Determination of isoprostanes in urine samples from Alzheimer patients using porous graphitic carbon liquid chromatography–tandem mass spectrometry

Bohnstedt, Kristina Claeson; Karlberg, Bo; Wahlund, Lars‐Olof; Eriksdotter, Maria; Basun, Hans; Schmidt, Staffan

doi:10.1016/s1570-0232(03)00600-7

Cited by 71 publications

(52 citation statements)

References 21 publications

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“…Some authors have claimed that urinary and plasma concentrations of isoprostanes are also increased in AD patients to an extent correlated with the degree of cognitive impairment (84,85 ), although this was not confirmed in other studies (86,87 ). The reason for this discrepancy is possibly because the samples were not taken at the same stage of the disease or because various medications that the patients were taking might have affected the outcome.…”

Section: Isoprostanesmentioning

confidence: 91%

Biomarkers of Oxidative Damage in Human Disease

et al. 2006

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Oxidative/nitrosative stress, a pervasive condition of increased amounts of reactive oxygen/nitrogen species, is now recognized to be a prominent feature of many acute and chronic diseases and even of the normal aging process. However, definitive evidence for this association has often been lacking because of recognized shortcomings with biomarkers and/or methods available to assess oxidative stress status in humans. Emphasis is now being placed on biomarkers of oxidative stress, which are objectively measured and evaluated as indicators of normal biological processes, pathogenic processes, or pharmacologic responses to therapeutic intervention. To be a predictor of disease, a biomarker must be validated. Validation criteria include intrinsic qualities such as specificity, sensitivity, degree of inter-and intraindividual variability, and knowledge of the confounding and modifying factors. In addition, characteristics of the sampling and analytical procedures are of relevance, including constraints and noninvasiveness of sampling, stability of potential biomarkers, and the simplicity, sensitivity, specificity, and speed of the analytical method. Here we discuss some of the more commonly used biomarkers of oxidative/nitrosative damage and include selected examples of human studies.

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Section: Isoprostanesmentioning

confidence: 91%

Biomarkers of Oxidative Damage in Human Disease

et al. 2006

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“…Since F 2 -IsoPs are a mixture are comprised of 4 regioisomers each of which are theoretically comprised of 8 racemic diastereomers, different isomers have been measured to reflect overall levels of lipid peroxidation. In studies of neurodegeneration, F 2 -IsoPs have been quantified by one of four different methods: commercially available enzymelinked immunosorbent assays (ELISAs) [103], two different gas chromatography-(GC-) mass spectrometry (MS) stable isotope dilution methods that we refer to as the "original method" [104] or "modified method" [105], and most recently by liquid chromatography-(LC-) MS [106]. The two GC-MS methods are similar, and quantify subsets of F 2 -IsoPs that co-elute with the deuterated internal standards used; this will be key to comparing studies presented below.…”

Section: Biofluid Studiesmentioning

confidence: 99%

“…We have reviewed this topic in detail previously [124] and find that two studies are important in untangling these conflicting studies. An investigation of peripheral F 2 -IsoPs in LOAD with a new LC-MS-MS method sensitively quantified the four classes of F 2 -IsoPs in urine: iPF 2α -III, iPF 2α -IV, iPF 2α -V, and iPF 2α -VI [106]; yet, these investigators were unable to detect a significant difference in urine iPF 2α concentrations between AD patients and controls. Most importantly, the same investigator who repeatedly reported increased plasma F 2 -IsoPs in MCI and LOAD by the modified GC-MS method recently reported that no increase was seen in a separate set of samples [125].…”

Section: Biofluid Studiesmentioning

confidence: 99%

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Sonnen¹,

Breitner²,

Lovell³

et al. 2008

Free Radical Biology and Medicine

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“…2 For the determination of 8-iso-PG F 2␣ (8-iso-PGF 2␣ ) in cell culture supernatant we adopted the high-performance liquid chromatography (HPLC)-tandem mass spectrometry method described by Bohnstedt et al 23 The limit of detection for 8-iso-PGF 2␣ was 1.5 pg/mL, and the relative standard deviation was 6.8%.…”

Section: Detection Of Oxidative Stressmentioning

confidence: 99%

Effect of Telmisartan on Nitric Oxide–Asymmetrical Dimethylarginine System

et al. 2008

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Abstract-Telmisartan, in addition to blocking angiotensin (Ang) II type 1 receptor (AT 1 R), activates peroxisome proliferator activated receptor ␥ (PPAR␥) signaling that interferes with nitric oxide (NO) system. Because aging of endothelial cells (ECs) is hallmarked by a reduction in NO synthesis, we hypothesized that telmisartan increases NO formation by regulated asymmetrical dimethylarginine (ADMA)-dimethylarginine dimethylaminohydrolase (DDAH)-system through blocking AT 1 R and activating PPAR␥ signaling. To test this hypothesis, ECs were cultured with telmisartan, eprosartan, Ang II, and GW9662 (PPAR␥ antagonist) until the twelfth passage. During the process of aging, PPAR␥ protein expression decreased significantly, whereas the expression of AT 1 R increased. Telmisartan reversed these effects and dose-dependently decreased reactive oxygen species and 8-iso-prostaglandin (PG) F 2␣ formation. This effect was associated with an upregulated activity and protein expression of DDAH, accompanied by a decrease in ADMA concentration, an increase in NO metabolites, and delayed senescence. Blockade of PPAR␥ signaling by GW9662 or PPAR␥ small-interference RNA prevented the effect of telmisartan on ADMA-DDAH-NO system. Coincubation with Ang II did not affect the effect of telmisartan-delayed senescence, whereas Ang II itself accelerated endothelial aging. Moreover, AT 1 R blocker eprosartan that did not influence PPAR␥ protein expression had no effect on ADMA system and senescence. We have demonstrated that telmisartan mainly by activating PPAR␥ signaling can alter the catabolism and release of ADMA as an important cardiovascular risk factor. We therefore propose that telmisartan translationally and posttranslationally upregulated DDAH expression via activation of PPAR␥ signaling, causing ADMA to diminish and increase NO synthesis sufficient to delay senescence. Key Words: telmisartan Ⅲ angiotensin II type 1 receptor Ⅲ peroxisome proliferator activated receptor ␥ Ⅲ oxidative stress Ⅲ asymmetrical dimethylarginine Ⅲ nitric oxide Ⅲ aging A ging is a well-documented risk factor for cardiovascular diseases. One of the possible physiopathological mechanisms through which increasing age may lead to cardiovascular damage is the promotion of endothelial dysfunction. 1 Aged human endothelial cells (ECs), which produce less NO, more asymmetrical dimethylarginine (ADMA), a novel cardiovascular risk factor, and more reactive oxygen species (ROS), 2-5 could account for endothelial dysfunction and development of cardiovascular diseases. 6 -10 We and other have previously demonstrated that aging of human ECs can be altered by several different factors contributing to delay or accelerate the process of aging. [2][3][4][5]11,12 These results suggest that the process of endothelial aging may be an influenceable process and raise the possibility of therapies for preventing various cardiovascular diseases in the elderly.Telmisartan, a highly lipophilic angiotensin (Ang) II type 1 receptor (AT 1 R) blocker (ARB), is used for the treatme...

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Determination of isoprostanes in urine samples from Alzheimer patients using porous graphitic carbon liquid chromatography–tandem mass spectrometry

Cited by 71 publications

References 21 publications

Biomarkers of Oxidative Damage in Human Disease

Biomarkers of Oxidative Damage in Human Disease

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Effect of Telmisartan on Nitric Oxide–Asymmetrical Dimethylarginine System

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