Stabilization of synaptic membranes by α-tocopherol against the damaging action of phospholipases. Possible mechanism of biological action of vitamin E

Erin, A. N.; Gorbunov, Nikolai V.; Brusovanik, V. I.; Tyurin, V. A.; Prilipko, L. L.

doi:10.1016/0006-8993(86)91253-9

Cited by 34 publications

(8 citation statements)

References 12 publications

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“…Although the mode of vitamin E action on keratinocytes remains to be further defined, a likely mechanism might be the stabilizing action on cellular membrane amplified by the application of vitamin E acetate ointment at high dose levels. Erin et al [27] have reported that the stabilization by vitamin E against the damaging action of phospholipases is due to the binding of phospholipid hydrolysis products but not to the inhibition of enzymes, and its action is a possible mechanism of biological action of vitamin E on biomembrane. In this study, vitamin E at high dose levels is postulated to protect dose-dependently the keratinocytes from damaging action of chemical irritants by the formation of a complex with the phospholipid hydrolysis products of the membrane.…”

Section: Discussionmentioning

confidence: 99%

Vitamin E ointment at high dose levels suppresses contact dermatitis in rats by stabilizing keratinocytes

et al. 2002

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Section: Discussionmentioning

confidence: 99%

Vitamin E ointment at high dose levels suppresses contact dermatitis in rats by stabilizing keratinocytes

et al. 2002

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“…Others used dietary vitamin E-deficient Wistar rats and found the synapse-to-neuron ratio decreased by 30%, and both the numerical density of the synapses and total synaptic area decreased significantly as well, suggesting that decreases in vitamin E intake could significantly affect the structural dynamics of hippocampal cholinergic synapses (Fattoretti et al, 1995). By using fluorescent and EPR spin probing techniques in investigation of rat brain synaptosomal membranes, Erin et al (1986) observed stabilization of synaptosomal membranes by ␣-tocopherol, suggesting a possible mechanism for the effect of vitamin E on biological membranes. In addition, synaptophysin, one of the presynaptic vesicle membrane proteins, was significantly increased in the brains of rats treated with vitamin E (Ferri et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Presynaptic Defects Underlying Impaired Learning and Memory Function in Lipoprotein Lipase-Deficient Mice

Xian¹,

Liu²,

Yu³

et al. 2009

J. Neurosci.

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Lipoprotein lipase (LPL) is predominantly expressed in adipose and muscle where it plays a crucial role in the metabolism of triglyceriderich plasma lipoproteins. LPL is also expressed in the brain with highest levels found in the pyramidal cells of the hippocampus, suggesting a possible role for LPL in the regulation of cognitive function. However, very little is currently known about the specific role of LPL in the brain. We have generated a mouse model of LPL deficiency which was rescued from neonatal lethality by somatic gene transfer. These mice show no exogenous and endogenous LPL expression in the brain. To study the role of LPL in learning and memory, the performance of LPL-deficient mice was tested in two cognitive tests. In a water maze test, LPL-deficient mice exhibited increased latency to escape platform and increased mistake frequency. Decreased latency to platform in the step-down inhibitory avoidance test was observed, consistent with impaired learning and memory in these mice. Transmission electron microscopy revealed a significant decrease in the number of presynaptic vesicles in the hippocampus of LPL-deficient mice. The levels of the presynaptic marker synaptophysin were also reduced in the hippocampus, whereas postsynaptic marker postsynaptic density protein 95 levels remained unchanged in LPL-deficient mice. Theses findings indicate that LPL plays an important role in learning and memory function possibly by influencing presynaptic function.

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“…Vitamin E has been shown to stabilize synaptosomal membranes against the damaging action of the phospholipases. This stabilization is caused by reconstitution of the transmembrane potential and an increase of microviscosity of the phospholipase‐treated membranes 112…”

Section: Molecular Checkpoints In Neuronal Cell Death: Opportunities mentioning

confidence: 99%

Tocotrienol: The Natural Vitamin E to Defend the Nervous System?

Sen

Khanna

Roy

2004

Annals of the New York Academy of Sciences

119

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Vitamin E is essential for normal neurological function. It is the major lipid-soluble, chain-breaking antioxidant in the body, protecting the integrity of membranes by inhibiting lipid peroxidation. Mostly on the basis of symptoms of primary vitamin E deficiency, it has been demonstrated that vitamin E has a central role in maintaining neurological structure and function. Orally supplemented vitamin E reaches the cerebrospinal fluid and brain. Vitamin E is a generic term for all tocopherols and their derivatives having the biological activity of RRR-alpha-tocopherol, the naturally occurring stereoisomer compounds with vitamin E activity. In nature, eight substances have been found to have vitamin E activity: alpha-, beta-, gamma- and delta-tocopherol; and alpha-, beta-, gamma- and delta-tocotrienol. Often, the term vitamin E is synonymously used with alpha-tocopherol. Tocotrienols, formerly known as zeta, , or eta-tocopherols, are similar to tocopherols except that they have an isoprenoid tail with three unsaturation points instead of a saturated phytyl tail. Although tocopherols are predominantly found in corn, soybean, and olive oils, tocotrienols are particularly rich in palm, rice bran, and barley oils. Tocotrienols possess powerful antioxidant, anticancer, and cholesterol-lowering properties. Recently, we have observed that alpha-tocotrienol is multi-fold more potent than alpha-tocopherol in protecting HT4 and primary neuronal cells against toxicity induced by glutamate as well as by a number of other toxins. At nanomolar concentration, tocotrienol, but not tocopherol, completely protected neurons by an antioxidant-independent mechanism. Our current work identifies two major targets of tocotrienol in the neuron: c-Src kinase and 12-lipoxygenase. Dietary supplementation studies have established that tocotrienol, fed orally, does reach the brain. The current findings point towards tocotrienol as a potent neuroprotective form of natural vitamin E.

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Stabilization of synaptic membranes by α-tocopherol against the damaging action of phospholipases. Possible mechanism of biological action of vitamin E

Cited by 34 publications

References 12 publications

Vitamin E ointment at high dose levels suppresses contact dermatitis in rats by stabilizing keratinocytes

Vitamin E ointment at high dose levels suppresses contact dermatitis in rats by stabilizing keratinocytes

Presynaptic Defects Underlying Impaired Learning and Memory Function in Lipoprotein Lipase-Deficient Mice

Tocotrienol: The Natural Vitamin E to Defend the Nervous System?

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