Quantitation of mercapturic acid conjugates of 4-hydroxy-2-nonenal and 4-oxo-2-nonenal metabolites in a smoking cessation study

Kuiper, Heather C.; Langsdorf, Brandi L.; Miranda, Cristobal L.; Joss, Jacqueline D; Jubert, Carole; Mata, John E.; Stevens, Jan F.

doi:10.1016/j.freeradbiomed.2009.10.025

Cited by 29 publications

(26 citation statements)

References 42 publications

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“…The low protective effect at higher concentrations of ONE might be due to high reactivity of this aldehyde to cellular thiols and nucleophiles and/or the electrophilicity of the reduced product ONOL. 34,40) Reverse transcription-PCR analysis revealed that the mRNA for AKR1B14 is expressed in rat brain, lung, heart, stomach, liver, adrenal gland, kidney, ovary and testis, although the expression level was high in the adrenal gland and female rat liver (data not shown), as reported previously. 16,21) Considering its tissue distribution and broad substrate specificity (Table 1), AKR1B14 may be involved in detoxification of the reactive carbonyl compounds generated from lipid peroxidation and glycation, in addition to the regulation of adrenal catecholamine release through the PGF 2a synthase activity.…”

supporting

confidence: 82%

Rat Aldose Reductase-Like Protein (AKR1B14) Efficiently Reduces the Lipid Peroxidation Product 4-Oxo-2-nonenal

Endo

Matsunaga

Fujita

et al. 2010

Biological & Pharmaceutical Bulletin

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The aldo-keto reductase (AKR) superfamily is a rapidly growing group of pyridine nucleotide-dependent oxidoreductases that metabolize carbohydrates, steroids, prostaglandins, and other endogenous aldehydes and ketones, as well as xenobiotic compounds.1,2) Aldose reductase (AR), which belongs to the AKR1B subfamily, is a nicotinamide adenine dinucleotide phosphate reduced form (NADPH)-dependent enzyme that catalyses the first step in the polyol pathway and has been implicated in the onset of secondary complications of diabetes in humans.3,4) AR shows broad substrate specificity for various aldehydes and aldoses, and is involved in various physiological roles, including the metabolism of retinoids, steroids and xenobiotics, and defensive mechanisms for oxidative stress. [5][6][7][8] Beside AR, multiple AR-like proteins (ARLPs) that show high sequence similarity (67-71%) to ARs have been identified in human and rodent tissues. While one ARLP (AKR1B10) is ubiquitously expressed in human tissues, 8,9) two ARLPs, androgen-dependent vas deferens protein (AKR1B7) 10) and fibroblast growth factor-inducible protein (AKR1B8), 11) are distributed tissue-specifically in mice. The two mouse ARLPs reduce aldehydes, but are clearly distinct from mouse AR in their poor efficiency in reducing glucose.12,13) AKR1B7 and AKR1B8 differ in their substrate specificity and inhibitor sensitivity. Compared to AKR1B7, 10,12) AKR1B8 exhibits high catalytic efficiency for cytotoxic 4-hydroxynonenal (HNE) derived from lipid peroxidation, 13) but has poor reactivity towards isocaproaldehyde resulting from the side chain cleavage of cholesterol during steroidogenesis.10) AKR1B7 is insensitive to AR inhibitors (ARIs) 10) and exhibits prostaglandin (PG) F 2a synthase activity, which is not detected in the ARI-sensitive AKR1B8. 14)In rats, two ARLPs, AKR1B13 and AKR1B14, have been identified, 15,16) and are thought to be orthologs of mouse AKR1B8 and AKR1B7, respectively, based on high sequence identity of 95% (AKR1B13 versus AKR1B8) and 87% (AKR1B14 versus AKR1B7). AKR1B13 is distributed in almost all rat tissues, and exhibits similar substrate specificity and inhibitor sensitivity to AKR1B8. 17) AKR1B14 and AKR1B7 are similar in their high expression in the adrenal glands and induction by adrenocorticotropic hormone, 10,16,18) but differ in their distribution and gene regulation in other tissues. AKR1B7 is also expressed in mouse vas deferens, intestine and liver, and is up-regulated by androgen, pituitary tropic hormones and agonists of nuclear receptors (liver X receptor-a, pregnane X receptor and constitutive androstane receptor). 10,19,20) In contrast, AKR1B14 is highly expressed in female rat liver through female-specific secretion pattern of growth hormone, 21) and its expression in male rat liver is up-regulated by oxidative stress. 22) Thus, these differences have suggested that AKR1B14 plays a physiological role distinct from its mouse ortholog, AKR1B7. However, there is no report on the detailed properties of AKR1B14, except for its ro...

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supporting

confidence: 82%

Rat Aldose Reductase-Like Protein (AKR1B14) Efficiently Reduces the Lipid Peroxidation Product 4-Oxo-2-nonenal

Endo

Matsunaga

Fujita

et al. 2010

Biological & Pharmaceutical Bulletin

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“…Depletion of vitamin C levels in smokers was ameliorated within 3 months by supplementation with a vitamin cocktail containing vitamin C, alpha-tocopherol and folate [35]. Vitamin C supplementation was also effective at reducing levels of lipid peroxidation byproducts in smokers’ urine [36]. Using a metabolic approach, antioxidant supplementation in smokers was found to alter lipid profiles in plasma in a manner consistent with reductions in oxidative stress [37].…”

Section: Discussionmentioning

confidence: 99%

Effect of smoking reduction and cessation on the plasma levels of the oxidative stress biomarker glutathione – Post-hoc analysis of data from a smoking cessation trial

Mons

Muscat

Modesto

et al. 2016

Free Radical Biology and Medicine

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Cigarette smoke contains high concentrations of free radical components that induce oxidative stress. Smoking-induced oxidative stress is thought to contribute to chronic obstructive pulmonary disease, cardiovascular disease and lung cancer through degenerative processes in the lung and other tissues. It is uncertain however whether smoking cessation lowers the burden of oxidative stress. We used data from a randomized controlled cessation trial of 434 current smokers for a post-hoc examination of the effects of smoking cessation on blood plasma levels of total glutathione (tGSH), the most abundant endogenous antioxidant in cells, and total cysteine (tCys), an amino acid and constituent of glutathione. Smoking status was validated based on serum cotinine levels. Multivariate linear mixed models were fitted to examine the association of smoking cessation and change in cigarette consumption with tGSH and tCys. After 12 months follow-up, quitters (n=55) had significantly increased levels of tGSH compared to subjects who continued to smoke (P<0.01). No significant change in tGSH was found for subjects who continued to smoke but reduced their intensity of smoking. No significant effect of smoking cessation or reduction was observed on levels of tCys. These results suggest that smoking cessation but not smoking reduction reduces levels of oxidative stress.

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“…Decrease in plasma vitamin C was ameliorated by supplements of a vitamin cocktail containing vitamin C, α-tocopherol, and folate in smokers [29]. Vitamin C supplements were effective at reducing levels of lipid peroxidation in smokers [30]. Antioxidant supplements altered plasma lipid profiles in smokers in a manner consistent with the reduction in oxidative stress [31].…”

Section: Anthocyanin Supplements Increase Oxidative Stress In Young Hmentioning

confidence: 96%

Single Oral Administration of Anthocyanin Rescues Smoking-Induced Endothelial Dysfunction in Young Smokers but Facilitates Oxidative Stress in Non-Smokers

Akane¹,

Tomisawa²,

Osanai³

et al. 2018

FNS

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Objectives: Smoking causes endothelial dysfunction, but it still remains unclear whether oral administration of anthocyanin brings benefits to endothelial function and redox states in young healthy smokers. We tested the hypothesis that supplement anthocyanin may rescue endothelial dysfunction and redox states in young healthy smokers. Methods: Young healthy male non-smoker (n = 8) and smokers (n = 14) were enrolled to measure the derivatives of reactive oxygen metabolites (d-ROMs) and biological antioxidant potential (BAP) levels and brachial artery flow-mediated dilation (FMD) before and 2 hours after one cigarette smoking or resting under administration of blackcurrant supplements (anthocyanins 210 mg) or not. Results: FMD, d-ROMs, and BAP at baseline were similar between non-smokers and smokers. One cigarette smoking induced a decrease in FMD at 2 hours (9.0% ± 2.6% vs 7.5% ± 2.3%, p < 0.05) without affecting plasma levels of d-ROMs and BAP in young healthy smokers. Single oral administration of anthocyanin at 210 mg abolished smoking-induced decrease in FMD (8.3% ± 3.4% vs 9.5% ± 3.6%, p = ns) without changes in plasma levels of d-ROMs and BAP in young smokers. In non-smokers, however, administration of anthocyanin at 210 mg slightly but significantly elevated plasma level of d-ROMs at 2 hours (249.6 ± 30.3 vs How to cite this paper: Yoshizaki, A., Tomisawa, T., Osanai, T., Nanashima, N., Kitajima, M., Mikami, K., Fujita, T., Maeda, H. and Kato, Y. (2018)

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Quantitation of mercapturic acid conjugates of 4-hydroxy-2-nonenal and 4-oxo-2-nonenal metabolites in a smoking cessation study

Cited by 29 publications

References 42 publications

Rat Aldose Reductase-Like Protein (AKR1B14) Efficiently Reduces the Lipid Peroxidation Product 4-Oxo-2-nonenal

Rat Aldose Reductase-Like Protein (AKR1B14) Efficiently Reduces the Lipid Peroxidation Product 4-Oxo-2-nonenal

Effect of smoking reduction and cessation on the plasma levels of the oxidative stress biomarker glutathione – Post-hoc analysis of data from a smoking cessation trial

Single Oral Administration of Anthocyanin Rescues Smoking-Induced Endothelial Dysfunction in Young Smokers but Facilitates Oxidative Stress in Non-Smokers

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