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Vitamin E Nicotinate

View Article: PubMed Central - PubMed

ABSTRACT

Vitamin E refers to a family of compounds that function as lipid-soluble antioxidants capable of preventing lipid peroxidation. Naturally occurring forms of vitamin E include tocopherols and tocotrienols. Vitamin E in dietary supplements and fortified foods is often an esterified form of α-tocopherol, the most common esters being acetate and succinate. The vitamin E esters are hydrolyzed and converted into free α-tocopherol prior to absorption in the intestinal tract. Because its functions are relevant to many chronic diseases, vitamin E has been extensively studied in respect to a variety of diseases as well as cosmetic applications. The forms of vitamin E most studied are natural α-tocopherol and the esters α-tocopheryl acetate and α-tocopheryl succinate. A small number of studies include or focus on another ester form, α-tocopheryl nicotinate, an ester of vitamin E and niacin. Some of these studies raise the possibility of differences in metabolism and in efficacy between vitamin E nicotinate and other forms of vitamin E. Recently, through metabolomics studies, we identified that α-tocopheryl nicotinate occurs endogenously in the heart and that its level is dramatically decreased in heart failure, indicating the possible biological importance of this vitamin E ester. Since knowledge about vitamin E nicotinate is not readily available in the literature, the purpose of this review is to summarize and evaluate published reports, specifically with respect to α-tocopheryl nicotinate with an emphasis on the differences from natural α-tocopherol or α-tocopheryl acetate.

No MeSH data available.


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Levels of α-tocopheryl nicotinate in the heart of healthy control rats and rats with heart failure. Pulmonary arterial hypertension-induced right-sided heart failure was generated by administering ovalbumin and SU5416 to Sprague-Dawley rats [16]. Homogenates of right-heart ventricular tissues were injected into a reverse-phase column of an Acquity ultra-performance liquid chromatography (UPLC) system. Mass spectrometry (MS) was performed using a quadrupole-time-of-flight mass spectrometer. The box-and-whisker plot represents the levels of the metabolite corresponding to α-tocopheryl nicotinate (m/z 536.4077) in arbitrary units (a.u.). * denotes significant difference between each other at p < 0.05.
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antioxidants-06-00020-f002: Levels of α-tocopheryl nicotinate in the heart of healthy control rats and rats with heart failure. Pulmonary arterial hypertension-induced right-sided heart failure was generated by administering ovalbumin and SU5416 to Sprague-Dawley rats [16]. Homogenates of right-heart ventricular tissues were injected into a reverse-phase column of an Acquity ultra-performance liquid chromatography (UPLC) system. Mass spectrometry (MS) was performed using a quadrupole-time-of-flight mass spectrometer. The box-and-whisker plot represents the levels of the metabolite corresponding to α-tocopheryl nicotinate (m/z 536.4077) in arbitrary units (a.u.). * denotes significant difference between each other at p < 0.05.

Mentions: Vitamin E nicotinate is an ester of vitamin E and niacin (vitamin B3). Figure 1 shows the chemical structures of α-tocopherol, niacin (nicotinic acid), and α-tocopheryl nicotinate. We came across α-tocopheryl nicotinate only when we performed metabolomics analysis in a list of differentially expressed metabolites between controls and rats with heart failure. In order to understand the mechanism of right-sided heart failure induced by pulmonary arterial hypertension, we subjected Sprague-Dawley rats to the SU5416/ovalbumin model of pulmonary arterial hypertension [16]. The right ventricles of these rats had severe damage to cardiomyocytes and exhibited severe fibrosis [17]. We then took the right ventricles from these rats as well as from healthy control rats and submitted them to metabolomics analysis. Among a number of metabolites that were found to have at least 2-fold changes in their contents with a probability of p ≤ 0.05, a metabolite with a molecular mass of 536.4077 was found to be 28-fold different with p = 0.02859. These results suggested that, compared with the control, the right ventricles of rats with pulmonary arterial hypertension and right-sided heart failure were found to have 28-fold less α-tocopheryl nicotinate (Figure 2). To confirm the metabolomics experiments performed with ultra-performance liquid chromatography and quadrupole-time-of-flight mass spectrometry, we performed mass spectrometry–mass spectrometry analysis. The results showed that the metabolite that was found to be decreased 28-fold in rats with right-sided heart failure had exactly the same mass as α-tocopheryl nicotinate standard from Sigma-Aldrich (St. Louis, MO, USA) (Figure 3). These rats were fed Laboratory Rodent Diet 5001 from LabDiet (St. Louis, MO, USA), which contains dl-α-tocopheryl acetate as a source of vitamin E. Thus, α-tocopheryl nicotinate is likely formed endogenously from dietary vitamin E and niacin. These results demonstrated that (i) α-tocopheryl nicotinate endogenously occurs in rat hearts and (ii) this cardiac α-tocopheryl nicotinate is dramatically reduced in heart failure. These findings highlight the possible pathophysiological importance of vitamin E nicotinate.


Vitamin E Nicotinate
Levels of α-tocopheryl nicotinate in the heart of healthy control rats and rats with heart failure. Pulmonary arterial hypertension-induced right-sided heart failure was generated by administering ovalbumin and SU5416 to Sprague-Dawley rats [16]. Homogenates of right-heart ventricular tissues were injected into a reverse-phase column of an Acquity ultra-performance liquid chromatography (UPLC) system. Mass spectrometry (MS) was performed using a quadrupole-time-of-flight mass spectrometer. The box-and-whisker plot represents the levels of the metabolite corresponding to α-tocopheryl nicotinate (m/z 536.4077) in arbitrary units (a.u.). * denotes significant difference between each other at p < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5384183&req=5

antioxidants-06-00020-f002: Levels of α-tocopheryl nicotinate in the heart of healthy control rats and rats with heart failure. Pulmonary arterial hypertension-induced right-sided heart failure was generated by administering ovalbumin and SU5416 to Sprague-Dawley rats [16]. Homogenates of right-heart ventricular tissues were injected into a reverse-phase column of an Acquity ultra-performance liquid chromatography (UPLC) system. Mass spectrometry (MS) was performed using a quadrupole-time-of-flight mass spectrometer. The box-and-whisker plot represents the levels of the metabolite corresponding to α-tocopheryl nicotinate (m/z 536.4077) in arbitrary units (a.u.). * denotes significant difference between each other at p < 0.05.
Mentions: Vitamin E nicotinate is an ester of vitamin E and niacin (vitamin B3). Figure 1 shows the chemical structures of α-tocopherol, niacin (nicotinic acid), and α-tocopheryl nicotinate. We came across α-tocopheryl nicotinate only when we performed metabolomics analysis in a list of differentially expressed metabolites between controls and rats with heart failure. In order to understand the mechanism of right-sided heart failure induced by pulmonary arterial hypertension, we subjected Sprague-Dawley rats to the SU5416/ovalbumin model of pulmonary arterial hypertension [16]. The right ventricles of these rats had severe damage to cardiomyocytes and exhibited severe fibrosis [17]. We then took the right ventricles from these rats as well as from healthy control rats and submitted them to metabolomics analysis. Among a number of metabolites that were found to have at least 2-fold changes in their contents with a probability of p ≤ 0.05, a metabolite with a molecular mass of 536.4077 was found to be 28-fold different with p = 0.02859. These results suggested that, compared with the control, the right ventricles of rats with pulmonary arterial hypertension and right-sided heart failure were found to have 28-fold less α-tocopheryl nicotinate (Figure 2). To confirm the metabolomics experiments performed with ultra-performance liquid chromatography and quadrupole-time-of-flight mass spectrometry, we performed mass spectrometry–mass spectrometry analysis. The results showed that the metabolite that was found to be decreased 28-fold in rats with right-sided heart failure had exactly the same mass as α-tocopheryl nicotinate standard from Sigma-Aldrich (St. Louis, MO, USA) (Figure 3). These rats were fed Laboratory Rodent Diet 5001 from LabDiet (St. Louis, MO, USA), which contains dl-α-tocopheryl acetate as a source of vitamin E. Thus, α-tocopheryl nicotinate is likely formed endogenously from dietary vitamin E and niacin. These results demonstrated that (i) α-tocopheryl nicotinate endogenously occurs in rat hearts and (ii) this cardiac α-tocopheryl nicotinate is dramatically reduced in heart failure. These findings highlight the possible pathophysiological importance of vitamin E nicotinate.

View Article: PubMed Central - PubMed

ABSTRACT

Vitamin E refers to a family of compounds that function as lipid-soluble antioxidants capable of preventing lipid peroxidation. Naturally occurring forms of vitamin E include tocopherols and tocotrienols. Vitamin E in dietary supplements and fortified foods is often an esterified form of &alpha;-tocopherol, the most common esters being acetate and succinate. The vitamin E esters are hydrolyzed and converted into free &alpha;-tocopherol prior to absorption in the intestinal tract. Because its functions are relevant to many chronic diseases, vitamin E has been extensively studied in respect to a variety of diseases as well as cosmetic applications. The forms of vitamin E most studied are natural &alpha;-tocopherol and the esters &alpha;-tocopheryl acetate and &alpha;-tocopheryl succinate. A small number of studies include or focus on another ester form, &alpha;-tocopheryl nicotinate, an ester of vitamin E and niacin. Some of these studies raise the possibility of differences in metabolism and in efficacy between vitamin E nicotinate and other forms of vitamin E. Recently, through metabolomics studies, we identified that &alpha;-tocopheryl nicotinate occurs endogenously in the heart and that its level is dramatically decreased in heart failure, indicating the possible biological importance of this vitamin E ester. Since knowledge about vitamin E nicotinate is not readily available in the literature, the purpose of this review is to summarize and evaluate published reports, specifically with respect to &alpha;-tocopheryl nicotinate with an emphasis on the differences from natural &alpha;-tocopherol or &alpha;-tocopheryl acetate.

No MeSH data available.


Related in: MedlinePlus