Effects of the Kupffer cell inactivator gadolinium chloride on rat liver oxygen uptake and content of mitochondrial cytochromes

Ferreira, Jorge; Tapia, Gladys; Videla, Luis A.

doi:10.1016/s0014-5793(98)00356-1

Cited by 11 publications

(3 citation statements)

References 23 publications

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“…This competition is due to the fact that the cristal radius of gadolinium is similar to that of calcium, while the valency of the former is higher (Klein et al, 1994;Roland et al, 1999). GdCl 3 moderately alters microvascular perfusion in rat liver (Rüttinger et al, 1996) and reversibly decreases O 2 consumption by lowering the levels of mitochondrial cytochromes c 1 and c (Ferreira et al, 1998). Moreover, gadolinium increases the expression of hepatic cytokines and several cytokine-regulated transcription factors, such as c-JUN, C/EBP-b, and C/EBP-d (Decker, 1990;Rai et al, 1996).…”

Section: Toxicological Effects Of Lanthanidesmentioning

confidence: 99%

Toxicological and cytophysiological aspects of lanthanides action.

Pałasz¹,

Czekaj²

2000

Acta Biochim Pol

214

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Lanthanides, also called rare-earth elements, are an interesting group of 15 chemically active, mainly trivalent, f-electronic, silvery-white metals. In fact, lanthanides are not as rare as the name implies, except for promethium, a radioactive artificial element not found in nature. The mean concentrations of lanthanides in the earth's crust are comparable to those of life-important elements like iodine, cobalt and selenium. Many lanthanide compounds show particular magnetic, catalytic and optic properties, and that is why their technical applications are so extensive. Numerous industrial sources enable lanthanides to penetrate into the human body and therefore detailed toxicological studies of these metals are necessary. In the liver, gadolinium selectively inhibits secretion by Kupffer cells and it decreases cytochrome P450 activity in hepatocytes, thereby protecting liver cells against toxic products of xenobiotic biotransformation. Praseodymium ion (Pr3+) produces the same protective effect in liver tissue cultures. Cytophysiological effects of lanthanides appear to result from the similarity of their cationic radii to the size of Ca2+ ions. Trivalent lanthanide ions, especially La3+ and Gd3+, block different calcium channels in human and animal cells. Lanthanides can affect numerous enzymes: Dy3+ and La3+ block Ca2+-ATPase and Mg2+-ATPase, while Eu3+ and Tb3+ inhibit calcineurin. In neurons, lanthanide ions regulate the transport and release of synaptic transmitters and block some membrane receptors, e.g. GABA and glutamate receptors. It is likely that lanthanides significantly and uniquely affect biochemical pathways, thus altering physiological processes in the tissues of humans and animals.

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Section: Toxicological Effects Of Lanthanidesmentioning

confidence: 99%

Toxicological and cytophysiological aspects of lanthanides action.

Pałasz¹,

Czekaj²

2000

Acta Biochim Pol

214

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“…In addition, Shen et al (24) and Fu et al (25) demonstrated that Gd promoted cell proliferation in mouse embryo fibroblast NIH3T3 cells. Ferreira et al (26) indicated that no effect was noted in regards to the viability of Kupffer cells after GdCl 3 exposure. Our data also revealed that there was no viability impact (Fig.…”

Section: Discussionmentioning

confidence: 99%

Caspase‑dependent apoptotic death by gadolinium chloride (GdCl3) via reactive oxygen species production and MAPK signaling in rat C6 glioma cells

Tsai¹,

Chen

Hsiao³

et al. 2018

Oncol Rep

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Gadolinium (Gd) compounds serve as magnetic resonance imaging contrast agents and exert certain anticancer activities. Yet, the molecular signaling underlying the antitumor effect of Gd chloride (GdCl 3) on glioma remains unclear. In the present study, we aimed to ascertain the apoptotic mechanisms of GdCl 3 on rat glioma C6 cells. Our results demonstrated that GdCl 3 significantly reduced cell viability and shrunk cell morphology of C6 cells in a concentration-dependent manner. GdCl 3 led to apoptotic C6 cell death as detected by TUNEL staining. An increase in cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9 occurred in GdCl 3-treated C6 cells as detected by immunoblotting analysis. The activities of caspase-3, caspase-8 and caspase-9 were increased, and the specific inhibitors of caspase-3/-8/-9 individually reversed cell viability, which caused apoptotic death in C6 cells prior to GdCl 3 exposure. GdCl 3 also caused an elevation in the cytoplasmic Ca 2+ level and reactive oxygen species (ROS) production, as well as the loss of mitochondrial membrane potential (ΔΨm) as shown by flow cytometric analysis in C6 cells. The results from the immunoblotting analysis demonstrated that there were upregulated protein levels of cytochrome c and Bax but a downregulated protein level of Bcl-2 in C6 cells after GdCl 3 treatment. Additionally, GdCl 3 decreased the protein levels of phosphorylated-extracellular signal-regulated kinases, phosphorylated-c-Jun N-terminal kinase and phosphorylated-p38 mitogen-activated protein kinases in C6 cells. In conclusion, ROS production and MAPKs signaling pathways contribute to GdCl 3-induced caspase cascade-mediated apoptosis in C6 cells. Our findings provide a better understanding of the molecular mechanisms underlying the role of GdCl 3 in rat glioma C6 cells.

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“…Indeed, a decrease in cell viability, an increase in cell death through apoptosis, and autophagic activation have been associated with Gd (III) toxicity [10,30,34,40,[46][47][48]51,58,60,64,70,99,113]. Mitochondrial dysfunction [38,42,51,91,108,109] and suppressing mitochondria membrane potential [62,101] were also described. Besides cytotoxic, genotoxic potential has also been attributed to Gd (III) exposure [28,45,62], and DNA cleavage of peripheral blood lymphocytes was reported [70,103].…”

Section: Reference Study Design Main Findingsmentioning

confidence: 99%

Toxicity Mechanisms of Gadolinium and Gadolinium-Based Contrast Agents—A Review

Coimbra,

Rocha,

Sousa

et al. 2024

IJMS

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Gadolinium-based contrast agents (GBCAs) have been used for more than 30 years to improve magnetic resonance imaging, a crucial tool for medical diagnosis and treatment monitoring across multiple clinical settings. Studies have shown that exposure to GBCAs is associated with gadolinium release and tissue deposition that may cause short- and long-term toxicity in several organs, including the kidney, the main excretion organ of most GBCAs. Considering the increasing prevalence of chronic kidney disease worldwide and that most of the complications following GBCA exposure are associated with renal dysfunction, the mechanisms underlying GBCA toxicity, especially renal toxicity, are particularly important. A better understanding of the gadolinium mechanisms of toxicity may contribute to clarify the safety and/or potential risks associated with the use of GBCAs. In this work, a review of the recent literature concerning gadolinium and GBCA mechanisms of toxicity was performed.

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Effects of the Kupffer cell inactivator gadolinium chloride on rat liver oxygen uptake and content of mitochondrial cytochromes

Cited by 11 publications

References 23 publications

Toxicological and cytophysiological aspects of lanthanides action.

Toxicological and cytophysiological aspects of lanthanides action.

Caspase‑dependent apoptotic death by gadolinium chloride (GdCl3) via reactive oxygen species production and MAPK signaling in rat C6 glioma cells

Toxicity Mechanisms of Gadolinium and Gadolinium-Based Contrast Agents—A Review

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