Pulmonary surfactant protein A inhibits the lipid peroxidation stimulated by linoleic acid hydroperoxide of rat lung mitochondria and microsomes

Terrasa, Ana M.; Guajardo, Margarita H.; Sanabria, Elizabeth de Armas; Catalá, Ángel

doi:10.1016/j.bbalip.2005.05.007

Cited by 19 publications

(13 citation statements)

References 38 publications

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“…This putative role (i.e. its involvement in redox regulation, in addition to its well-described role in innate immunity) builds on several reports that have described an antioxidant function for SP-A [101][102][103].…”

Section: Discussionmentioning

confidence: 71%

“…We speculate that this increase occurs because of the lack of SP-A, an important host defense protein that plays an antioxidant or oxidant scavenger role in the alveolus. This is based on several converging lines of evidence including: 1) the attribution of an antioxidant role to SP-A [101][102][103]; 2) the demonstration that SP-A is highly susceptible to oxidative modification by carbonylation) [53] and to ozone-induced oxidation of methionine residues [34], and that its function is disrupted by these oxidative modifications) [9,[31][32][33][34]; and 3) the description of other systems in which proteins serve as "sacrificial antioxidants" [104][105][106][107][108][109].…”

Section: Discussionmentioning

confidence: 99%

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The impact of surfactant protein-A on ozone-induced changes in the mouse bronchoalveolar lavage proteome

et al. 2009

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BackgroundOzone is a major component of air pollution. Exposure to this powerful oxidizing agent can cause or exacerbate many lung conditions, especially those involving innate immunity. Surfactant protein-A (SP-A) plays many roles in innate immunity by participating directly in host defense as it exerts opsonin function, or indirectly via its ability to regulate alveolar macrophages and other innate immune cells. The mechanism(s) responsible for ozone-induced pathophysiology, while likely related to oxidative stress, are not well understood.MethodsWe employed 2-dimensional difference gel electrophoresis (2D-DIGE), a discovery proteomics approach, coupled with MALDI-ToF/ToF to compare the bronchoalveolar lavage (BAL) proteomes in wild type (WT) and SP-A knockout (KO) mice and to assess the impact of ozone or filtered air on the expression of BAL proteins. Using the PANTHER database and the published literature most identified proteins were placed into three functional groups.ResultsWe identified 66 proteins and focused our analysis on these proteins. Many of them fell into three categories: defense and immunity; redox regulation; and protein metabolism, modification and chaperones. In response to the oxidative stress of acute ozone exposure (2 ppm; 3 hours) there were many significant changes in levels of expression of proteins in these groups. Most of the proteins in the redox group were decreased, the proteins involved in protein metabolism increased, and roughly equal numbers of increases and decreases were seen in the defense and immunity group. Responses between WT and KO mice were similar in many respects. However, the percent change was consistently greater in the KO mice and there were more changes that achieved statistical significance in the KO mice, with levels of expression in filtered air-exposed KO mice being closer to ozone-exposed WT mice than to filtered air-exposed WT mice.ConclusionWe postulate that SP-A plays a role in reactive oxidant scavenging in WT mice and that its absence in the KO mice in the presence or absence of ozone exposure results in more pronounced, and presumably chronic, oxidative stress.

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

The impact of surfactant protein-A on ozone-induced changes in the mouse bronchoalveolar lavage proteome

et al. 2009

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“…The cell viabilities are expressed as a percentage of control cells treated with vehicle alone. *Significant difference from the cells treated with 9,10-PQ (open bars), P<0.05 hydrophilic member of surfactant apoproteins SPA is reported to inhibit lipid peroxidation (Terrasa et al 2005), ROS generation (Crowther et al 2004) and type II alveolar cell apoptosis (White and Strayer 2001). Additionally, another soluble protein SPD seems to have the capacity to protect mice from allergic inflammation (Takeda et al 2003) and acute hyperoxic lung injury (Jain et al 2008).…”

Section: Discussionmentioning

confidence: 97%

9,10-Phenanthrenequinone promotes secretion of pulmonary aldo-keto reductases with surfactant

et al. 2012

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9,10-Phenanthrenequinone (9,10-PQ), a major quinone in diesel exhaust particles, induces apoptosis via the generation of reactive oxygen species (ROS) because of 9,10-PQ redox cycling. We have found that intratracheal infusion of 9,10-PQ facilitates the secretion of surfactant into rat alveolus. In the cultured rat lung, treatment with 9,10-PQ results in an increase in a lower-density surfactant by ROS generation through redox cycling of the quinone. The surfactant contains aldo-keto reductase (AKR) 1C15, which reduces 9,10-PQ and the enzyme level in the surfactant increases on treatment with 9,10-PQ suggesting an involvement of AKR1C15 in the redox cycling of the quinone. In six human cell types (A549, MKN45, Caco2, Hela, Molt4 and U937) only type II epithelial A549 cells secrete three human AKR1C subfamily members (AKR1C1, AKR1C2 and AKR1C3) with the surfactant into the medium; this secretion is highly increased by 9,10-PQ treatment. Using in vitro enzyme inhibition analysis, we have identified AKR1C3 as the most abundantly secreted AKR1C member. The AKR1C enzymes in the medium efficiently reduce 9,10-PQ and initiate its redox cycling accompanied by ROS production. The exposure of A549 cells to 9,10-PQ provokes viability loss, which is significantly protected by the addition of the AKR1C3 inhibitor and antioxidant enzyme and by the removal of the surfactants from the culture medium. Thus, the AKR1C enzymes secreted in pulmonary surfactants probably participate in the toxic mechanism triggered by 9,10-PQ.

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“…Additional studies of lipid peroxidation of rat lung mitochondria or microsomes using equal amounts of albumin and even higher compared to SPA were carried out. Our results indicate that under our experimental conditions, BSA was unable to inhibit lipid peroxidation stimulated by linoleic acid hydroperoxide of rat lung mitochondria or microsomes, thus indicating that this effect is specific to SP-A [39]. …”

Section: Lipid Peroxidation Studiesmentioning

confidence: 99%

Five Decades with Polyunsaturated Fatty Acids: Chemical Synthesis, Enzymatic Formation, Lipid Peroxidation and Its Biological Effects

Catalá

2013

Journal of Lipids

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I have been involved in research on polyunsaturated fatty acids since 1964 and this review is intended to cover some of the most important aspects of this work. Polyunsaturated fatty acids have followed me during my whole scientific career and I have published a number of studies concerned with different aspects of them such as chemical synthesis, enzymatic formation, metabolism, transport, physical, chemical, and catalytic properties of a reconstructed desaturase system in liposomes, lipid peroxidation, and their effects. The first project I became involved in was the organic synthesis of [1-14C] eicosa-11,14-dienoic acid, with the aim of demonstrating the participation of that compound as a possible intermediary in the biosynthesis of arachidonic acid “in vivo.” From 1966 to 1982, I was involved in several projects that study the metabolism of polyunsaturated fatty acids. In the eighties, we studied fatty acid binding protein. From 1990 up to now, our laboratory has been interested in the lipid peroxidation of biological membranes from various tissues and different species as well as liposomes prepared with phospholipids rich in PUFAs. We tested the effect of many antioxidants such as alpha tocopherol, vitamin A, melatonin and its structural analogues, and conjugated linoleic acid, among others.

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Pulmonary surfactant protein A inhibits the lipid peroxidation stimulated by linoleic acid hydroperoxide of rat lung mitochondria and microsomes

Cited by 19 publications

References 38 publications

The impact of surfactant protein-A on ozone-induced changes in the mouse bronchoalveolar lavage proteome

The impact of surfactant protein-A on ozone-induced changes in the mouse bronchoalveolar lavage proteome

9,10-Phenanthrenequinone promotes secretion of pulmonary aldo-keto reductases with surfactant

Five Decades with Polyunsaturated Fatty Acids: Chemical Synthesis, Enzymatic Formation, Lipid Peroxidation and Its Biological Effects

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