The uremic toxin indoxyl sulfate exacerbates reactive oxygen species production and inflammation in 3T3-L1 adipose cells

Inflammation and oxidative stress are common features of patients with chronic kidney disease (CKD) and many uremic solutes retained in these patients could be involved in these processes, among which protein-bound solutes such as indoxyl sulfate (IS). White adipose tissue recently gained attention...

Full description

Saved in:
Bibliographic Details
Published in:Free radical research 2016-03, Vol.50 (3), p.337-344
Main Authors: Stockler-Pinto, Milena B., Saldanha, Juliana F., Yi, Dan, Mafra, Denise, Fouque, Denis, Soulage, Christophe O.
Format: Article
Language:English
Subjects:
3T3-L1 Cells
Adipocytes - metabolism
Adipocytes - pathology
Adipocytes - secretion
Animals
Antioxidant
cardiovascular
cytokines
Indican - pharmacology
Inflammation
Interleukin-6 - secretion
Life Sciences
Mice
NADPH Oxidases - drug effects
Oxidative Stress - drug effects
Reactive Oxygen Species - pharmacology
Renal Insufficiency, Chronic - complications
Renal Insufficiency, Chronic - metabolism
Renal Insufficiency, Chronic - pathology
Toxins, Biological - pharmacology
Tumor Necrosis Factor-alpha - secretion
Uremia - etiology
Uremia - metabolism
Uremia - pathology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Inflammation and oxidative stress are common features of patients with chronic kidney disease (CKD) and many uremic solutes retained in these patients could be involved in these processes, among which protein-bound solutes such as indoxyl sulfate (IS). White adipose tissue recently gained attention as an important source of inflammation and oxidative stress. To examine the effect of IS on adipocytes, 3T3-L1 adipose cells were incubated with IS to mimic the conditions encountered in uremic patients. Incubation of adipose cells with IS increased reactive oxygen species production generated mainly through activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase since it was prevented by the NADPH oxidase inhibitor apocynin. Exposure to IS furthermore exacerbated the secretion of tumor necrosis factor-α and interleukin-6 by adipose cells. This inflammatory response was prevented by NADPH oxidase inhibition pinpointing the pivotal role of intracellular oxidative stress. IS induces adipocyte perturbation and promotes inflammatory state mainly through induction of oxidative stress. IS, a uremic toxin, accumulates in CKD patients could, therefore, be an important mediator of adipocyte dysfunction in these patients.
ISSN:1071-5762
1029-2470
DOI:10.3109/10715762.2015.1125996