Gamma-tocopherol detoxification of nitrogen dioxide: superiority to alpha-tocopherol.

Cooney, Robert V.; Franke, Adrian A.; Harwood, Patricia J.; Hatch‐Pigott, V.; Custer, Laurie J.; Mordan, Lawrence J.

doi:10.1073/pnas.90.5.1771

Cited by 310 publications

(193 citation statements)

References 40 publications

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“…The destruction of ß-carotene in the NO2 exposure was inhibited little by a-toc or the polyunsaturated fatty esters, and slightly by ascorbyl palmitate, indicating that the reactivity of ß-carotene toward N 0 2 is higher than that of these biomaterials which are known to scavenge NO2 and consequently release HNO2 [13,14]. Interaction of ß- carotene with NO2 released little HNO2 or NO under the present conditions and nitrogen atoms from NO2 might be tightly bound to the ß-carotene molecule.…”

Section: Discussionmentioning

confidence: 97%

“…In contrast, oc-toc, ML, EIPA and EDHA caused the loss of much less N0 2 (+HN0 2 ). Because it has been shown that oc-toc [13] and the polyunsaturated fatty esters [14] can convert NO2 into HNO2, these compounds may have converted some of the NO2 into HNO2 under the present conditions. When N0 2 in air was introduced into «-hexane containing 50 nmol ß-carotene during a period of 10 min, the characteristic absorption spectrum of the solution with a maximum at NO2 (52-67 ppm) in air (total amounts 210-270 nmol) was introduced into 5.0 ml of «-hexane containing 50 nmol of the substrate at a flow rate of 10 ml/min for 10 min.…”

Section: Resultsmentioning

confidence: 99%

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β‐Carotene effectively scavenges toxic nitrogen oxides: nitrogen dioxide and peroxynitrous acid

Kikugawa¹,

Hiramoto²,

Tomiyama³

et al. 1997

FEBS Letters

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ß-Carotene absorbed 2 equimolar amounts of N0 2 accompanying the complete destruction of ß-carotene. Electron spin resonance study using 2-phenyl-4,4,5,5-tetramethylimidazoline-3-oxide-l-oxyl revealed that no significant amounts of NO were released by the interaction. Nitrogen atoms derived from N0 2 were tightly bound to the ß-carotene molecules. Destruction of ß-carotene was inhibited little by a-tocopherol and polyunsaturated fatty esters, and slightly by ascorbyl palmitate, indicating that ß-carotene was a more effective scavenger of N0 2 . ONOOH/ONOO -and 3-morpholinosydononimine similarly destroyed ß-carotene. The results suggest that ß-carotene contributes to the prevention of cytotoxicity and genotoxicity of N0 2 and ONOOH/ONOO" derived from NO.

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Section: Discussionmentioning

confidence: 97%

Section: Resultsmentioning

confidence: 99%

β‐Carotene effectively scavenges toxic nitrogen oxides: nitrogen dioxide and peroxynitrous acid

Kikugawa¹,

Hiramoto²,

Tomiyama³

et al. 1997

FEBS Letters

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“…In vivo studies have shown that gamma-tocopherol is able to neutralize nitric dioxide, (61,62) a compound that inhibits collagen synthesis. (63) As a result of this reaction, nitric oxide (NO) is produced, (61) which can uncouple bone resorption and formation, reduce bone resorption, and stimulate bone formation.…”

Section: Discussionmentioning

confidence: 99%

“…(63) As a result of this reaction, nitric oxide (NO) is produced, (61) which can uncouple bone resorption and formation, reduce bone resorption, and stimulate bone formation. (64,65) On the other hand, high NO levels in presence of proinflammatory cytokines may inhibit osteoblast growth and differentiation.…”

Section: Discussionmentioning

confidence: 99%

Effects of vitamin E on bone turnover markers among US postmenopausal women

Hamidi

Corey

Cheung

2012

Journal of Bone and Mineral Research

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Increased oxidative stress and inflammation resulting from aging and declining estrogen levels can lead to increased bone loss in postmenopausal women. Alpha-tocopherol and gamma-tocopherol, the two predominant isomers of vitamin E, have antioxidant and anti-inflammatory properties, but their effects on bone metabolism have not been well studied in humans. We examined the associations between dietary and total (diet and supplements) alpha-tocopherol intake, serum alpha-tocopherol and gamma-tocopherol levels and their ratio, and bone turnover markers (BTMs) among postmenopausal women aged !45 years. We used cross-sectional data from the National Health and Nutrition Examination Survey 1999-2002. Multiple regression models with adjustments for relevant confounders were used to examine the associations between intake and serum levels of tocopherols, and serum bone-specific alkaline phosphatase (BAP), a biomarker of bone formation, and urinary N-telopeptides/creatinine (uNTx/Cr), a biomarker of bone resorption. The study sample included 497 postmenopausal women who were not taking estrogen, steroids, or osteoporosis medications, were free from kidney and liver disease, cancer, and rheumatoid arthritis, and were fasting >9 hours prior to examination. Participants had a mean age of 65.5 AE 0.6 years and over 45% used vitamin E (alpha-tocopherol) supplements in the past month. Vitamin E supplement users had significantly lower serum gamma-tocopherol, higher serum alpha-tocopherol levels, and higher ratio of serum alpha-tocopherol to gamma-tocopherol than nonusers. High serum gamma-tocopherol levels and low ratio of serum alpha-tocopherol to gamma-tocopherol were associated with increased BAP levels (p < 0.01 for both). There were no associations between any of the vitamin E variables and uNTx/Cr. In conclusion, we hypothesize that gamma-tocopherol may uncouple bone turnover, resulting in more bone formation than resorption. Vitamin E supplements in the form of alpha-tocopherol suppress serum gamma-tocopherol levels and may have negative effects on bone formation. Further research is needed to investigate the potential anabolic effect of gamma-tocopherol from food sources on bone. ß

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“…Previous findings in isolated insulin-secreting cells (Cooney et al, 1995) also showed that the vitamin E gtocopherol, a major antioxidant in Western diets, could reverse the effects of IL-1, probably by detoxifying the nitrogen dioxide formed thereby preventing lipid peroxidation (Cooney et al, 1993). Interestingly, in vivo administration of E-vitamin was found to decrease or delay the onset of IDDM in BB rats (Murthy et al, 1992), and to reduce the incidence of IDDM in the NOD mouse (Hayward et al, 1992).…”

Section: Il-1 Stimulates Islet Nitric Oxide Formation and Causes Apopmentioning

confidence: 94%

Aspects of the involvement of interleukin-1 and nitric oxide in the pathogenesis of insulin-dependent diabetes mellitus

Sjöholm

1998

Cell Death Differ

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The possible involvement of the cytokine interleukin-1 (IL-1) and nitric oxide (NO) in the pathogenesis of insulin-dependent diabetes mellitus (IDDM) is reviewed and current and potential therapies are discussed. IDDM is a common disorder in the Western world and it is rising in incidence. In IDDM, isletinfiltrating macrophages produce IL-1 which is cytotoxic specifically to b-cells in vitro. IL-1 increases b-cell formation of NO, ceramide, prostaglandins, heat-shock proteins, and activates a protease. Additionally, IL-1 depresses b-cell energy production, insulin gene expression and cyclic AMP synthesis, and impacts negatively on different parts of the insulin stimulus-secretion coupling, actions mimicked by NO. Conversely, blocking NO formation prevented many of these effects in most reports published. Also, changes in cyclic AMP and prostaglandins seem unlikely events in mediating the cytotoxicity of IL-1, while the role of ceramide remains less clear. Peptides capable of blocking b-cell IL-1 receptors, and agents blocking NO synthesis may prove valuable in preserving b-cell function in IDDM. Although IDDM causes immense morbidity and expense, uniformly effective preventive or b-cell protective therapy is not currently available. If IL-1 is causing b-cell dysfunction in human IDDM through NO production, several processes in the IL-1-NO connection are appropriate targets for agents protecting b-cells from destruction and functional inhibition in IDDM.

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Gamma-tocopherol detoxification of nitrogen dioxide: superiority to alpha-tocopherol.

Cited by 310 publications

References 40 publications

β‐Carotene effectively scavenges toxic nitrogen oxides: nitrogen dioxide and peroxynitrous acid

β‐Carotene effectively scavenges toxic nitrogen oxides: nitrogen dioxide and peroxynitrous acid

Effects of vitamin E on bone turnover markers among US postmenopausal women

Aspects of the involvement of interleukin-1 and nitric oxide in the pathogenesis of insulin-dependent diabetes mellitus

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