In vivo lipid peroxidation in man as measured by the respiratory excretion of ethane, pentane, and other low-molecular-weight hydrocarbons

Wade, C R; Rij, AndréM. van

doi:10.1016/0003-2697(85)90433-6

Cited by 80 publications

(18 citation statements)

References 10 publications

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“…Second, tissue oxygen tension may influence the formation of the alkanes (27,28). Third, the alkanes may be metabolized differently (29). Finally, with the use of the present method the quantitation of pentane is more accurate than that of ethane (14).…”

Section: Daysmentioning

confidence: 88%

Immaturity-Dependent Free Radical Activity in Premature Infants

et al. 1994

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To examine the role of immaturity in the free radicalmediated rate of lipid peroxidation in premature infants, we studied 27 infants [gestational age, 27.1 (SD 2.4) wk; birth weight, 970 (SD 330) g]. Ethane and pentane were quantitated in expired air during the first 18 d of life. During the first 2 postnatal d ethane [24.1 (SEM 7.8) pmol x kg-' x min-'1 and pentane [24.2 (SEM 4.1) pmol x kg-' x min-'1 were stable but increased during d 5 to maxima of 79.1 (15.8) pmol x kg-' x min-' and 62.1 (8.1) pmol X kg-' X min-', respectively. Maximum ethane and pentane correlated with gestational age (r = -0.42, p = 0.03 and r = -0.52, p = 0.005, respectively) and birth weight (r = -0 . 3 8 ,~ = 0.05 and r = -0.59, p = 0.001, respectively). Infants with high maximum expired ethane and pentane (exceeding 40 pmol x kg-' x min-') had higher odds of dying or having bronchopulmonary dysplasia than those with low ethane and pentane (odds ratio, 6.5; 95% confiThe newborn at term is better protected against the effects of free oxygen radicals than are prematurely born and adult individuals (1, 2). The reasons for such resistance are possibly the high activity of antioxidant enzymes and the capacity for induction of activity of these enzymes in response to oxidative challenge (1, 3, 4). Additionally, the concentrations of antioxidants are low in the premature infant (2,5). Moreover, the prematurely born infant is f~equently exposed to conditions associated with increased generation of free oxygen radicals, such as dence interval, 1.1 to 38.5; p < 0.05 for ethane and odds ratio, 5.6; 95% confidence interval, 1.1 to 2 9 . 3 ;~ < 0.05 for pentane). We conclude that degree of prematurity is the single most important factor explaining free radicalmediated lipid peroxidation in premature infants. A therapeutic intervention to limit the effects of free radicals should be started during the 1st postnatal d in premature infants to be effective. Lipid peroxidation generates volatile products, e.g. ethane and pentane, the concentrations of which in expired air serve as indicators of the free radical activity (13,14). The aim of the present investigation was to analyze the factors associated with free radical activity by quantifying ethane and pentane in expired air. PATIENTS AND METHODSreperfusion and hyperoxia (69 7)-1 t -h~ been proposed patients.

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Section: Daysmentioning

confidence: 88%

Immaturity-Dependent Free Radical Activity in Premature Infants

et al. 1994

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“…Breath ethane output has received less attention in human studies as a measure of lipid peroxidation, likely because pentane represents the majority of PUFA (n-6) in the body (37). However, breath ethane output is a well-recognized index of lipid peroxidation (38)(39)(40) and has been reported to be elevated in smokers (41) and children with liver disease (42).…”

Section: Discussionmentioning

confidence: 99%

Lipid peroxidation during n−3 fatty acid and vitamin E supplementation in humans

Allard

Kurian²,

Aghdassi³

et al. 1997

Lipids

151

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The purpose of this study was to investigate in healthy humans the effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) intake, alone or in combination with dL-alpha-tocopherol acetate (vitamin E) supplements on lipid peroxidation. Eighty men were randomly assigned in a double-blind fashion to take daily for 6 wk either menhaden oil (6.26 g, n-3 fatty acids) or olive oil supplements with either vitamin E (900 IU) or its placebo. Antioxidant vitamins, phospholipid composition, malondialdehyde (MDA), and lipid peroxides were measured in the plasma at baseline and week 6. At the same time, breath alkane output was measured. Plasma alpha-tocopherol concentration increased in those receiving vitamin E (P < 0.0001). In those supplemented with n-3 fatty acids, EPA and DHA increased in plasma phospholipids (P < 0.0001) and plasma MDA and lipid peroxides increased (P < 0.001 and P < 0.05, respectively). Breath alkane output did not change significantly and vitamin E intake did not prevent the increase in lipid peroxidation during menhaden oil supplementation. The results demonstrate that supplementing the diet with n-3 fatty acids resulted in an increase in lipid peroxidation, as measured by plasma MDA release and lipid peroxide products, which was not suppressed by vitamin E supplementation.

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“…It has been reported that background levels of ethane can be washed out of the lung in 4 min by breathing hydrocarbon-free air (16). However, others have shown that steady state was not achieved even after 2 h of breathing ethane-free air (48). Recently, von Basum et al (47) have reported a real-time method for the analysis of breath ethane.…”

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confidence: 99%