Perturbation of Transferrin by Thiol Oxidation affects mitochondrial Ferritin behavior & triggers...
- OLCIAS
- Jul 6, 2023
- 2 min read
Talk Title: Perturbation of Transferrin by Thiol Oxidation affects mitochondrial Ferritin behavior & triggers Ferroptosis - the complex Neurochemistry of Parkinsonian neurons
Author: Narendra Singh Amity University Kolkata, India Email: todaysman63@gmail.com Co-author: Ruchita Karmakar Amity University Kolkata ,India Email: ruchitakarmakar@gmail.com Volume: Parkinson's Disease 2023_CN37_AA05 The International Live Conference on Parkinson's Disease Date: July 15, 2023 Time: 8 PM Indian Standard Time Location: Online Conference Theme: The Future of Parkinson's Disease Research and Clinical Practice Abstract: Parkinson’s disease (PD) is a common neurodegenerative disorder that is associated with degeneration of dopaminergic neurons in the substantia nigra. Although the etiology of parkinsonian neurodegeneration is complex, there is strong evidence that mitochondrial impairment and oxidative stress play key roles in PD pathogenesis. The normal substantia nigra has a higher concentration of iron than the liver, which is the body’s main iron store. The redox properties and coordination chemistry of iron make it ideally suited for a variety of biological functions. These same properties make it potentially dangerous, by virtue of its ability to generate reactive oxygen species. Therefore, iron transport, storage, and levels in cytoplasm and organelles must be tightly coordinated and controlled. The majority of cellular iron is directed to mitochondria, in part because of their high content of iron–sulfur clusters, which are essential for mitochondrial respiration. A potential role for iron accumulation in PD pathogenesis is supported by the fact that mutations in genes related to iron homeostasis are associated with a higher relative risk for developing PD. Despite the importance of iron in mitochondrial function and its potential role in PD pathogenesis, our understanding of how iron accumulates in neurons and how it is transported into mitochondria is rudimentary.
