NDLI: Comparative cytotoxicity of 5-aminosalicylic acid (mesalazine) and related compounds in different cell lines

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Comparative cytotoxicity of 5-aminosalicylic acid (mesalazine) and related compounds in different cell lines

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Cell Biology and Toxicology : Volume 13, Issue 4-5, July 1997

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Cell Biology and Toxicology : Volume 13, Issue 1, January 1997

Comparative cytotoxicity of 5-aminosalicylic acid (mesalazine) and related compounds in different cell lines

Content Provider	Springer Nature Link
Author	ble, E. Janssen, L. Dierickx, P.J.
Copyright Year	1997
Abstract	Nonsteroidal anti-inflammatory drugs can cause serious side-effects such as tubulo-interstitial nephritis. Mesalazine (5-ASA, 5-aminosalicylic acid) is used for the treatment of colitis ulcerosa, Crohn disease, and other diseases; it has been found to induce necrosis of both proximal convoluted tubules and renal papillaries. The comparative cytotoxicity of 3-, 4-, and 5- aminosalicylic acid, acetylsalicylic acid (AcSA), and the parent compound salicylic acid (SA) was investigated for the free acids and for their sodium salts. The interaction with endogenous glutathione (GSH) was also investigated. Four established cell lines were used: MDCK, LLC-PK1, NRK as renal cells, and HepG2 as hepatic cells. The free acid compounds were less toxic than their corresponding salts. Acidic 5-ASA was the most toxic of the three isomers in MDCK and LLC-PK1 cells, while NRK and HepG2 were more susceptible to acidic 3-ASA. Addition of NaOH modified the relative toxicity of 3-ASA and 5-ASA. The LLC-PK1 and HepG2 cells were more sensitive to the test chemicals as their salts than were the NRK and MDCK cells. SA and 5-ASA decreased the GSH content in renal cells and increased it in HepG2. GSH depletion with l-buthionine-(S,R)-sulfoximine enhanced the toxicity only for SA in NRK and for 5-ASA and AcSA in HepG2. No correlation between endogenous GSH and the susceptibility of MDCK and LLC-PK1 to the test compounds was observed. The results suggest that no typical nephrotoxic effect occurred. No explanation could be found for the tubulo-interstitial nephritis caused by 5-ASA therapy.
Starting Page	445
Ending Page	451
Page Count	7
File Format	PDF
ISSN	07422091
Journal	Cell Biology and Toxicology
Volume Number	13
Issue Number	6
e-ISSN	15736822
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	1997-01-01
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Pharmacology/Toxicology Veterinary Medicine Animal Anatomy / Morphology / Histology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Health, Toxicology and Mutagenesis Toxicology

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