Determination of Aldehydes and Other Lipid Peroxidation Products in Biological Samples by Gas Chromatography-Mass Spectrometry

Luo, Xiao-Jun; Yazdanpanah, Mehrdad; Bhooi, N.; Lehotay, Denis C.

doi:10.1006/abio.1995.1353

Cited by 189 publications

(123 citation statements)

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“…The GC-MS method employed in the present study has the advantages of mass specificity, high sensitivity allowing for detection of HNE at the level of 50 fmol (Luo et al, 1995), mild derivatization conditions to minimize the artifactual production of lipid peroxidation aldehydic products during the experimental processes (see below), and simultaneous detection and quantification of both HNE and MDA in one sample. The use of stable, deuterated internal standards has addressed early concerns that the recovery of HNE might not be quantitative (Luo et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

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Levels of 4-Hydroxynonenal and Malondialdehyde Are Increased in Brain of Human Chronic Users of Methamphetamine

Fitzmaurice

Tong²,

Yazdanpanah³

et al. 2006

J Pharmacol Exp Ther

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Animal studies suggest that the widely used psychostimulant drug methamphetamine (MA) can harm brain dopamine neurones, possibly by causing oxidative damage. However, evidence of oxidative damage in brain of human MA users is lacking. We tested the hypothesis that levels of two "gold standard" products generated from lipid peroxidation, 4-hydroxynonenal (one of the most reactive lipid peroxidation aldehyde products) and malondialdehyde, would be elevated in post mortem brain of 16 dopamine-deficient chronic MA users compared with those in 21 matched control subjects. Derivatized aldehyde concentrations were determined by gas chromatography-mass spectrometry. In the MA group, we found significantly increased levels of 4-hydroxynonenal and malondialdehyde in the dopamine-rich caudate nucleus (by 67 and 75%, respectively) and to a lesser extent in frontal cortex (48 and 36%, respectively) but not in the cerebellar cortex. Approximately half of the MA users had levels of 4-hydroxynonenal falling above the upper limit of the control range in caudate and frontal cortex. A subgroup of MA users with high brain drug levels had higher concentrations of the aldehydes. Our data suggest that MA exposure in human causes, as in experimental animals, above-normal formation of potentially toxic lipid peroxidation products in brain. This provides evidence for involvement of oxygen-based free radicals in the action of MA in both dopamine-rich (caudate) and -poor (cerebral cortex) areas of human brain.

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Section: Discussionmentioning

confidence: 99%

“…HNE and MDA were measured by gas chromatography (GC)-negative ion chemical ionization-mass spectrometry (MS) using minor modifications of the method of Luo et al (1995). All samples were analyzed in replicate by an unbiased observer (M.Y.)…”

Section: Methodsmentioning

confidence: 99%

Levels of 4-Hydroxynonenal and Malondialdehyde Are Increased in Brain of Human Chronic Users of Methamphetamine

Fitzmaurice

Tong²,

Yazdanpanah³

et al. 2006

J Pharmacol Exp Ther

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“…Blood samples were taken before and during lipid/saline infusion for assays of plasma glucose, insulin, C-peptide, triacyl- Laboratory methods Plasma glucose, insulin, C-peptide, triacylglycerols and NEFAs were assayed as previously described [8]. Plasma MDA and 4-HNE were analysed by a modification of a previously described method [28,29], on a Hewlett-Packard 5973N MSD GC-MS equipped with an HP-5 MS column and performed in negative-ion chemical ionisation.…”

Section: Methodsmentioning

confidence: 99%

Oral taurine but not N-acetylcysteine ameliorates NEFA-induced impairment in insulin sensitivity and beta cell function in obese and overweight, non-diabetic men

2007

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Aims/hypothesis Antioxidants have been shown to ameliorate lipid-induced impairment of insulin action and beta cell function, both in vitro and in animal studies. The aim of the present study was to examine the effects of two orally administered antioxidants, N-acetylcysteine (NAC) and taurine (TAU), on lipotoxicity in humans. Methods Nine non-diabetic men, who were either overweight or obese, underwent three studies each, 4-6 weeks apart, in random order: (1) i.v. infusion of saline for 48 h (SAL); (2) i.v. infusion of Intralipid and heparin for 48 h to mimic chronic elevation of plasma NEFA (IH); and (3) IH infusion for 48 h with concurrent oral NAC (IH+NAC). Six men underwent similar studies except for study 3, where instead of NAC they received a 2 week pretreatment with oral TAU (IH+TAU). Results For both the NAC and TAU studies, a 48 h IH infusion alone without antioxidant impaired insulin sensitivity (S I , 63% and 62% of SAL in NAC and TAU studies, respectively) and beta cell function, as evidenced by a reduction in disposition index (DI, 55% and 54% of SAL in NAC and TAU studies, respectively). NAC failed to prevent the lipid-induced increase in levels of the plasma oxidative stress marker malondialdehyde and did not prevent the lipid-induced reduction in S I or DI, whereas TAU completely prevented the rise in malondialdehyde and decreased 4-hydroxynonenal, and significantly improved S I (91% of SAL) and DI (81% of SAL). Conclusions/interpretation Oral TAU ameliorates lipidinduced functional beta cell decompensation and insulin resistance in humans, possibly by reducing oxidative stress.ClinicalTrials.gov ID no. NCT0018873

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“…Samples were analyzed for malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) by a modification of a previously described method (49). Briefly, plasma aldehydes and 100 pmol of benzaldehyde-ring-D5 (internal standard) were derivatized by pentafluorobenzyl hydroxylamine hydrochloride (PFBHA ⅐ HCl) to form the aldehydes-PFBHA derivative.…”

Section: Methodsmentioning

confidence: 99%

N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress

Haber

Lam

Yü

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

202

135

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-Exposure to high concentrations of glucose and insulin results in insulin resistance of metabolic target tissues, a characteristic feature of type 2 diabetes. High glucose has also been associated with oxidative stress, and increased levels of reactive oxygen species have been proposed to cause insulin resistance. To determine whether oxidative stress contributes to insulin resistance induced by hyperglycemia in vivo, nondiabetic rats were infused with glucose for 6 h to maintain a circulating glucose concentration of 15 mM with and without coinfusion of the antioxidant N-acetylcysteine (NAC), followed by a 2-h hyperinsulinemic-euglycemic clamp. High glucose (HG) induced a significant decrease in insulin-stimulated glucose uptake [tracer-determined disappearance rate (R d), control 41.2 Ϯ 1.7 vs. HG 32.4 Ϯ 1.9 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 , P Ͻ 0.05], which was prevented by NAC (HG ϩ NAC 45.9 Ϯ 3.5 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 ). Similar results were obtained with the antioxidant taurine. Neither NAC nor taurine alone altered Rd. HG caused a significant (5-fold) increase in soleus muscle protein carbonyl content, a marker of oxidative stress that was blocked by NAC, as well as elevated levels of malondialdehyde and 4-hydroxynonenal, markers of lipid peroxidation, which were reduced by taurine. In contrast to findings after long-term hyperglycemia, there was no membrane translocation of novel isoforms of protein kinase C in skeletal muscle after 6 h. These data support the concept that oxidative stress contributes to the pathogenesis of hyperglycemia-induced insulin resistance. euglycemic clamp; insulin resistance; protein carbonyls; protein kinase C; antioxidants INSULIN RESISTANCE is one of the earliest detectable predictors of type 2 diabetes (47, 51, 39) and, along with relative insulin deficiency (39, 56), strongly contributes to the development of overt hyperglycemia. Hyperglycemia is in large part responsible for a host of complications found in diabetic subjects (15,83,86) and can worsen insulin resistance (11,38,72,73,75). The effect of hyperglycemia per se to induce insulin resistance in vivo was first demonstrated by Rossetti et al. (75) in the partially pancreatectomized rat model, which is characterized by moderate fasting hyperglycemia, glucose intolerance, and normal fasting insulin levels. In that study, phlorizin was used to normalize plasma glucose without affecting insulin secretion. Use of a hyperinsulinemic-euglycemic clamp revealed that the decreased insulin-stimulated glucose utilization was completely normalized in the phlorizin-treated rats, indicating a direct role of glucose in the induction of insulin resistance. Several mechanisms have been proposed to mediate hyperglycemia-induced insulin resistance, including the hexosamine biosynthetic pathway (4,31,67,74,87) and protein kinase C (55,68,78

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Determination of Aldehydes and Other Lipid Peroxidation Products in Biological Samples by Gas Chromatography-Mass Spectrometry

Cited by 189 publications

References 0 publications

Levels of 4-Hydroxynonenal and Malondialdehyde Are Increased in Brain of Human Chronic Users of Methamphetamine

Levels of 4-Hydroxynonenal and Malondialdehyde Are Increased in Brain of Human Chronic Users of Methamphetamine

Oral taurine but not N-acetylcysteine ameliorates NEFA-induced impairment in insulin sensitivity and beta cell function in obese and overweight, non-diabetic men

N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress

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