Cellular mechanisms of vitamin E uptake: relevance in α-tocopherol metabolism and potential implications for disease

Mardones, Pablo; Rigotti, Attilio

doi:10.1016/j.jnutbio.2004.02.006

Cited by 104 publications

(71 citation statements)

References 79 publications

(105 reference statements)

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“…Indeed, the concentration of a-tocopherol in plasma and muscles is linked to the a-tocopherol incorporation rate which depends on the quantity of specific receptors such as scavenger receptor class B, type I (SR-BI) (24,25) . These receptors are efficient vectors for a-tocopherol incorporation in muscle cells through their specific recognition of HDL (24) . One has to be cautious when interpretating plasma a-tocopherol concentrations during training periods.…”

Section: Vitamin Ementioning

confidence: 99%

Does physical exercise modify antioxidant requirements?

Margaritis

Rousseau

2008

Nutr. Res. Rev.

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Physical training is known to induce a biochemical adaptive response which might require an increase in the ingestion and/or the absorption of micronutrients. A question that is still being raised is whether acute or chronic exercise modifies antioxidant requirements. First, the present review brings to light the most crucial studies on the topic. Second, it interprets the established relationships between antioxidant micronutrient intakes and the adaptive response of antioxidant systems. Finally, it exposes the major questions connected with antioxidant micronutrient requirements for athletes. To this effect, the training-load interaction with nutrition is taken into account. As oxidative stress cannot be avoided, the imbalance between oxidants and antioxidants can be alleviated to minimise oxidative damage and outcomes. There is growing evidence that one specific antioxidant cannot by itself prevent oxidative stress-induced damage, as direct adverse effects of supplementation are attributed to undesirable synergic effects. Other effects can be supposed that limit the endogenous adaptive effect of training. High doses of antioxidant supplements can minimise the effects of radical oxygen species themselves or generate pro-oxidant effects. Effects are only exhibited when nutritional status is deficient. There are no convincing effects of supplementation in well-trained athletes. Risk/benefit analysis emerges on evidence for an unknown risk of supranutritional intakes, a supposed impairment of adaptive effects and a still unknown long-term risk. Appropriate status can be achieved by a diversified and balanced diet, adapted to specific needs, by awareness of high-density food intakes (avoiding products containing a low density of micronutrients).

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Section: Vitamin Ementioning

confidence: 99%

Does physical exercise modify antioxidant requirements?

Margaritis

Rousseau

2008

Nutr. Res. Rev.

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“…A number of genes other than that encoding α-TTP are implicated in the uptake, retention and secretion of α-T ( Kaempf-Rotzoll et al, 2003;Mardones and Rigotti, 2004;Schneider, 2005). These include genes encoding scavenger receptor B-1 (SR-B1) (Goti et al, 2001;Mardones et al, 2002;Reboul et al, 2006), phosphilipid transfer protein (Desrumaux et al, 1999;Desrumaux et al, 2005;Huuskonen et al, 2001;Jiang et al, 2002), apolipoprotein E (Reich et al, 2001;Vatassery et al, 2006) lipoprotein lipase (Goti et al, 2002) and tocopherol binding proteins (Kempna et al, 2003;Stocker and Azzi, 2000).…”

Section: Proteins Other Than α-Ttp That May Modify Tissue α-T Concentmentioning

confidence: 99%

Mice lacking α-tocopherol transfer protein gene have severe α-tocopherol deficiency in multiple regions of the central nervous system

et al. 2008

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Ataxia with vitamin E deficiency is caused by mutations in α-tocopherol transfer protein (α-TTP) gene and it can be experimentally generated in mice by α-TTP gene inactivation (α-TTP-KO). This study compared α-tocopherol (α-T) concentrations of five brain regions and of four peripheral organs from 5 months old, male and female, wild-type (WT) and α-TTP-KO mice. All brain regions of female WT mice contained significantly higher α-T than those from WT males. α-T concentration in the cerebellum was significantly lower than that in other brain regions of WT mice. These sex and regional differences in brain α-T concentrations do not appear to be determined by α-TTP expression which was undetectable in all brain regions. All the brain regions of α-TTP-KO mice were severely depleted in α-T. The concentration of another endogenous antioxidant, total glutathione, was unaffected by gender but was decreased slightly but significantly in most brain regions of α-TTP-KO mice. The results show that both gender and the hepatic α-TTP, but not brain α-TTP gene expression are important in determining α-T concentrations within the brain. Interestingly, functional abnormality (ataxia) develops only very late in α-TTP-KO mice in spite of the severe α-tocopherol deficiency in brain starting at an early age.

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“…38 Furthermore, SR-BI mediates the uptake of ␣-tocopherol by tissues. 39 As a result, biliary secretion and the levels of ␣-tocopherol in selected tissues such as brain, lung, and gonads were decreased, whereas circulating ␣-tocopherol levels were increased in SR-BI knockout mice. 40 Thus, reduced bioavailability of these dietary antioxidants might also have contributed to the increased oxidative stress observed in SR-BI knockout mice.…”

Section: Van Eck Et Almentioning

confidence: 99%

Increased Oxidative Stress in Scavenger Receptor BI Knockout Mice With Dysfunctional HDL

Eck

Hoekstra

Hildebrand

et al. 2007

ATVB

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Objective-In the current study the effect of disruption of SR-BI, a prominent regulator of HDL metabolism, on the activity of the HDL-associated antioxidant enzymes PON1 and PAF-AH as well as in vivo oxidative stress were investigated. Methods and Results-SR-BI deficiency resulted in 1.4-fold (PϽ0.001) and 1.6-fold (PϽ0.01) lower serum paraoxonase and arylesterase activity of PON1, respectively. Furthermore, a trend to slightly lower PAF-AH activity was observed. In vivo oxidative stress was evaluated by measuring isoprostane F2␣-VI (iPF2␣-VI) and protein carbonyls. Compared with wild-type animals, SR-BI knockouts had 1.4-fold (PϽ0.05) higher levels of plasma iPF2␣-VI, whereas urinary excretion was increased 2-fold (PϽ0.0001). Plasma carbonyls were 1.5-fold (PϽ0.05) higher in SR-BI knockout animals. Furthermore, iPF2␣-VI and carbonyl levels were 2.1-fold (PϽ0.01) and 1.4-fold (PϽ0.01), respectively, increased in livers of SR-BI knockout mice, and in reaction to the increased oxidative stress the expression of several endogenous antioxidant systems was upregulated. On challenging the SR-BI knockout mice with an atherogenic Western-type diet, a further increase in oxidative stress in these animals was observed. Conclusion-SR-BI deficiency results in a reduced activity of the antioxidant enzyme PON1 and a significant increase in oxidative stress, potentially contributing to the proatherogenic effect of SR-BI deficiency. (Arterioscler Thromb Vasc

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Cellular mechanisms of vitamin E uptake: relevance in α-tocopherol metabolism and potential implications for disease

Cited by 104 publications

References 79 publications

Does physical exercise modify antioxidant requirements?

Does physical exercise modify antioxidant requirements?

Mice lacking α-tocopherol transfer protein gene have severe α-tocopherol deficiency in multiple regions of the central nervous system

Increased Oxidative Stress in Scavenger Receptor BI Knockout Mice With Dysfunctional HDL

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