Antioxidant defense in renal proximal tubular cells from normal and diabetic rats
Abstract
Primary cultures of proximal tubular (PT) cells from streptozotocin (STZ) diabetic rats had higher basal and toxicant‐stimulated reactive oxygen species and mitochondrial membrane potential and were more susceptible to oxidant injury as compared to those from age‐matched control rats. Both N‐acetyl‐L‐cysteine (NAC) and a cell‐permeable catalase derivative (Cat‐SKL) protected. Despite higher basal oxidant stress, mitochondria of diabetic PT cells had higher GSH content. Protein levels of mitochondrial GSH transporters were slightly higher in diabetes, that of superoxide dismutase 2 (SOD2) was modestly elevated, and that of total thioredoxin 2 (Trx2) was decreased at 30 days and increased at 90 days. Levels of 3‐nitrotyrosine‐modified proteins in mitochondria were somewhat higher at both times in diabetic rats. 4‐Hydroxy‐2‐nonenal (HNE)‐modified proteins were mostly increased at 30 days but decreased at 90 days. Thus, redox processes and mitochondrial energetics are markedly altered due to diabetes and change as nephropathy progresses. (Supported by DOD Grant PR64340)
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 01, 2010
- Source ID
- 10.1096/fasebj.24.1_supplement.569.6
Entities
People
- David A. Putt
- Lawrence Harold Lash
- Qing Zhong
- Stanley R. Terlecky
Organizations
- United States Department of Defense
- Wayne State University