Ethanolamine plasmalogens prevent the oxidation of cholesterol by reducing the oxidizability of cholesterol in phospholipid bilayers

Maeba, Ryouta; Ueta, Nobuo

doi:10.1194/jlr.m200340-jlr200

Cited by 74 publications

(49 citation statements)

References 42 publications

(34 reference statements)

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“…Less than 0.2% of the total radioactivity was found in the aqueous layer. This distribution of the radiolabel is in agreement with the literature values for AAPH-oxidized cholesterol [25]. The presence of SM inhibited the formation of all products to the same extent (results not shown).…”

Section: Oxidation Of Labeled Cholesterolsupporting

confidence: 80%

“…The inhibition was much greater when labeled cholesterol was incorporated into pure SM liposomes, although these liposomes were considerably more turbid compared to the PC-containing liposomes. Although previous studies [25] reported some inhibition of cholesterol oxidation by egg PE, both PE and PS modestly stimulated the oxidation in our experimental system. The reason for this discrepancy is not clear, but there are several differences in the experimental conditions between the two studies.…”

Section: Specificity Of Sm Effectmentioning

confidence: 44%

“…Although we have not conclusively identified the oxidation products in this study, the major products formed by AAPH oxidation of cholesterol are known to be 7-oxo (keto) cholesterol, 7α-and 7β-hydroxy cholesterol, and 5,6-epoxy cholesterol [24,25]. Based on the R f values reported in the literature [22], we tentatively identified the polar (origin) spot as a mixture of 7α-and 7β-hydroxy cholesterol, and the less polar spot as predominantly 7-oxo cholesterol.…”

Section: Oxidation Of Labeled Cholesterolmentioning

confidence: 99%

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Protection of membrane cholesterol by sphingomyelin against free radical-mediated oxidation

Sargis

Subbaiah

2006

Free Radical Biology and Medicine

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Although the free radical-mediated oxidation of free cholesterol (FC) is critical in the generation of regulatory sterols and in atherogenesis, the physiological regulation of this process is poorly understood. We tested the hypothesis that sphingomyelin (SM), a major phospholipid of cell membranes, which is closely associated with FC, protects FC against oxidation, because of its unique structure, and affinity to the sterol. We employed phosphatidylcholine (PC) liposomes containing varying amounts of SM, and either radioactive FC or a fluorescent analog, dehydroergosterol (DHE), and determined the oxidative decay of the sterol in presence of 2,2′ azo bis(2-amidinopropane hydrochloride) (AAPH). Incorporation of 25 mol% of SM in the liposomes inhibited the oxidation of FC or DHE by up to 50%. This inhibition was specific for SM among phospholipids, and was abolished by sphingomyelinase treatment. SM was not degraded during the oxidation reaction, and its effect was not dependent upon the nature of the oxidizing agent, because it also inhibited sterol oxidation by FeSO 4 /ascorbate, and by cholesterol oxidase. These studies show that SM plays a physiological role in the regulation of cholesterol oxidation by free radicals.

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Section: Oxidation Of Labeled Cholesterolsupporting

confidence: 80%

Section: Specificity Of Sm Effectmentioning

confidence: 44%

Section: Oxidation Of Labeled Cholesterolmentioning

confidence: 99%

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Protection of membrane cholesterol by sphingomyelin against free radical-mediated oxidation

Sargis

Subbaiah

2006

Free Radical Biology and Medicine

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“…5). DHAP-AT is an important enzyme required for synthesis of plasmalogens (Purdue et al, 1997), which are strong antioxidant phospholipids important for scavenging ROS and preventing cell membrane oxidation (Maeba and Ueta, 2003). Our study suggests that a decrease in DHAP-AT activity reduced plasmalogens, which likely increases the vulnerability of late OL-progenitors to oxidative-stress.…”

Section: Discussionmentioning

confidence: 78%

Lipopolysaccharide-induced peroxisomal dysfunction exacerbates cerebral white matter injury: Attenuation by N-acetyl cysteine

Paintlia

Contreras

et al. 2008

Experimental Neurology

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Cerebral white matter injury during prenatal maternal infection characterized as periventricular leukomalacia (PVL) is the main substrate for cerebral palsy (CP) in premature infants. Previously, we reported that maternal LPS exposure causes oligodendrocyte (OL)-injury/hypomyelination in the developing brain which can be attenuated by an antioxidant agent, N-acetyl cysteine (NAC). Herein, we elucidated the role of peroxisomes in LPS-induced neuroinflammation and cerebral white matter injury. Peroxisomes are important for detoxification of reactive oxidative species (ROS) and metabolism of myelin-lipids in OLs. Maternal LPS exposure induced selective depletion of developing OLs in the fetal brain which was associated with ROS generation, glutathione depletion and peroxisomal dysfunction. Likewise, hypomyelination in the postnatal brain was associated with decrease in peroxisomes in OLs after maternal LPS exposure. Conversely, NAC abolished these LPS-induced effects in the developing brain. CP brains imitated these changes in peroxisomal/myelin proteins in the postnatal brain after maternal LPS exposure. In vitro studies revealed that proinflammatory cytokines cause OL-injury via peroxisomal dysfunction and ROS generation. NAC or WY14643 (peroxisome proliferators activated receptor (PPAR)-α agonist) reverses these effects of proinflammatory cytokines in the wild-type OLs, but not in PPAR-α (−/−) OLs. Similarly treated B12 oligodenroglial cells co-transfected with PPAR-α siRNAs/pTK-PPREx3-Luc, and LPS exposed PPAR-α (−/−) pregnant mice treated with NAC or WY14643 further suggested that PPAR-α activity mediates NAC-induced protective effects. Collectively, these data provide unprecedented evidence that LPS-induced peroxisomal dysfunction exacerbates cerebral white matter injury and NACinduced protection is via a PPAR-α dependent mechanism expands therapeutic avenues for PVL and related demyelinating diseases.

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“…18 Plasmalogens may also act as antioxidants, thus protecting cells from oxidative stress. 19 Rüdiger and colleagues 15 reported the highest concentration of plasmalogens in poractant alfa (3.8 mol%), which is 2.5 times greater than beractant and 4 times greater than SF-RI1. On an in-vitro basis, plasmalogens and PUFA-PL contribute substantially to the lowering of surface viscosity.…”

Section: The Biochemistry Of Surfactantsmentioning

confidence: 99%

Surfactants in the Management of Respiratory Distress Syndrome in Extremely Premature Infants

Ramanathan

2006

The Journal of Pediatric Pharmacology and Therapeutics

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Respiratory distress syndrome (RDS) is primarily due to decreased production of pulmonary surfactant, and it is associated with significant neonatal morbidity and mortality. Exogenous pulmonary surfactant therapy is currently the treatment of choice for RDS, as it demonstrates the best clinical and economic outcomes. Studies confirm the benefits of surfactant therapy to include reductions in mortality, pneumothorax, and pulmonary interstitial emphysema, as well as improvements in oxygenation and an increased rate of survival without bronchopulmonary dysplasia. Phospholipids (PL) and surfactant-associated proteins (SP) play key roles in the physiological activity of surfactant. Different types of natural and synthetic surfactant preparations are currently available. To date, natural surfactants demonstrate superior outcomes compared to the synthetic surfactants, at least during the acute phase of RDS. This disparity is often attributed to biochemical differences including the presence of surfactant-associated proteins in natural products that are not found in the currently available synthetic surfactants. Comparative trials of the natural surfactants strive to establish the precise differences in clinical outcomes among the different preparations. As new surfactants become available, it is important to evaluate them relative to the known benefits of the previously existing surfactants. In order to elucidate the role of surfactant therapy in the management of RDS, it is important to review surfactant biochemistry, pharmacology, and outcomes from randomized clinical trials.

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Ethanolamine plasmalogens prevent the oxidation of cholesterol by reducing the oxidizability of cholesterol in phospholipid bilayers

Cited by 74 publications

References 42 publications

Protection of membrane cholesterol by sphingomyelin against free radical-mediated oxidation

Protection of membrane cholesterol by sphingomyelin against free radical-mediated oxidation

Lipopolysaccharide-induced peroxisomal dysfunction exacerbates cerebral white matter injury: Attenuation by N-acetyl cysteine

Surfactants in the Management of Respiratory Distress Syndrome in Extremely Premature Infants

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