Abstract
Parkinson's disease (PD) is characterized by progressive motor impairment attributed to progressive loss of dopaminergic neurons in the substantia nigra (SN) pars compacta. In addition to an accumulation of iron, there is also an increased production of reactive oxygen/nitrogen species (ROS/RNS) and inflammatory markers. These observations suggest that iron dyshomeostasis may be playing a key role in neurodegeneration. However, the mechanisms underlying this metal-associated oxidative stress and neuronal damage have not been fully elucidated. To determine peripheral levels of iron, ferritin, and transferrin in PD patients and its possible relation with oxidative/nitrosative parameters, whilst attempting to identify a profile of peripheral biomarkers in this neurological condition. Forty PD patients and 46 controls were recruited to compare serum levels of iron, ferritin, transferrin, oxidative stress markers (superoxide dismutase (SOD), catalase (CAT), nitrosative stress marker (NOx), thiobarbituric acid reactive substances (TBARS), non-protein thiols (NPSH), advanced oxidation protein products (AOPP), ferric reducing ability of plasma (FRAP) and vitamin C) as well as inflammatory markers (NTPDases, ecto-5’-nucleotidase, adenosine deaminase (ADA), ischemic-modified albumin (IMA) and myeloperoxidase). Iron levels were lower in PD patients, whereas there was no difference in ferritin and transferrin. Oxidative stress (TBARS and AOPP) and inflammatory markers (NTPDases, IMA, and myeloperoxidase) were significantly higher in PD, while antioxidants FRAP, vitamin C, and non-protein thiols were significantly lower in PD. The enzymes SOD, CAT, and ecto-5’-nucleotidase were not different among the groups, although NOx and ADA levels were significantly higher in the controls. Our data corroborate the idea that ROS/RNS production and neuroinflammation may dysregulate iron homeostasis and collaborate to reduce the periphery levels of this ion, contributing to alterations observed in the pathophysiology of PD.
Highlights
Oxidative stress is a present factor throughout the average aging process
Previous studies suggest that altered iron homeostasis may be involved with Parkinson’s disease (PD) pathogenesis, where lower levels of serum iron were found in individuals who developed the disease [3, 4]
Since nitric oxide (NO) has been linked to iron metabolism [30] and proposed as a major upstream event in PD pathogenesis [31], we evaluated the involvement of nitrosative stress in this disease
Summary
Oxidative stress is a present factor throughout the average aging process. it is higher in at least 60 different age-related diseases, such as Parkinson’s disease (PD) [1]. In PD, oxidative stress is a result of mitochondrial deficiency, in addition to a chronic inflammatory process, in which both produce reactive oxygen species (ROS) and reactive nitrogen species (RNS). These reactive species meet the accumulated iron in the brain and harm structures, leading to the death of dopaminergic neurons in the substantia nigra. This process creates a cycle of cell damage, neuroinflammation, and ROS/RNS production, resulting in neuronal death [2]. Other oxidative stress and inflammatory markers are being studied: advanced oxidation protein products (AOPP), ferric reducing ability of plasma (FRAP), nitric oxide (NO), thiobarbituric acid reactive substances (TBARS), vitamin C and non-protein thiols (NPSH) as well as ATP and ADP NTPDases, ecto-5’-nucleotidase, adenosine deaminase (ADA), myeloperoxidase and ischemic-modified albumin (IMA)
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