Korean J Physiol Pharmacol.  2003 Feb;7(1):33-37.

Overexpressed Mitochondrial Thioredoxin Protects PC12 Cells from Hydrogen Peroxide and Serum-deprivation

• Lee YS
• Yu SA

Abstract

Oxidative damage to mitochondria is a critical mechanism in necrotic or apoptotic cell death induced by many kinds of toxic chemicals. Thioredoxin (Trx) family proteins are known to play protective roles in organisms under oxidative stress through redox reaction by using reducing equivalents of cysteines at a conserved active site, Cys-X-X-Cys. Whereas biological and physiological properties of Trx1 are well characterized, significance of mitochondrial thioredoxin (Trx2) is not well known. Therefore, we addressed physiological role of Trx2 in PC12 cells under oxidative stress. In PC12 cells, transiently overexpressed Trx2 significantly reduced cell death induced by hydrogen peroxide, whereas mutant Trx2, having serine residues instead of two cysteine residues at the active site did not. In addition, stably expressed Trx2 protected PC12 cells from serum deprivation. These results suggest that Trx2 may play defensive roles in PC12 cells by reducing oxidative stress to mitochondria.

Keyword

Mitochondrial thioredoxin (Trx2); Oxidative stress; Serum deprivation; PC12 cells; Cell death

MeSH Terms

Animals
Catalytic Domain
Cell Death
Cysteine
Humans
Hydrogen Peroxide*
Hydrogen*
Mitochondria
Oxidation-Reduction
Oxidative Stress
PC12 Cells*
Serine
Thioredoxins*
Cysteine
Hydrogen
Hydrogen Peroxide
Serine
Thioredoxins