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In Vitro Toxicological Assessment of Gadodiamide in Normal Brain SVG P12 Cells

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cris.lastimport.scopus2026-02-26T16:01:55Z
dc.creatorTsai, Yuh-feng
dc.creatorYang, Jai-sing
dc.creatorTsai, Fuu-jen
dc.creatorLu, Chi-cheng
dc.creatorChiu, Yu-jen
dc.creatorTsai, Shih-chang
dc.date2021-09
dc.date.accessioned2021-11-08T06:33:31Z
dc.date.accessioned2025-07-27T15:03:18Z
dc.date.available2021-11-08T06:33:31Z
dc.date.issued2021-11-08T06:33:31Z
dc.description.abstractBackground/Aim: Magnetic resonance imaging (MRI) is a technique for evaluating patients with primary and metastatic tumors. The contrast agents improve the diagnostic accuracy of MRI. Large quantities of a contrast agent must be administrated into the patient to obtain useful images, which leads to cell injury. Gadolinium has been reported to cause central lobular necrosis of the liver and nephrogenic systemic fibrosis. However, the toxicity caused on brain tissue is uncertain. Materials and Methods: This study mainly aimed on the in vitro study of high concentration (2 and 5-fold of normal concentration) gadolinium-based contrast agents (GBCAs), gadodiamide (Omniscan (R)), on normal brain glial SVG P12 cells. MTT assay, DAP1 staining, immunofluorescent staining, LysoTracker Red staining, and western blotting analysis were applied on the cells. Results: The viability of gadodiamide (13, 2.6, 5.2, 13 and 26 mM)-treated SVG P12 cells was significantly reduced after 24 h of incubation. Gadodiamide caused significant autophagic flux at 2.6, 52 and 13.0 mM as seen by acridine orange (AO) staining, LC-3-GFP and LysoTracker Red staining. The expression levels of autophagy-related proteins such as heeling , ATG-5, ATG-14 and LC-3 II were up-regulated after 24 h of gadodiamide incubation. Autophagy inhibitors including 3-methyladenine (3-MA), chloroquine (CQ) and bafilomycin Al (Baf) significantly alleviated the autophagic cell death effect of gadodiamide on normal brain glial SVG P12 cells. Gadodiamide induced significant apoptotic effects at 52 mM and 13.0 mM as seen by DAPI staining and the pan-caspase inhibitor significantly alleviated the apoptotic effect. Gadodiamide at 5.2 mM and 13.0 mM inhibited antiapoptotic protein expression levels of Bcl-2 and Bcl-XL, while promoted pro-apoptotic protein expression levels of Bax, BAD, cytochrome c, Apaf-1 cleaved-caspase-9 and cleaved-caspase-3. Conclusion: Normal brain glial SVG P12 cells treated with high concentrations of gadodiamide can undergo autophagy and apoptosis.
dc.format.extent109 bytes
dc.format.mimetypetext/html
dc.identifier.doi10.21873/invivo.12544
dc.identifier.issn0258-851X
dc.identifier.urihttps://ir.ntus.edu.tw/handle/987654321/64479
dc.languageen_US
dc.publisherATHENS, GREECE:INT INST ANTICANCER RESEARCH
dc.relationIN VIVO, 35(5), p.2621-2630
dc.subjectBrain glial SVG P12 cells
dc.subjectgadodiamide
dc.subjectautophagy
dc.subjectapoptosis
dc.titleIn Vitro Toxicological Assessment of Gadodiamide in Normal Brain SVG P12 Cells
dc.typearticle
dspace.entity.typePublication

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