer cells blocked this increase of hepatic oxygen consumption after femur fracture but had no effect in sham-operated animals."( Adaptive Kupffer cell alterations after femur fracture trauma in rats.
Baker, CC; Bracey, LW; Huynh, T; Lemasters, JJ, 1997
)
1.02
"Gadolinium chloride treatment reduced total hepatic microsomal P450 as well as aniline hydroxylase activity by approximately 30% in males and 20% in females."( Gadolinium chloride reduces cytochrome P450: relevance to chemical-induced hepatotoxicity.
Badger, DA; Kuester, RK; Sauer, JM; Sipes, IG, 1997
)
2.46
"Gadolinium chloride pretreatment eliminated the rise in lung iNOS activity and protein expression and significantly attenuated the increase in pulmonary exhaled NO product, but it had no effect on arterial pressure."( Contribution of macrophages to pulmonary nitric oxide production in septic shock.
Fujii, Y; Goldberg, P; Hussain, SN, 1998
)
1.02
"Rats treated with gadolinium chloride to deplete macrophages showed a significant drop in apoptosis, suggesting a causal relationship between macrophages and epithelial cell apoptosis."( Castration-induced prostate epithelial cell apoptosis results from targeted oxidative stress attack of M1
Augusto, TM; Baratti, MO; Barbosa, GO; Bruni-Cardoso, A; Carvalho, HF; Cesar, CL; Corrêa-da-Silva, F; Damas-Souza, DM; Felisbino, SL; Ferrucci, D; Menezes, GB; Moraes-Vieira, PM; Nishan, U; Oliveira, SBP; Rosa-Ribeiro, R; Santana, JCO; Silva, JAF; Siqueira-Berti, A; Stach-Machado, DR, 2019
)
0.84
"Pretreatment with gadolinium chloride increased the severity of cholestasis and signs of liver damage."( In vivo effect of selective macrophage suppression on the development of intrahepatic cholestasis in mice.
Alexeenko, TV; Cherkanova, MS; Filjushina, EE; Goncharova, IA; Klishevich, MS; Korolenko, TA; Savchenko, NG; Zhanaeva, SY, 2008
)
0.67
"Pretreatment with gadolinium chloride to deplete Kupffer cells before IR: 1) blocked the increase in serum bile acids, 2) attenuated TNFalpha but not IL1beta/IL6 levels, 3) inhibited the altered hepatic transporter expression, and 4) blocked the decrease in HNF1alpha nuclear protein levels."( Kupffer cell-mediated downregulation of hepatic transporter expression in rat hepatic ischemia-reperfusion.
Chen, C; Klaassen, CD; Maher, JM; Tanaka, Y, 2006
)
0.66
"Treatment with gadolinium chloride (GdCl3) selectively reduced the capacity of Kupffer cells to generate superoxide by 65% and attenuated liver injury by 73% at 4 h and 58-69% at 24 h."( Activation of Kupffer cells and neutrophils for reactive oxygen formation is responsible for endotoxin-enhanced liver injury after hepatic ischemia.
Farhood, A; Fisher, MA; Jaeschke, H; Liu, P; McGuire, GM; Smith, CW, 1995
)
0.63
"Pretreatment with gadolinium chloride (0.5 mg/100 gm body wt, intravenously, 21 hr before saline solution or lipopolysaccharide administration), liposome-encapsulated dichloromethylene diphosphonate (40 mumol/100 gm body wt, intravenously, 44 hr before saline solution or lipopolysaccharide injection), dexamethasone (40 micrograms/100 gm body wt, intravenously, 1 hr before saline solution or lipopolysaccharide administration) or diethylcarbamazine (repeated doses, 10 mg/100 gm body wt, intravenously, 1 hr before saline solution or lipopolysaccharide injection) counteracted the lipopolysaccharide inhibitory effect on hepatic hyaluronan uptake."( Modulation of hepatic sinusoidal endothelial cell function by Kupffer cells: an example of intercellular communication in the liver.
Bagby, GJ; Deaciuc, IV; Niesman, MR; Skrepnik, N; Spitzer, JJ, 1994
)
0.61
"Pretreatment with gadolinium chloride (GdCl3), which reduces KC function, attenuated the liver leukostasis and NPS elicited by gut I/R."( Role of Kupffer cells in gut ischemia/reperfusion-induced hepatic microvascular dysfunction in mice.
Granger, DN; Horie, Y; Russell, J; Shanley, TP; Wolf, R, 1997
)
0.62
"Pretreatment with gadolinium chloride or cyclosporin A inhibited the elevations in hepatic cytokines and attenuated Cd-induced liver damage, assessed on the basis of serum alanine aminotransferase and sorbitol dehydrogenase activities."( Attenuation of cadmium-induced liver injury in senescent male fischer 344 rats: role of Kupffer cells and inflammatory cytokines.
DeCicco, LA; Rikans, LE; Yamano, T, 2000
)
0.63
"Pretreatment with gadolinium chloride, an inhibitor of Kupffer cell function, significantly decreased LDH and PNP efflux during reperfusion by approximately 60% and 50%, respectively."( Antioxidants and gadolinium chloride attenuate hepatic parenchymal and endothelial cell injury induced by low flow ischemia and reperfusion in perfused rat livers.
Bailey, SM; Reinke, LA, 2000
)
0.97
"Pretreatment with gadolinium chloride, a selective blocker of Kupffer cells, considerably potentiated damage to hepatocytes leading to generalization of this process, delayed inflammatory infiltration, and inhibited reparative processes."( Liver resistance to toxic effects of CCl(4) under conditions of gadolinium chloride depression of Kupffer cells.
Cyrendorzhiev, DD; Kutina, SN; Zubakhin, AA, 2000
)
0.87

Toxicity

ExcerptReferenceRelevance
"Acetaminophen is a mild analgesic and antipyretic agent that is safe and effective when taken in therapeutic doses."( Modulation of macrophage functioning abrogates the acute hepatotoxicity of acetaminophen.
Gardner, CR; Jollow, DJ; Laskin, DL; Price, VF, 1995
)
0.29
" One possibility is that Kupffer cells participant in this mechanism since CCl4 elevates calcium, and the release of toxic eicosanoids and cytokines by Kupffer cells is calcium-dependent."( The involvement of Kupffer cells in carbon tetrachloride toxicity.
Edwards, MJ; Kauffman, FC; Keller, BJ; Thurman, RG, 1993
)
0.29
" From these experiments, we conclude that retinol pretreatment decreases the severity of 2-nitronaphthalene and paraquat-induced pulmonary toxicity, apparently by inhibiting the inflammatory responses associated with the progression of toxic injury."( Modulation of chemical-induced lung and liver toxicity by all-trans-retinol in the male Sprague-Dawley rat.
Sauer, JM; Sipes, IG, 1995
)
0.29
"We have established conditions in which soluble Al is toxic to the yeast Saccharomyces cerevisiae."( A1 toxicity in yeast. A role for Mg?
Gardner, RC; MacDiarmid, CW, 1996
)
0.29
" Rats were pretreated with LPS (100 micrograms/kg) 2 hr before treatment with a minimally toxic dose of allyl alcohol mg/kg), and liver toxicity was assessed 18 hr later from activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in plasma and from histologic changes in liver sections."( Bacterial endotoxin enhances the hepatotoxicity of allyl alcohol.
Brown, AP; Ganey, PE; Grimes, SD; Schultze, AE; Sneed, RA, 1997
)
0.3
"Fumonisin B1 (FB1) is a toxic and carcinogenic mycotoxin produced by Fusarium verticillioides found on corn worldwide."( Fumonisin B1 hepatotoxicity in mice is attenuated by depletion of Kupffer cells by gadolinium chloride.
He, Q; Kim, J; Sharma, RP, 2005
)
0.55
" Yeast suspensions were used to examine the toxic effects of contaminants on the cyclic behaviour of metabolite changes during anaerobic glycolysis."( Effect of the periodic properties of toxic stress on the oscillatory behaviour of glycolysis in yeast-evidence of a toxic effect frequency.
André, C; Gagné, F, 2017
)
0.46

Pharmacokinetics

ExcerptReferenceRelevance
"Factor X (FX), a plasma glycoprotein playing a central role in coagulation has a long circulatory half-life compared to closely related coagulation factors."( Coagulation factor X interaction with macrophages through its N-glycans protects it from a rapid clearance.
Cherel, G; Christophe, OD; Denis, CV; Kurdi, M; Lenting, PJ, 2012
)
0.38

Dosage Studied

ExcerptRelevanceReference
" These studies were designed to determine if shorter dosing regimens of retinol potentiate carbon tetrachloride (CCl4)."( The role of inflammatory cells and cytochrome P450 in the potentiation of CCl4-induced liver injury by a single dose of retinol.
Badger, DA; Hoglen, NC; Jolley, CS; Sauer, JM; Sipes, IG, 1996
)
0.29
" But no relationship was observed between GdCl3 dosage and enzyme activities."( Modulation of Kupffer cells on hepatic drug metabolism.
Chen, J; Ding, H; Shi, GG; Tong, J; Wu, JY; Wu, SC; Yin, DK; Yuan, XF, 2004
)
0.32
" HO-1 expression was undetectable in hepatic parenchymal cells from rats receiving Methocel control or a single dose of ethinyl estradiol, however cytosolic HO-1 immunoreactivity in these cells after repeated dosing of ethinyl estradiol was pronounced."( Hepatic expression of heme oxygenase-1 and antioxidant response element-mediated genes following administration of ethinyl estradiol to rats.
Barron, AM; Leone, A; Lord, P; McMillian, MK; Morio, LA; Nie, AY; Parker, JB; Sawant, SP; Taggart, P, 2006
)
0.33
" Dose-response curves to methoxamine (alpha(1)-adrenergic agonist) were obtained in the absence or the presence of the nitric oxide synthase inhibitor N-monomethyl-L-arginine."( Decreased intrahepatic response to alpha(1)-adrenergic agonists in lipopolysaccharide-treated rats is located in the sinusoidal area and depends on Kupffer cell function.
Abraldes, JG; Groszmann, RJ; Haq, O; Iwakiri, Y; Lee, CH; Loureiro-Silva, MR, 2007
)
0.34
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (1)

RoleDescription
TRP channel blockerAn agent that inhibits the passage of cations through the transient receptor potential (TRP) channels.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (1)

ClassDescription
gadolinium coordination entity
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Research

Studies (542)

TimeframeStudies, This Drug (%)All Drugs %
pre-199012 (2.21)18.7374
1990's176 (32.47)18.2507
2000's212 (39.11)29.6817
2010's134 (24.72)24.3611
2020's8 (1.48)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 35.48

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index35.48 (24.57)
Research Supply Index6.34 (2.92)
Research Growth Index5.77 (4.65)
Search Engine Demand Index49.09 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (35.48)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials1 (0.18%)5.53%
Reviews3 (0.53%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other563 (99.29%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]