Salsolinol, a catechol neurotoxin, induces oxidative modification of cytochrome c.

Abstract

Methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), an endogenous neurotoxin, is known to perform a role in the pathogenesis of Parkinson's disease (PD). In this study, we evaluated oxidative modification of cytochrome c occurring after incubation with salsolinol. When cytochrome c was incubated with salsolinol, protein aggregation increased in a dosedependent manner. The formation of carbonyl compounds and the release of iron were obtained in salsolinol- treated cytochrome c. Salsolinol also led to the release of iron from cytochrome c. Reactive oxygen species (ROS) scavengers and iron specific chelator inhibited the salsolinol-mediated cytochrome c modification and carbonyl compound formation. It is suggested that oxidative damage of cytochrome c by salsolinol might induce the increase of iron content in cells, subsequently leading to the deleterious condition which was observed. This mechanism may, in part, provide an explanation for the deterioration of organs under neurodegenerative disorders such as PD.

• Authors: Jung Hoon Kang
• Journal: BMB reports (BMB Rep) Vol. 46 Issue 2 Pg. 119-23 (Feb 2013) ISSN: 1976-670X [Electronic] Korea (South)
• PMID: 23433116 (Publication Type: Journal Article)

Chemical References

• Isoquinolines
• Neurotoxins
• Reactive Oxygen Species
• Copper
• Cytochromes c
• salsolinol
• Iron

Topics

• Animals
• Cell Line, Tumor
• Copper (chemistry)
• Cytochromes c (metabolism)
• DNA Damage (drug effects)
• Iron (chemistry)
• Isoquinolines (toxicity)
• Neurotoxins (toxicity)
• Oxidative Stress (drug effects)
• Protein Carbonylation (drug effects)
• Rats
• Reactive Oxygen Species (metabolism)