Damaging effects of advanced glycation end-products in the murine macrophage cell line J774A.1

The interaction of reducing sugars, such as aldose, with proteins and the subsequent molecular rearrangements, produces irreversible advanced glycation end-products (AGEs), a heterogeneous class of non-enzymatic glycated proteins or lipids. AGEs form cross-links, trap macromolecules and release reac...

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Bibliographic Details
Published in:	Toxicology in vitro Vol. 16; no. 4; pp. 339 - 347
Main Authors:	Bassi, A.M, Ledda, S, Valentini, S, De Pascale, M.C, Rossi, S, Odetti, P, Cottalasso, D
Format:	Journal Article Conference Proceeding
Language:	English
Published:	Oxford Elsevier Ltd 01-08-2002 Elsevier Science
Subjects:	Age Animals Arginine - adverse effects Arginine - analogs & derivatives Arginine - pharmacokinetics Biological and medical sciences Cell Line Cell metabolism, cell oxidation Cell physiology Chromatography, High Pressure Liquid Diabetes Mellitus - physiopathology Fundamental and applied biological sciences. Psychology Glycation End Products, Advanced - adverse effects Glycoxidation In vitro cytotoxicity Lipid Peroxidation Lysine - adverse effects Lysine - analogs & derivatives Lysine - pharmacokinetics Macrophages - pathology Mice Molecular and cellular biology Oxidative Stress Pentosidine Ribose - metabolism TBARs PBS Oxidative stress Glycoxidation CML TBARs In vitro cytotoxicity RAGE GS MTT Pentosidine HCl NRU DMEM LDH FBS NGS HFBA Age Vertebrata Mammalia Cell line Monocyte Mouse Toxicity Reaction product Rodentia Cytotoxicity In vitro Glycation
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Summary:	The interaction of reducing sugars, such as aldose, with proteins and the subsequent molecular rearrangements, produces irreversible advanced glycation end-products (AGEs), a heterogeneous class of non-enzymatic glycated proteins or lipids. AGEs form cross-links, trap macromolecules and release reactive oxygen intermediates. AGEs are linked to aging, and increase in several related diseases. The aim of this study was to assess, in a murine macrophage cell line, J774A.1, the effects of 48 h of exposure to glycated serum containing a known amount of pentosidine, a well-known AGE found in the plasma and tissues of diabetic and uremic subjects. Fetal bovine serum was incubated with ribose (50 m m) for 7 days at 37 °C to obtain about 10 nmol/ml of pentosidine. The cytotoxic parameters studied were cell morphology and viability by neutral red uptake, lactate dehydrogenase release and tetrazolium salt test. In the medium and in the intracellular compartment, bound and free pentosidine were evaluated by HPLC, as sensitive and specific glycative markers, and thiobarbituric acid reactive substances (TBARs), as index of the extent of lipid peroxidation. Our results confirm that macrophages are able to take up pentosidine. It is conceivable that bound pentosidine is degraded and free pentosidine is released inside the cell and then into the medium. The AGE increase in the medium was combined with an increase in TBARs, meaning that an oxidative stress occurred; marked cytotoxic effects were observed, and were followed by the release of free pentosidine and TBARs into the culture medium.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-2 ObjectType-Feature-1 content type line 23 SourceType-Conference Papers & Proceedings-1 ObjectType-Conference-3
ISSN:	0887-2333 1879-3177
DOI:	10.1016/S0887-2333(02)00016-4