Premium
Antioxidant defense in renal proximal tubular cells from normal and diabetic rats
Author(s) -
Lash Lawrence Harold,
Putt David A.,
Terlecky Stanley R.,
Zhong Qing
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.569.6
Subject(s) - mitochondrion , streptozotocin , sod2 , oxidative stress , chemistry , medicine , diabetic nephropathy , endocrinology , superoxide dismutase , reactive oxygen species , glutathione , thioredoxin , diabetes mellitus , antioxidant , biochemistry , biology , enzyme
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)