Genetic vitamin E deficiency does not affect MPTP susceptibility in the mouse brain (original) (raw)
Related papers
Vitamin E therapy in Parkinson's disease
Toxicology, 2003
Though the etiology is not well understood, late-onset Parkinson's disease (PD) appears to result from several key factors including exposure to unknown environmental toxicants, toxic endogenous compounds and genetic alterations. A plethora of scientific evidence suggest that these environmental and endogenous factors cause PD by producing mitochondrial (mito) oxidative stress and damage in the substantia nigra, leading to cell death. Thus assuming a critical role for mito oxidative stress in PD, therapies to treat or prevent PD must target these mito and protect them against oxidative damage. The focus of this article is to briefly review the experimental and clinical evidence for the role of environmental toxicants and mito oxidative stress/damage in PD as well as discuss the potential protective role of mito d-a-tocopherol (T) enrichment and vitamin E therapy in PD. New experimental data are presented that supports the enrichment of mito with T as a critical event in cytoprotection against toxic mito-derived oxidative stress. We propose that chronic, high dose vitamin E dietary supplementation or parenteral vitamin E administration (e.g. vitamin E succinate) may serve as a successful therapeutic strategy for the prevention or treatment of PD (by enriching substantia nigra mito with protective levels of T). #
Effects of vitamin E on neurodegenerative diseases: an update
Acta Neurobiologiae Experimentalis, 2021
Vitamin E deficiency is associated with many neurological problems. Although the mechanisms of vitamin E action in neurodegenerative diseases are not clear, there are many possible mechanisms. Examples of such mechanisms are the protective effects of vitamin E against oxidative stress damage and its suppressive role in the expression of many genes involved in the development of neurodegeneration. Many studies have evaluated the relationship between vitamin E intake or vitamin E levels in body fluids and neurodegenerative diseases. Some studies concluded that vitamin E can play a protective role in neurodegeneration with respect to diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), stroke and amyotrophic lateral sclerosis (ALS). Vitamin E supplementation was also associated with risk factors for some neurodegenerative diseases. In this review, we discuss the possible effects of vitamin E on the development and course of AD, PD, stroke and ALS, and the potential mechanisms involved.
Neuroscience Letters, 2005
Dopaminergic cell death in the ventral and dorsal tiers of substantia nigra pars copmacta (SNc) and their prevention by anti-oxidant diet was immunohistochemically studied in the zitter mutant rats, which are characterized by abnormal metabolism of superoxide. Similar to previous reports, the number of SNc neurons in Nissl-stained section decreased with age. Tyrosine hydroxylase (TH) immunohistochemistry demonstrated that the dopaminergic neurons in the ventral tier of SNc degenerated early, whereas the dorsal tier gradually degenerated with age. Thus, the ventral tier dopaminergic neurons are affected first, but the dorsal tier neurons do become impact by the zi/zi mutation. Following 9-month period after weaning, zitter rats supplemented with 500 mg d,l-␣-tocophenol (VE(+))/kg diet exhibited a significant increased of surviving TH-immunoreactive neurons in both the tiers of SNc as compared with the zi/zi rats with control and VE(−) diets. These results suggest that VE supplement may slow the dopaminergic cell loss in zitter mutant rat, and further support that degeneration of the dopaminergic neurons in this mutant rat is caused by oxidant stress. Thus, the zitter rat may represent a good model for studying the dopaminergic cell death by superoxide species.
Vitamin E and neurodegenerative diseases
Molecular Aspects of Medicine, 2007
Vitamin E is essential for neurological function. This fact, together with a growing body of evidence indicating that neurodegenerative processes are associated with oxidative stress, lead to the convincing idea that several neurological disorders may be prevented and/or cured by the antioxidant properties of vitamin E.
Vitamin E and Neurodegenerative Disorders Associated with Oxidative Stress
Nutritional Neuroscience, 2002
Several neurodegenerative disorders are associated with oxidative stress that is manifested by lipid peroxidation, protein oxidation and other markers. Included in these disorders in which oxidative stress is thought to play an important role in their pathogenesis are Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), tardive dyskinesia, Huntington's disease (HD), and multiple sclerosis. This review presents some of the chemistry of vitamin E as an antioxidant and summarizes studies in which vitamin E has been employed in these disorders and models thereof.
Journal of the Neurological Sciences, 1988
Longitudinal studies were carried out over 55 weeks in vitamin E deficient and control rats. It was shown that neurological tissues (brain, cord and nerve) retained a greater percentage of vitamin E (~-tocopherol) than other tissues (serum, liver and adipose tissue), and that there was no evidence for compensation by other antioxidant enzyme systems (superoxide dismutase and giutathione peroxidase). An increased uptake of 0t-[3H]tocopherol (150~ of controls) was observed in peripheral nerve of deficient animals from 11 weeks, whereas similar increases were not found in brain and cord until 36 weeks. These results were correlated with tests of neurological function which included electrophysiological studies and measurement of axonal transport. Recordings of somatosensory evoked potentials showed a significant delay (P < 0.001) of central conduction velocity after 40 weeks of deficiency, whereas peripheral conduction was unchanged. After 40 weeks of deficiency, abnormal electromyographic activity of the hind limbs was obtained which was suggestive of chronic partial denervation. By 52 weeks there were significant reductions of both fast anterograde (P < 0.02) and retrograde (P < 0.05) transport of acetylcholinesterase in the deficient rats.
Parkinsonism & Related Disorders, 2008
Background: Free radical formation and oxidative stress might play an important role in the pathogenesis of Parkinson's disease (PD). In vitro data indicate that neuromelanin (NM) pigment is formed the excess cytosolic catecholamine that is not accumulated into synaptic vesicles via the vesicular monoamine transporter 2 (VMAT2). We designed this study to investigate the neuroprotective effects of vitamin E in the early model of PD. Methods: Male rats (n = 40) with unbiased rotational behavior were randomly divided into five groups: sham operated group (SH, n = 8), vehicle-treated SH group (SH + V, n = 8), vitamin E-treated SH group (SH + E, n = 8), vehicle-treated lesion group (L + V, n = 8) and vitamin E-treated lesion group (L + E, n = 8). Unilateral intrastriatal 6-hydroxydopamine (12.5 µl) lesioned rats were treated intramuscularly with αtocopherol acid succinate (24 I.U/kg, intramuscular [i.m.]) 1 h before surgery and three times per week for 2 month post-surgery. To evaluate the vitamin E pretreatment efficacy, tyrosine hydroxylase (TH) immunoreactivity and immunostaining intensity (ISI) for monoamine transporter 2 were used. Results: TH immunohistochemical analyses showed a reduction of 20% in locus coeruleus (LC) cell number of vitamin E pretreated lesioned group but the cell number dropped to 60% in the lesioned group. The ISI of the cells was measured for VMAT2 in LC. Lesioned groups: 1) had the lowest VMAT2 ISI of all neurons; 2) There was an inverse relationship between VMAT2 ISI and NM pigment in the locus and 3) Neurons with the highest VMAT2 ISI also had high TH ISI. Conclusion: The data support the hypothesis that repeated i.m. administration of vitamin E exerts a protective effect on the LC neurons in the early model of PD. Iran.
Annals of Neurology, 1994
Four patients with vitamin E deficiency and sensory ataxia were studied using E*8Fldopa positron emission tomography. The 2 most disabled patients, who had severe and prolonged vitamin E deficiency due to abetalipoproteinemia, showed reduced {"FF)dopa uptake in both putamen and caudate. Putaminal uptake was in a similar range to that seen in Parkinson's disease. Studies of E3H)mazindol binding in the striatum of vitamin E-deficient rats indicated a reduced number of dopamine terminals, which was most severe in ventrolateral striatum. These observations suggest that severe and prolonged vitamin E deficiency results in loss of nigrostriatal nerve terminals, and support the hypothesis that oxidative stress may contribute to the etiology of Parkinson's disease.
Journal of Alzheimer's Disease, 2003
Compensatory upregulation in endogenous antioxidants has been shown to accompany certain genetic and dietary deficiencies that promote oxidative stress, including that related to Alzheimer's disease. We compared antioxidant levels in brain tissue of normal and transgenic mice lacking apolipoprotein E following dietary deprivation of vitamin E or folate. As described previously, ApoE-deficient mice displayed increased levels of the endogenous antioxidant glutathione as compared to normal mice, and increased these levels further following folate deprivation. By contrast, glutathione was depleted following vitamin E deprivation in brain tissue of normal and ApoE-deficient mice. TBAR analyses confirmed increased oxidative damage following vitamin E deprivation. However, combined deprivation of folate and vitamin E resulted in levels of glutathione intermediate between those observed following deprivation of either agent, indicating that the lack of compensatory increase in glutathione following vitamin E deprivation was not due to overt neurotoxicity. Similar results were observed for total antioxidant levels in brain tissue. The differential response to vitamin E and folate deprivation is consistent with the possibility that specific differences in oxidative damage may result from deficiencies in either of these agents. The lack of a compensatory response to vitamin E deprivation highlights the importance of dietary vitamin E in prevention of chronic neurodegeneration.