Abstract

Background Halogenative and nitrosative stress are two types of oxidative stress that have been proposed as pathogenic mechanisms in Parkinson’s disease (PD). They can be caused by over-stimulation of phagocytes. We hypothesize that maintained phagocyte overstimulation leads to both halogenative and nitrosative stress in Parkinson’s disease, which are present in serum and cerebrospinal fluid of patients. These types of oxidative stress could modify proteins related to the pathogenesis of Parkinson’s disease.

Highlights

  • Halogenative and nitrosative stress are two types of oxidative stress that have been proposed as pathogenic mechanisms in Parkinson’s disease (PD)

  • In our lab, it has been detected the presence of halogenative stress in serum and, to a lesser extent, cerebrospinal fluid of Parkinsonian patients leading to excess of advanced oxidized protein products or AOPP

  • Nitrosative stress is present in serum and cerebrospinal fluid of patients with early PD, characterized by the selective increase of 3-nitrotyrosine proteins other than nitroalbumin and free 3-nitrotyrosine

Read more

Summary

Background

Halogenative and nitrosative stress are two types of oxidative stress that have been proposed as pathogenic mechanisms in Parkinson’s disease (PD). They can be caused by over-stimulation of phagocytes. We hypothesize that maintained phagocyte overstimulation leads to both halogenative and nitrosative stress in Parkinson’s disease, which are present in serum and cerebrospinal fluid of patients. These types of oxidative stress could modify proteins related to the pathogenesis of Parkinson’s disease

Materials and methods
Results
Conclusions

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.