Programmed Lipid Peroxidation of Biomembranes Generating Kinked Phospholipids Permitting Local Molecular Mobility: A Peroxidative Theory of Fluidity Management

Jain, Sudhir; Thomas, M. Joy; Kumar, Pratap; Laloraya, Malini

doi:10.1006/bbrc.1993.2084

Cited by 17 publications

(5 citation statements)

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“…Such a parameter common to all phenomena studied could be membrane fluidity. In agreement with reports from the literature, 47 incubation with XO/HX decreased membrane viscosity in endothelial cells. This mechanism was prevented by SOD.…”

Section: Discussionsupporting

confidence: 93%

Effects of Superoxide Anions on Endothelial Ca ²⁺ Signaling Pathways

Graier

Hoebel

Paltauf-Doburzynska

et al. 1998

ATVB

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Abstract-Although the involvement of free radicals in the development of endothelial dysfunction under pathological conditions, like diabetes and hypercholesterolemia, has been proposed frequently, there is limited knowledge as to how superoxide anions (O 2 Ϫ ) might affect endothelial signal transduction. In this study, we investigated the effects of preincubation with the O 2 Ϫ -generating system xanthine oxidase/hypoxanthine (XO/HX) on mechanisms for Ca 2ϩ signaling in cultured porcine aortic endothelial cells. Incubation of cells with XO/HX yielded increased intracellular Ca 2ϩ release and capacitative Ca 2ϩ entry in response to bradykinin and ATP in a time-and concentration-dependent manner. This effect was prevented by superoxide dismutase but not by the tyrosine kinase inhibitor tyrphostin A48. In addition, capacitative Ca 2ϩ entry induced by the receptor-independent stimulus 2,5-di-(tert-butyl)-1,4-benzohydroquinone or thapsigargin was enhanced in O 2 Ϫ -exposed cells (ϩ38% and ϩ32%, respectively). Increased Ca 2ϩ release in response to bradykinin in XO/HX-pretreated cells might be due to enhanced formation of inositol-1,4,5-trisphosphate (ϩ140%). Exposure to XO/HX also affected other signal transduction mechanisms involved in endothelial Ca 2ϩ signaling, such as microsomal cytochrome P450 epoxygenase and membrane hyperpolarization to Ca 2ϩ store depletion with thapsigargin (ϩ103% and ϩ48%, respectively) and tyrosine kinase activity (ϩ97%). A comparison of bradykinin-initiated intracellular Ca 2ϩ release and thapsigargin-induced hyperpolarization with membrane viscosity modulated by XO/HX (decrease in viscosity) or cholesterol (increase in viscosity) reflected a negative correlation between bradykinin-initiated Ca 2ϩ release and membrane viscosity. Because intracellular Ca 2ϩ is a main regulator of endothelial vascular function, our data suggest that O 2 Ϫ anions are involved in regulation of the vascular endothelium.

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Section: Discussionsupporting

confidence: 93%

Effects of Superoxide Anions on Endothelial Ca ²⁺ Signaling Pathways

Graier

Hoebel

Paltauf-Doburzynska

et al. 1998

ATVB

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“…It is also reported that early pregnancy associated elevation in free radical generation and SOD suppression, 16 resulting in lipid kinky and the increase in membrane fluidity. 23 In an attempt to understand the adverse effects of CrVI on female reproductive system, we studied the status of antioxidants in the rat uterus. In the background of the existing information, it is hypothesized that lactational exposure to CrVI would disrupt uterine function by inducing oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Lactational hexavalent chromium exposure-induced oxidative stress in rat uterus is associated with delayed puberty and impaired gonadotropin levels

Samuel

Stanley

Roopha³

et al. 2010

Hum Exp Toxicol

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Hexavalent chromium (CrVI) is a transition element utilized in many fields of modern industries. CrVI is a reproductive metal toxicant that can traverse the placental barrier and cause a wide range of fetal effects. Therefore, the present study was carried out to determine the CrVI-induced utero-toxicity. In the present study, lactating rats received drinking water containing CrVI (50 mg/L and 200 mg/L) from postnatal days (PND) 1-21. During PND 1-21, the pups received CrVI via the mother’s milk. Pups from both control and treatment groups were continued on regular diet and water from PND-21 onwards and euthanized on PND-45 and -65. Specific activities antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST) were estimated. Hydrogen peroxide (H 2O2), lipid peroxidation (LPO) and serum gonadotropins viz. Luteinizing hormone (LH) and follicle stimulating hormone (FSH) were also assayed. Specific activities of SOD, CAT, GPX, GR and GST and serum testosterone and progesterone were significantly decreased, while H2O2 , LPO and serum FSH was increased in 50—parts per million (ppm) and 200 ppm—treated rats in an age-dependent manner. These results suggest that lactational CrVI exposure induces oxidative stress in rat uterus by decreasing antioxidant enzymes, which were associated with delayed puberty and altered steroids and gonadotrophin levels.

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“…We previously reported that Ox-PAPC causes depletion of cholesterol in the plasma membrane in HAEC (39), which may alter membrane fluidity and thus recycling efficiency of quinone molecule. Previous reports also showed that the incorporation of oxidized phospholipids into the membrane can alter membrane structure (40,41) and fluidity (42). To our knowledge, no studies on the effects of changes in membrane fluidity on the PMET system have been reported.…”

Section: Discussionmentioning

confidence: 82%

Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell

Lee

Kim

et al. 2009

Journal of Lipid Research

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Oxidized-1-palmitoyl-2-arachidonyl-sn -glycerol-3-phosphocholine (Ox-PAPC) has been demonstrated to accumulate in atherosclerotic lesions and regulates expression of more than 1,000 genes in human aortic endothelial cell (HAEC). Among the most highly induced is heme oxygenase-1 (HO-1), a cell-protective antioxidant enzyme, which is sensitively induced by oxidative stress. To identify the pathway by which Ox-PAPC induces HO-1, we focused on the plasma membrane electron transport (PMET) complex, which contains ecto-NADH oxidase 1 (eNOX1) and NADPH:quinone oxidoreductase 1 (NQO1) and affects cellular redox status by regulating levels of NAD(P)H. We demonstrated that Ox-PAPC and its active components stimulated electron transfer through the PMET complex in HAECs from inside to outside [as determined by extracellular 2-(4-iodophenyl)-3-(44-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium (WST-1) reduction] and from outside to inside of the cell (as determined by intracellular NBT reduction). Chemical inhibitors of PMET system and siRNAs to PMET components (NQO1 and eNOX1) significantly decreased HO-1 induction by Ox-PAPC. We present evidence that Ox-PAPC activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in HAEC plays an important role in the induction of HO-1 and PMET inhibitors blocked Nrf2 activation by Ox-PAPC. We hypothesized that PMET activation by Ox-PAPC causes intracellular NAD(P)H depletion, which leads to the increased oxidative stress and HO-1 induction. Supporting this hypothesis, cotreatment of cells with exogenous NAD(P)H and Ox-PAPC significantly decreased oxidative stress and HO-1 induction by Ox-PAPC. Taken together, we demonstrated that the PMET system in HAEC plays an important role in the regulation of cellular redox status and HO-1 expression by Ox-PAPC.

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Programmed Lipid Peroxidation of Biomembranes Generating Kinked Phospholipids Permitting Local Molecular Mobility: A Peroxidative Theory of Fluidity Management

Cited by 17 publications

References 0 publications

Effects of Superoxide Anions on Endothelial Ca ²⁺ Signaling Pathways

Effects of Superoxide Anions on Endothelial Ca ²⁺ Signaling Pathways

Lactational hexavalent chromium exposure-induced oxidative stress in rat uterus is associated with delayed puberty and impaired gonadotropin levels

Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell

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Programmed Lipid Peroxidation of Biomembranes Generating Kinked Phospholipids Permitting Local Molecular Mobility: A Peroxidative Theory of Fluidity Management

Cited by 17 publications

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Effects of Superoxide Anions on Endothelial Ca 2+ Signaling Pathways

Effects of Superoxide Anions on Endothelial Ca 2+ Signaling Pathways

Lactational hexavalent chromium exposure-induced oxidative stress in rat uterus is associated with delayed puberty and impaired gonadotropin levels

Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell

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Effects of Superoxide Anions on Endothelial Ca ²⁺ Signaling Pathways

Effects of Superoxide Anions on Endothelial Ca ²⁺ Signaling Pathways