[26] α-carboxyethyl-6-hydroxychroman as urinary metabolite of vitamin E

Schultz, M.; Leist, Marcel; Elsner, Angelika; Brigelius‐Flohé, Regina

doi:10.1016/s0076-6879(97)82116-7

Cited by 36 publications

(25 citation statements)

References 10 publications

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“…26,[40][41][42] In tocopherol metabolism, cytochrome P450 enzymes catalyze the formation of biologically active carboxyethyl hydroxy chroman metabolites. 43,44 Carboxyethyl hydroxy chroman metabolites are water-soluble, low-molecular-weight compounds that accumulate in the absence of kidney function and are readily removed by dialysis, thus providing a favorable pharmacokinetic profile for use in a dialysis population. Likewise, low-molecular-weight thiol-containing antioxidants have dramatically increased area under the plasmaconcentration curve, probably because of reduced cellular uptake.…”

Section: Discussionmentioning

confidence: 99%

Provision of Antioxidant Therapy in Hemodialysis (PATH)

Himmelfarb

İkizler²,

Ellis³

et al. 2014

Journal of the American Society of Nephrology

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Increased markers of oxidative stress and acute-phase inflammation are prevalent in patients undergoing maintenance hemodialysis therapy (MHD), and are associated with increased mortality and hospitalization rates and decreased erythropoietin responsiveness. No adequately powered studies have examined the efficacy of antioxidant therapies on markers of inflammation and oxidative stress. We tested the hypothesis that oral antioxidant therapy over 6 months would decrease selected biomarkers of acute-phase inflammation and oxidative stress and improve erythropoietic response in prevalent MHD patients. In total, 353 patients were enrolled in a prospective, placebo-controlled, double-blind clinical trial and randomly assigned to receive a combination of mixed tocopherols (666 IU/d) plus a-lipoic acid (ALA; 600 mg/d) or matching placebos for 6 months (NCT00237718); 238 patients completed the study. High-sensitivity C-reactive protein (hsCRP) and IL-6 concentration were measured as biomarkers of systemic inflammation, and F2 isoprostanes and isofurans were measured as biomarkers of oxidative stress. The groups did not significantly differ at baseline. At 3 and 6 months, the treatment had no significant effect on plasma hsCRP, IL-6, F2 isoprostane, or isofuran concentrations and did not improve the erythropoietic response. No major adverse events were related to the study drug, and both groups had similar mortality and hospitalization rates during the study. In conclusion, the administration of mixed tocopherols and ALA was generally safe and well tolerated, but did not influence biomarkers of inflammation and oxidative stress or the erythropoietic response.

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Section: Discussionmentioning

confidence: 99%

Provision of Antioxidant Therapy in Hemodialysis (PATH)

Himmelfarb

İkizler²,

Ellis³

et al. 2014

Journal of the American Society of Nephrology

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“…The ICMs have also been found in cultured HepG2 cells (α-, γ-7'-COOH and α-, γ-5'-COOH [120,140,144] ). The catabolic end-products of vitamin E metabolism are the CEHC (CEHC, sometimes also referred to 3'-COOH or short-chain metabolites, SCM), which were an early focus of research on vitamin E metabolism [145,146] . In the 1980s and 1990s different CEHCs were identified as the first known metabolites of vitamin E degradation: α-CEHC [132,146] , γ-CEHC [147] and δ-CEHC [131] .…”

Section: Metabolism Of Tohmentioning

confidence: 99%

Complexity of vitamin E metabolism

Schmölz¹,

Birringer²,

Lorkowski³

et al. 2016

WJBC

176

138

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Bioavailability of vitamin E is influenced by several factors, most are highlighted in this review. While gender, age and genetic constitution influence vitamin E bioavailability but cannot be modified, life-style and intake of vitamin E can be. Numerous factors must be taken into account however, i.e. , when vitamin E is orally administrated, the food matrix may contain competing nutrients. The complex metabolic processes comprise intestinal absorption, vascular transport, hepatic sorting by intracellular binding proteins, such as the significant α-tocopherol-transfer protein, and hepatic metabolism. The coordinated changes involved in the hepatic metabolism of vitamin E provide an effective physiological pathway to protect tissues against the excessive accumulation of, in particular, non-α-tocopherol forms. Metabolism of vitamin E begins with one cycle of CYP4F2/CYP3A4-dependent ω-hydroxylation followed by five cycles of subsequent β-oxidation, and forms the water-soluble end-product carboxyethylhydroxychroman. All known hepatic metabolites can be conjugated and are excreted, depending on the length of their sidechain, either via urine or feces. The physiological handling of vitamin E underlies kinetics which vary between the different vitamin E forms. Here, saturation of the side-chain and also substitution of the chromanol ring system are important. Most of the metabolic reactions and processes that are involved with vitamin E are also shared by other fat soluble vitamins. Influencing interactions with other nutrients such as vitamin K or pharmaceuticals are also covered by this review. All these processes modulate the formation of vitamin E metabolites and their concentrations in tissues and body fluids. Differences in metabolism might be responsible for the discrepancies that have been observed in studies performed in vivo and in vitro using vitamin E as a REVIEW

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“…32 The 24-hour urinary excretion of 1,5,7,8-tetramethyl-2(2Ј-carboxyethyl)-6-hydroxychroman (␣-CEHC) was assessed by gas chromatography. 37 …”

Section: Measurement Of Vitamins C and E And ␣-Cehcmentioning

confidence: 99%

Long-Term Effects of Vitamin E, Vitamin C, and Combined Supplementation on Urinary 7-Hydro-8-Oxo-2′-Deoxyguanosine, Serum Cholesterol Oxidation Products, and Oxidation Resistance of Lipids in Nondepleted Men

Porkkala-Sarataho

Salonen

Nyyssönen

et al. 2000

ATVB

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Abstract-We studied the long-term effects of vitamins E and C and their combination on lipid peroxidation in vivo and in vitro. The Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) trial is a double-masked placebo-controlled randomized clinical trial to study the effects of vitamin C (500 mg of slow release ascorbate per day), vitamin E (182 mg of RRR-␣-tocopherol acetate per day), and the combination of both antioxidants. Lipid peroxidation measurements were carried out for 48 male participants at entry and at 12 and 36 months. Compared with placebo, vitamin E and the vitamin combination increased plasma lipid-standardized ␣-tocopherol during the first 12 months by 68.2% and 65.2% (PϽ0.001 for both), respectively, and reduced serum 7␤-hydroxycholesterol by 50.4% (Pϭ0.013) and 44.0% (Pϭ0.041), respectively. The net change of lipid standardized ␣-tocopherol was 63.8% after 36 months of vitamin E supplementation and 43.3% for the combination. Vitamin C supplementation elevated plasma total ascorbate level by 30.1% (Pϭ0.043) in 12 months and by 91.1% (Pϭ0.001) in 36 months.Neither vitamin E, vitamin C, nor the combination influenced the urinary excretion rate of 7-hydro-8-oxo-2Ј-deoxyguanosine or the antioxidative capacity of plasma. Vitamin E and the combination of vitamins E and C enhanced the oxidation resistance of isolated lipoproteins and total serum lipids. Our data indicate that long-term supplementation of nondepleted men with a reasonable dose of vitamin E alone or in combination with slow release vitamin C reduces lipid peroxidation in vitro and in vivo, whereas a relatively high dose of vitamin C alone does not. Key Words: antioxidants Ⅲ lipid peroxidation Ⅲ oxidation resistance Ⅲ 7-hydro-8-oxo-2Ј-deoxyguanosine Ⅲ oxysterols V itamins E 1-4 and C 5,6 are widely regarded as important dietary antioxidants. However, this concept is based on in vitro studies and on supplementation trials in which only measurements of lipid peroxidation ex vivo have been performed. 3 The evidence of the lipid peroxidation-inhibiting effects of vitamins E and C in vitro is plentiful. [1][2][3][4][5][6][7] In addition, oral vitamin E supplementation has consistently increased the oxidation resistance of isolated lipoproteins in vitro. 8 -13 Vitamin C has had been shown to have a similar effect in a few 14 -16 but not in all 17 studies. Vitamin C can also act as a pro-oxidant in certain conditions. 17,18 In theory, vitamin E could function as a mediator of lipid peroxidation if sufficient coantioxidants are not present. 19,20 However, this theory has not been tested in oral supplementation studies with in vivo measurements. There are no previous long-term placebocontrolled oral supplementation trials concerning the effects of these vitamins on lipid peroxidation in nonsmoking clinically healthy subjects.The assessment of oxidative stress and lipid peroxidation in vivo in humans is problematic. 7-Hydro-8-oxo-2Ј-deoxyguanosine (8-oxodG), a repair product of oxidative damage to DNA, has been used as an indicator...

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[26] α-carboxyethyl-6-hydroxychroman as urinary metabolite of vitamin E

Cited by 36 publications

References 10 publications

Provision of Antioxidant Therapy in Hemodialysis (PATH)

Provision of Antioxidant Therapy in Hemodialysis (PATH)

Complexity of vitamin E metabolism

Long-Term Effects of Vitamin E, Vitamin C, and Combined Supplementation on Urinary 7-Hydro-8-Oxo-2′-Deoxyguanosine, Serum Cholesterol Oxidation Products, and Oxidation Resistance of Lipids in Nondepleted Men

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