P2.038 The protective effect of vitamin E on Locus coeruleus in early model of Parkinson's disease in rat: immunoreactivity evidence

Pasbakhsh, Parichehr; Omidi, Negar; Omidi, Hamid

doi:10.1016/s1353-8020(08)70267-0

Cited by 10 publications

(13 citation statements)

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“…Vitamin E may have neuroprotective effects against ironinduced hippocampal and nigral neurotoxicity [21] . A higher intake of vitamin E may be associated with a decreasing risk of PD [22,23] . Vitamin E is generally believed to be protective against Cu-induced oxidative damage, too [8] .…”

Section: Discussionmentioning

confidence: 99%

Serum Vitamins and Heavy Metals in Blood and Urine, and the Correlations among Them in Parkinson’s Disease Patients in China

et al. 2011

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Background: Some heavy metals are suspected to be pathogenic and some vitamins protective against Parkinson’s disease (PD), and the interaction between heavy metals and vitamins could be associated with the pathophysiology of PD. Methods: Subjects comprised PD patients and sex- and age-matched controls recruited from an outpatient clinic in China. Morning blood and urine samples were used to measure concentrations of metals and vitamins. Results: The serum iron, whole-blood manganese, urine iron and copper levels were significantly higher in the PD patients than in the controls. The correlation coefficient between serum and urine concentrations of iron in the PD patients was significant. The serum vitamin E/urine copper ratio was significantly lower in the PD patients than in the controls. Serum vitamin E was negatively correlated with serum copper and was positively correlated with urine copper in the PD patients. Serum vitamin B₁₂ was positively correlated with serum zinc in the PD patients and was negatively correlated with urine zinc in the controls. Conclusions: Excessive intake of iron and copper, accumulation of manganese, vitamin E/copper imbalance in intake, and vitamin B₁₂ decrease by zinc deficiency in the body might be involved in the etiology of PD.

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Section: Discussionmentioning

confidence: 99%

Serum Vitamins and Heavy Metals in Blood and Urine, and the Correlations among Them in Parkinson’s Disease Patients in China

et al. 2011

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“…88 However, these vitamins are potent natural antioxidants that can be used in the treatment of PD. A double-blind placebo study using vitamin E found that tardive dyskinesia severity is reduced in patients who have received vitamin E. 89 In addition, vitamin E has been shown to be neuroprotective against free radical-mediated injury, protect neurons of the locus coeruleus from death in an early model of PD, 90,15 prevent the toxin-induced destruction of striatal dopaminergic terminals, 91 and regulate the levels of antioxidant defenses such as glutathione and SOD. 16,92 Similar to vitamin E, vitamin A and C have also shown neuroprotective effects alone or in combination with CoQ10.…”

Section: Endogenous Antioxidants Coenzyme Q10mentioning

confidence: 99%

Cellular and molecular mechanisms of antioxidants in Parkinson's disease

Sutachán

Casas

Albarracín

et al. 2012

Nutritional Neuroscience

105

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Parkinson's disease (PD) is a neurodegenerative movement disorder characterized by the degeneration and progressive loss of dopaminergic neurons in the substantia nigra pars compacta. It has been suggested that oxidative stress plays a role in the etiology and progression of PD. For instance, low levels of endogenous antioxidants, increased reactive species, augmented dopamine oxidation, and high iron levels have been found in brains from PD patients. In vitro and in vivo studies of Parkinson models evaluating natural and endogenous antioxidants such as polyphenols, coenzyme Q10, and vitamins A, C, and E have shown protective effects against oxidative-induced neuronal death. In this paper, we will review the mechanisms by which polyphenols and endogenous antioxidants can produce protection. Some of the mechanisms reviewed include: scavenging nitrogen and oxygen reactive species, regulation of signaling pathways associated with cell survival and inflammation, and inhibition of synphilin-1 and alpha-synuclein aggregation.

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“…28,29 Administration of vitamin E exerts a protective effect on the locus coeruleus (LC) neurons in an early model of Parkinson's disease (PD). 30 The activity of chaperone-mediated autophagy, a selective pathway for the degradation of cytosolic proteins in lysosomes, is enhanced during oxidative stress. Also Cao et al showed that vitamin E may partially inhibit activated chaperone-mediated autophagy during oxidative stress.…”

Section: Histological Findingsmentioning

confidence: 99%

Protective effects of vitamin E on central nervous system in streptozotocin-induced diabetic rats

Kabay¹,

Özden²,

Güven³

et al. 2009

CIM

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Objective: To evaluate the histopathological and antioxidant effects of vitamin E (VE) treatment on brain tissue in streptozotocin (STZ)-induced diabetic rats. Methods: Thirty two male Wistar albino rats were used. The study comprised four groups of 8 rats: Group A - untreated group, group B - diabetic group, group C - VE and group D - diabetic plus VE. In the diabetic groups, diabetes was induced by a single intraperitoneal injection of 65 mg/kg STZ. Vitamin E was given 50 mg/kg/day i.p. for three weeks. Concentrations of glucose, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were detected in the haemolysate. Results: Glucose concentrations were increased in the blood of the STZ-treated rats compared with those in the diabetic groups (group B and D). The MDA concentrations in the brain from diabetic rats increased, whereas the GPx, SOD, CAT concentrations decreased. Treatment with VE returned concentrations of MDA, GPx, SOD and CAT toward control values. The MDA concentration in the diabetic group (20.65±2.24 nmol/mg Hb) was decreased compared with the VE treated group (15.54±1.32 nmol/mg Hb). There were no pathological differences between untreated and VE treated rats’ brains. Neuronal ischemic damages were determined in STZ-induced diabetic rats. Ischemic neuronal alterations in group B (diabetic) had more damage than group D (diabetic + VE). Conclusion: The study revealed neuroprotective effects of VE on ischemic damage in diabetic central neuronal cells, caused by diabetic oxidative stress.

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P2.038 The protective effect of vitamin E on Locus coeruleus in early model of Parkinson's disease in rat: immunoreactivity evidence

Cited by 10 publications

References 0 publications

Serum Vitamins and Heavy Metals in Blood and Urine, and the Correlations among Them in Parkinson’s Disease Patients in China

Serum Vitamins and Heavy Metals in Blood and Urine, and the Correlations among Them in Parkinson’s Disease Patients in China

Cellular and molecular mechanisms of antioxidants in Parkinson's disease

Protective effects of vitamin E on central nervous system in streptozotocin-induced diabetic rats

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