Role of vitamin E as a lipid-soluble peroxyl radical scavenger: in vitro and in vivo evidence

2014 ◽  
Vol 66 ◽  
pp. 3-12 ◽  
Author(s):  
Etsuo Niki
2021 ◽  
Vol 11 (8) ◽  
pp. 1098
Author(s):  
Maria Ester La Torre ◽  
Ines Villano ◽  
Marcellino Monda ◽  
Antonietta Messina ◽  
Giuseppe Cibelli ◽  
...  

Microglia are the first line of defense at the level of the central nervous system (CNS). Phenotypic change in microglia can be regulated by various factors, including the orexin system. Neuroinflammation is an inflammatory process mediated by cytokines, by the lack of interaction of specific receptors such as the OX2-OX2R complex, caused by systemic tissue damage or, more often, associated with direct damage to the CNS. Chronic activation of microglia could lead to long-term neurodegenerative diseases. This review aims to explore how tocopherol (vitamin E) and the orexin system may play a role in the prevention and treatment of microglia inflammation and, consequently, in neurodegenerative diseases thanks to its antioxidant properties. The results of animal and in vitro studies provide evidence to support the use of tocopherol for a reduction in microglia inflammation as well as a greater activation of the orexinergic system. Although there is much in vivo and in vitro evidence of vitamin E antioxidant and protective abilities, there are still conflicting results for its use as a treatment for neurodegenerative diseases that speculate that vitamin E, under certain conditions or genetic predispositions, can be pro-oxidant and harmful.


1988 ◽  
Vol 255 (4) ◽  
pp. E518-E524 ◽  
Author(s):  
J. Hidalgo ◽  
L. Campmany ◽  
M. Borras ◽  
J. S. Garvey ◽  
A. Armario

The possibility that liver metallothionein (MT) can function as an antioxidant in vivo has been studied in the rat. It was found that the stress of food and water deprivation with or without physical immobilization consistently increased liver lipid peroxidation (LLP), suggesting that liver MT induction by stress might be related to the stress-induced LLP. This was supported by results with the lipid peroxidation promoter dimethyl sulfoxide (DMSO) and the natural antioxidant vitamin E. Whereas DMSO administration increased LLP levels in basal and stress situations, vitamin E decreased them. Liver MT levels were increased by DMSO in basal and stress situations, whereas they were decreased by vitamin E during stress. These in vivo results are consistent with an antioxidant role of liver MT suggested by previous in vitro results. However, liver MT preinduction by Zn treatment did not result in a lower MT response to stress. Instead a positive synergistic effect between Zn and stress appeared to be present. This result indicates that the mechanism of action of MT as antioxidant remains unclear.


1996 ◽  
Vol 134 (6) ◽  
pp. 758-763 ◽  
Author(s):  
K Möbius ◽  
A Redmann ◽  
HH Hiller ◽  
W Oelkers ◽  
V Bähr

Möbius K, Redmann A, Hiller HH, Oelkers W, Bähr V. Permissive role of α-tocopherol in the stimulation of aldosterone by sodium depletion in the guinea pig. Eur J Endocrinol 1996;134:758–63. ISSN 0804–4643 To investigate the role of vitamin E in aldosterone synthesis, in vivo and in vitro studies were done in α-tocopherol-depleted guinea pigs. Seventy-one days of low vitamin E intake (< 5 mg/kg feed) reduced the concentration of α-tocopherol in serum, liver and adrenals to low levels with no signs of hypovitaminosis. Aldosterone secretion was stimulated by 15 days on a low sodium diet (200 mg/kg feed) in controls and vitamin E-depleted animals. Sodium depletion in controls stimulated plasma aldosterone by 335%. Vitamin E depletion reduced the stimulation of plasma aldosterone to only 112% (p < 0.05). In vitro aldosterone secretion by adrenal cells from sodium-depleted animals was 252% higher than secretion by cells from controls. This enhancement of in vitro aldosterone secretion following in vivo sodium depletion was abolished completely by combined in vivo vitamin E and sodium depletion (p < 0.05). No significant differences between groups were found for plasma renin activity, adrenocorticotrophin and serum potassium, suggesting that intra-adrenal mechanisms like damage by enhanced lipid peroxidation in α-tocopherol-depleted animals rather than changes in humoral aldosterone-regulating factors are the cause of the attenuated aldosterone response to sodium depletion. Volker Bähr, Abteilung Endokrinologie, Medizinische Klinik, Klinikum Benjamin Franklin, Freie Universität Berlin, Hindenburgdamm 30, D-12000 Berlin, Germany


2014 ◽  
Vol 2014 ◽  
pp. 1-16 ◽  
Author(s):  
Shy Cian Khor ◽  
Norwahidah Abdul Karim ◽  
Wan Zurinah Wan Ngah ◽  
Yasmin Anum Mohd Yusof ◽  
Suzana Makpol

Sarcopenia is a geriatric syndrome that is characterized by gradual loss of muscle mass and strength with increasing age. Although the underlying mechanism is still unknown, the contribution of increased oxidative stress in advanced age has been recognized as one of the risk factors of sarcopenia. Thus, eliminating reactive oxygen species (ROS) can be a strategy to combat sarcopenia. In this review, we discuss the potential role of vitamin E in the prevention and treatment of sarcopenia. Vitamin E is a lipid soluble vitamin, with potent antioxidant properties and current evidence suggesting a role in the modulation of signaling pathways. Previous studies have shown its possible beneficial effects on aging and age-related diseases. Although there are evidences suggesting an association between vitamin E and muscle health, they are still inconclusive compared to other more extensively studied chronic diseases such as neurodegenerative diseases and cardiovascular diseases. Therefore, we reviewed the role of vitamin E and its potential protective mechanisms on muscle health based on previous and currentin vitroandin vivostudies.


2012 ◽  
Vol 82 (3) ◽  
pp. 228-232 ◽  
Author(s):  
Mauro Serafini ◽  
Giuseppa Morabito

Dietary polyphenols have been shown to scavenge free radicals, modulating cellular redox transcription factors in different in vitro and ex vivo models. Dietary intervention studies have shown that consumption of plant foods modulates plasma Non-Enzymatic Antioxidant Capacity (NEAC), a biomarker of the endogenous antioxidant network, in human subjects. However, the identification of the molecules responsible for this effect are yet to be obtained and evidences of an antioxidant in vivo action of polyphenols are conflicting. There is a clear discrepancy between polyphenols (PP) concentration in body fluids and the extent of increase of plasma NEAC. The low degree of absorption and the extensive metabolism of PP within the body have raised questions about their contribution to the endogenous antioxidant network. This work will discuss the role of polyphenols from galenic preparation, food extracts, and selected dietary sources as modulators of plasma NEAC in humans.


Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
HM Lee ◽  
TG Ahn ◽  
CW Kim ◽  
HJ An
Keyword(s):  

1987 ◽  
Vol 26 (01) ◽  
pp. 1-6 ◽  
Author(s):  
S. Selvaraj ◽  
M. R. Suresh ◽  
G. McLean ◽  
D. Willans ◽  
C. Turner ◽  
...  

The role of glycoconjugates in tumor cell differentiation has been well documented. We have examined the expression of the two anomers of the Thomsen-Friedenreich antigen on the surface of human, canine and murine tumor cell membranes both in vitro and in vivo. This has been accomplished through the synthesis of the disaccharide terminal residues in both a and ß configuration. Both entities were used to generate murine monoclonal antibodies which recognized the carbohydrate determinants. The determination of fine specificities of these antibodies was effected by means of cellular uptake, immunohistopathology and immunoscintigraphy. Examination of pathological specimens of human and canine tumor tissue indicated that the expressed antigen was in the β configuration. More than 89% of all human carcinomas tested expressed the antigen in the above anomeric form. The combination of synthetic antigens and monoclonal antibodies raised specifically against them provide us with invaluable tools for the study of tumor marker expression in humans and their respective animal tumor models.


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