Translator Disclaimer
1 December 2007 Oxidative stress and cellular stress response in diabetic nephropathy
Vittorio Calabrese, Cesare Mancuso, Maria Sapienza, Eduardo Puleo, Stella Calafato, Carolin Cornelius, Manuela Finocchiaro, Andrea Mangiameli, Maurizio Di Mauro, Anna Maria Giuffrida Stella, Pietro Castellino
Author Affiliations +
Abstract

 Oxidative stress has been suggested to play a main role in the pathogenesis of type 2 diabetes mellitus and its complications. As a consequence of this increased oxidative status, a cellular-adaptive response occurs requiring functional chaperones, antioxidant production, and protein degradation. This study was designed to evaluate systemic oxidative stress and cellular stress response in patients suffering from type 2 diabetes–induced nephropathy and in age-matched healthy subjects. Systemic oxidative stress has been evaluated by measuring advanced glycation end-products (pentosidine), protein oxidation (protein carbonyls [DNPH]), and lipid oxidation (4-hydroxy-2-nonenal [HNE] and F2-isoprostanes) in plasma, lymphocytes, and urine, whereas the lymphocyte levels of the heat shock proteins (Hsps) heme oxygenase-1 (HO-1), Hsp70, and Hsp60 as well as thioredoxin reductase-1 (TrxR-1) have been measured to evaluate the systemic cellular stress response. We found increased levels of pentosidine (P < 0.01), DNPH (P < 0.05 and P < 0.01), HNE (P < 0.05 and P < 0.01), and F2-isoprostanes (P < 0.01) in all the samples from type 2 diabetic patients with nephropathy with respect to control group. This was paralleled by a significant induction of cellular HO-1, Hsp60, Hsp70, and TrxR-1 (P < 0.05 and P < 0.01). A significant upregulation of both HO-1 and Hsp70 has been detected also in lymphocytes from type 2 diabetic patients without uraemia. Significant positive correlations between DNPH and Hsp60, as well as between the degree of renal failure and HO-1 or Hsp70, also have been found in diabetic uremic subjects. In conclusion, patients affected by type 2 diabetes complicated with nephropathy are under condition of systemic oxidative stress, and the induction of Hsp and TrxR-1 is a maintained response in counteracting the intracellular pro-oxidant status.

Vittorio Calabrese, Cesare Mancuso, Maria Sapienza, Eduardo Puleo, Stella Calafato, Carolin Cornelius, Manuela Finocchiaro, Andrea Mangiameli, Maurizio Di Mauro, Anna Maria Giuffrida Stella, and Pietro Castellino "Oxidative stress and cellular stress response in diabetic nephropathy," Cell Stress & Chaperones 12(4), 299-306, (1 December 2007). https://doi.org/10.1379/CSC-270.1
Received: 6 February 2007; Accepted: 1 April 2007; Published: 1 December 2007
JOURNAL ARTICLE
8 PAGES

This article is only available to subscribers.
It is not available for individual sale.
+ SAVE TO MY LIBRARY

SHARE
ARTICLE IMPACT
RIGHTS & PERMISSIONS
Get copyright permission
Back to Top