Polyunsaturated fatty acids stimulate superoxide formation in tumor cells: A mechanism for specific cytotoxicity and a model for tumor necrosis factor?

Peterson, Douglas A; Mehta, Naren; Butterfield, John T.; Hušák, M.; Christopher, M. M.; Jagarlapudi, Srinath; Eaton, John W.

doi:10.1016/s0006-291x(88)80600-4

Cited by 23 publications

(5 citation statements)

References 11 publications

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“…The mechanisms by which alterations in fatty acid composition modulate cellular susceptibility to oxidant stress remain to be defined. Based on reports that fatty acids alter PROS production in other cells and tissues [12][13][14][15][16][17], we hypothesized that supplementation with exogenous fatty acids altered intracellular H,O, concentrations and thereby affected cell susceptibility to oxidant stress. To test this hypothesis, PAEC were supplemented with 18:l or 18:3.…”

Section: Discussionmentioning

confidence: 99%

Oleic Acid Reduces Oxidant Stress in Cultured Pulmonary Artery Endothelial Cells

Hart

Gupta

Evanoff

1997

Experimental Lung Research

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Altering the fatty acid composition of cultured porcine pulmonary artery endothelial cells (PAEC) modulates their susceptibility to oxidant stress. This study demonstrates that supplementing PAEC with oleic acid (18:1 omega 9), but not gamma-linolenic acid (18:3 omega 6), provided dose-dependent protection from hydrogen peroxide (H2O2)-induced cytotoxicity. It was hypothesized that 18:1 reduced PAEC susceptibility to oxidant stress by altering H2O2 metabolism. To test this hypothesis, confluent PAEC monolayers were treated with 100-200 microM H2O2 or control conditions 24 h after supplementation with 0.1 mM 18:1, 18:3, or vehicle for 3 h. Intracellular [H2O2] in control cells (14.4-29.0 pM), estimated from the rate of aminotriazole-mediated inactivation of endogenous catalase activity, increased following treatment with 200 microM H2O2 (19.0-37.3 pM). Supplementation with 18:1 attenuated increases in intracellular [H2O2] only in oxidant-exposed cells, whereas supplementation with 18:3 attenuated intracellular [H2O2] only in control cells. Supplementation with 18:1 or 18:3 tended to reduce or enhance PAEC lipid hydroperoxide content following H2O2 exposure, respectively, but did not alter PAEC reduced glutathione content, the activities of glutathione peroxidase or catalase, or H2O2 uptake and release. Alteration of H2O2 metabolism in cultured PAEC may contribute to the ability of fatty acids to modulate cellular oxidant susceptibility.

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Section: Discussionmentioning

confidence: 99%

Oleic Acid Reduces Oxidant Stress in Cultured Pulmonary Artery Endothelial Cells

Hart

Gupta

Evanoff

1997

Experimental Lung Research

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“…Arachidonic acid and its diverse products regulate death in several cell types 30 . This is thought to be due to the fact that arachidonic acid products are second messengers in tumour necrosis factor-induced apoptosis 31 and the fact that oxygen radicals, which are produced during lipoxygenation of arachidonic acid, induce the production of reactive oxygen species and are involved in the induction of cell death 32 . Arachidonic acid also activates sphingo myelinase, leading to ceramide production and apoptosis 33 .…”

Section: Host Lipids Modulate Macrophage Deathmentioning

confidence: 99%

Evasion of innate immunity by Mycobacterium tuberculosis: is death an exit strategy?

2010

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Virulent Mycobacterium tuberculosis inhibits apoptosis and triggers necrosis of host macrophages to evade innate immunity and delay the initiation of adaptive immunity. By contrast, attenuated M. tuberculosis induces macrophage apoptosis, an innate defence mechanism that reduces bacterial viability. In this Opinion article, we describe how virulent M. tuberculosis blocks production of the eicosanoid lipid mediator prostaglandin E2 (PGE2). PGE2 production by infected macrophages prevents mitochondrial damage and initiates plasma membrane repair, two processes that are crucial for preventing necrosis and inducing apoptosis. Thus, M. tuberculosis-mediated modulation of eicosanoid production determines the death modality of the infected macrophage, which in turn has a substantial impact on the outcome of infection.

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“…Arachidonic acid and its diverse products regulate death in several cell types 40 . For example, arachidonic acid products are second messengers in TNF-induced apoptosis 41 , and oxygen radicals, which are produced during lipoxygenation of arachidonic acid, induce ROS production, which can induce cell death 42 . Arachidonic acid also activates sphingomyelinase leading to ceramide production and apoptosis 43 .…”

Section: Host Lipid Mediators Modulate Mtb Infected Macrophage Death mentioning

confidence: 99%

Dying to Live: How the Death Modality of the Infected Macrophage Affects Immunity to Tuberculosis

Divangahi

Behar²,

Remold³

2013

Advances in Experimental Medicine and Biology

108

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Polyunsaturated fatty acids stimulate superoxide formation in tumor cells: A mechanism for specific cytotoxicity and a model for tumor necrosis factor?

Cited by 23 publications

References 11 publications

Oleic Acid Reduces Oxidant Stress in Cultured Pulmonary Artery Endothelial Cells

Oleic Acid Reduces Oxidant Stress in Cultured Pulmonary Artery Endothelial Cells

Evasion of innate immunity by Mycobacterium tuberculosis: is death an exit strategy?

Dying to Live: How the Death Modality of the Infected Macrophage Affects Immunity to Tuberculosis

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