Plasma levels of antioxidant vitamins C and E are decreased in vascular parkinsonism
Introduction
It has been widely accepted that oxidative stress is an important final mechanism of cell death in many neurodegenerative disorders including Parkinson's disease (PD) [1], [2]. Vitamin C (ascorbate) is an important water-soluble antioxidant that protects neurons from oxidative damage directly and indirectly, by restoring the reduced form of vitamin E [3], [4]. Vitamin E is a lipid-soluble, chain-breaking antioxidant that protects cellular and subcellular membranes from lipid peroxidation [5]; vitamin A is another important lipid soluble antioxidant [6]. Data on the blood levels and dietary intake of antioxidant vitamins in PD are conflicting. Several authors have reported decreased ascorbate levels [7], [8], while others have reported either normal [9] or increased levels [10] and normal dietary intake [11], [12]. Blood levels and/or dietary intake of vitamin E have been reported either decreased [8], [12] or normal [10], [11], [13]. An increased risk for PD was observed with lower dietary intake of vitamin E, but not vitamin C or carotene in one study [12] or with decreased previous intake of vitamin C and probably carotene but not vitamin E in another study [14]. Methodological differences and differences in dietary habits of the various ethnic groups studied may account for these discrepancies.
Oxidative stress and/or deficiency of antioxidant vitamins such as C and E have also been shown to participate in neuronal ischemia [1] and in the process of atherogenesis [15], [16]. Vascular parkinsonism (VP) is a recently reestablished heterogeneous entity [17] and its clinical, pathological and pathophysiological characteristics are currently under investigation [18], [19], [20]. It is caused by multiple lacunar or nonlacunar infarcts in the basal ganglia or white matter, etat grible, Binswanger's disease or, rarely, a single focal ischemic infarct or hemorrhage [21]. Clinical characteristics useful for the differentiation from PD include gait disorder, postural instability, absence of tremor, older age, unsatisfactory response to l-dopa and various combinations of cognitive decline, pyramidal and pseudobulbar signs [18].
The aim of the present cross-sectional study was to determine the plasma levels of vitamins C, E and A in PD and vascular parkinsonism in the Greek population.
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Patients
A total of 72 patients, divided into three groups, were enrolled in the study: (a) The PD group comprised 44 patients fulfilling the criteria for both probable [22] and clinically definite PD [23], and without evidence of cerebrovascular disease in CT or MRI. (b) The VP group comprised 12 patients fulfilling the following criteria: akinetorigid parkinsonism with prominent gait difficulty and/or postural instability, minimal or no response to l-dopa, vascular disease in at least two vascular
Results
Results are summarized in Table 1 and Fig. 1A–C. Patients with VP had a higher age as compared to the other groups. However, age, sex, smoking habits, disease duration and stage did not affect any of the biochemical variables significantly (data not shown). The PD and mixed groups did not differ from the control group as concerns the ascorbate levels. The VP group had significantly lower levels of ascorbate as compared to all other groups. The PD group did not differ from the controls as
Discussion
Our results are compatible with the absence of any systemic abnormality of the antioxidant vitamins C, E and A in PD. Vitamin E levels seem to be normal in brain and the cerebrospinal fluid of PD patients [27], [28], while ascorbate has been reported decreased only in the amygdala but not in the substantia nigra, other brain areas or the cerebrospinal fluid [29], [30], [31]. Thus, an abnormality, if any, of the above substance(s) in PD, may be either restricted to specific neuronal
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2020, Nutraceuticals in Brain Health and BeyondThe effects of omega-3 fatty acids and vitamin E co-supplementation on clinical and metabolic status in patients with Parkinson's disease: A randomized, double-blind, placebo-controlled trial
2017, Neurochemistry InternationalCitation Excerpt :Previous reports have indicated that omega-3 fatty acids deficiency can reduce the nigrostriatal system's ability to maintain homeostasis under oxidative conditions, which may increase the risk of PD (Fabelo et al., 2011; Cardoso et al., 2014). Furthermore, few researchers have exhibited that concentrations of vitamin E were lower in PD patients than healthy subjects (Paraskevas et al., 2003; Fukushima et al., 2011). Our previous study among gestational diabetes (GDM) have demonstrated that co-supplementation with 1000 mg omega-3 fatty acids and 400 IU vitamin E daily for 6 weeks increased total antioxidant capacity (TAC) and nitric oxide (NO), and decreased malondialdehyde (MDA) values, but unaltered glutathione (GSH) and high-sensitivity C-reactive protein (hs-CRP) levels (Jamilian et al., 2016).
Neuropsychiatric Scurvy
2015, PsychosomaticsCitation Excerpt :In 1992, Yapa reported that subclinical evidence of vitamin C deficiency, such as the presence of corkscrew hairs, confirmed by serum vitamin C assays, correlated strongly with a diagnosis of Parkinson disease among elderly patients.13 Logroscino et al. found that a diet rich in non-heme iron is associated with an increased risk of the development of Parkinson disease, and this risk is further increased if the diet is poor in vitamin C.14 In vascular parkinsonism, serum levels of vitamin C, as well as vitamin E, tend to be lower than in controls.15 In another interesting study of patients with Parkinson disease, King et al.16 found that the serum vitamin C level did not differ between patients and healthy young controls.
Autophagy as an essential cellular antioxidant pathway in neurodegenerative disease
2014, Redox BiologyCitation Excerpt :In the brain, decreased glutathione levels have also been reported in aging [31] and sporadic Parkinson’s disease [32–38]. Plasma levels of ascorbate and α-tocopherol have been reported to be lower in vascular but not non-vascular Parkinson’s disease patients [39]. The coenzyme Q10 is more oxidized in platelets of Parkinson’s disease patients consistent with increased mitochondrial oxidative stress [40].
Inhibition of lipid peroxidation and protein oxidation by endogenous and exogenous antioxidants in rat brain microsomes in vitro
2012, Neuroscience LettersCitation Excerpt :In addition, the antioxidant activity of α-T increases under reducing conditions which allow oxidized α-T to be recycled back to the reduced form. However, neurodegenerative disorders are characterized by both a strong pro-oxidant conditions and a marked reduction in the amount of reducing agents [26]. Keeping this in mind, our results, obtained in the absence of reducing agents, are in line with the pathophysiology of neurodegenerative disorders and contribute to explain the low antioxidant activity of α-T.
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