Abstract
Tamoxifen (TAM) is a nonsteroidal triphenylethylene antiestrogenic drug widely used in the treatment and prevention of breast cancer. TAM brings about a collapse of the mitochondrial membrane potential. It acts both as an uncoupling agent and as a powerful inhibitor of mitochondrial electron transport chain. The effect of catechin pretreatment on the mitochondrial toxicity of TAM was studied in liver mitochondria of Swiss albino mice. TAM treatment caused a significant increase in the mitochondrial lipid peroxidation (LPO) and the protein carbonyls (PCs). It also caused a significant increase in superoxide radical production. Pretreatment of mice with catechin (40 mg/kg) showed significant protection as demonstrated by marked attenuation of increased oxidative stress parameters such LPO, PCs, and superoxide production. It also restored the decreased nonenzymatic and enzymatic antioxidants of mitochondria. The inhibitory effect of catechin on TAM-induced oxidative damage suggests that it may have potential benefits in prevention of human diseases where reactive oxygen species have some role as causative agents.
Original language | English (US) |
---|---|
Pages (from-to) | 110-117 |
Number of pages | 8 |
Journal | Journal of Biochemical and Molecular Toxicology |
Volume | 21 |
Issue number | 3 |
DOIs | |
State | Published - 2007 |
Externally published | Yes |
Keywords
- Catechin
- Lipid peroxidaion
- Mitochondria
- Oxidative stress
- Protein oxidation
- Tamoxifen
ASJC Scopus subject areas
- Biochemistry
- Molecular Medicine
- Molecular Biology
- Toxicology
- Health, Toxicology and Mutagenesis