Abstract
An important drug used in the treatment of Parkinson’s disease is amantadine. We are the first to perform a comprehensive study based on various glycation and oxidation factors, determining the impact of amantadine on protein glycoxidation. Sugars (glucose, fructose, galactose) and aldehydes (glyoxal, methylglyoxal) were used as glycation agents, and chloramine T was used as an oxidant. Glycoxidation biomarkers in albumin treated with amantadine were generally not different from the control group (glycation/oxidation factors), indicating that the drug did not affect oxidation and glycation processes. Molecular docking analysis did not reveal strong binding sites of amantadine on the bovine serum albumin structure. Although amantadine poorly scavenged hydroxyl radical and hydrogen peroxide, it had significantly lower antioxidant and antiglycation effect than all protein oxidation and glycation inhibitors. In some cases, amantadine even demonstrated glycoxidant, proglycation, and prooxidant properties. In summary, amantadine exhibited weak antioxidant properties and a lack of antiglycation activity.
Author contributions
MN did laboratory determinations, interpreted the data, prepared the graphic part of the manuscript, wrote the manuscript, and expressed final approval of the version to be published. MZP interpreted the data. JRL interpreted the data. AZ conceptualised and reviewed the article, and provided final approval of the version to be published. MM conceptualised the article, did laboratory determinations, interpreted the data, prepared the graphic part of the manuscript, wrote the manuscript, reviewed the article, and granted final approval of the version to be published.
Disclosure statement
The authors report no conflicts of interest.
Data availability statement
The data that support the findings of this study are available from the corresponding author upon reasonable request. Some data may not be made available because of privacy or ethical restrictions.