Type II pneumocytes secrete vitamin E together with surfactant lipids

Rüstow, Bernd; Haupt, Renate; Stevens, Paul A.; Kunze, D

doi:10.1152/ajplung.1993.265.2.l133

Cited by 38 publications

(26 citation statements)

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“…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). Considering that the pulmonary surfactant contains α-tocopherol (Rüstow et al 1993) in addition to the two antioxidant proteins, the enhanced surfactant secretion is feasibly a cytoprotective response of alveolar type II cells to oxygen radical formation on 9,10-PQ exposure. Experiments on rat alveolar type II primary cells have shown that DEP components, particularly polyaromatic hydrocarbons, induce the release of phosphatidylcholine into the alveolar space through a nitric-oxide-dependent signaling pathway (Juvin et al 2002).…”

Section: Discussionmentioning

confidence: 99%

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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Section: Discussionmentioning

confidence: 99%

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

et al. 2012

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“…But there are some studies about oxidative substances, including nitrogen dioxide, which allow us to postulate that these air pollutants would be responsible for the decreasing of the type II pneumocyte cytosomes in city pigeons. So, oxidizing gases originate a decrease in the phospholipidic component of the surfactant (LaCagnin et al, 1990); they seem to affect negatively the polyunsaturated phospholipids (Seeger et al, 1985) which are necessary for normal functioning of surfactant (Van Golde et al, 1988;Rü stow et al, 1993); and, on the other hand, SP-A (surfactant protein A) and lysozyme, two components of surfactant in mammalian lung (Kuroki et al, 1988;Ryan et al, 1989;Voorhout et al, 1991;Haller et al, 1992), are damaged by oxidizing agents, such as ozone and nitrogen dioxide Oosting et al, 1991Oosting et al, , 1992Ryan et al, 1989;Mü ller et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Incidence of air pollution in the pulmonary surfactant system of the pigeon (Columba livia)

Lorz

López

1997

Anat. Rec.

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Background: The integrity of both pulmonary surfactant and surfactant producing cells, type II pneumocytes, is essential for normal pulmonary function. Almost all studies about air pollution effects on the pulmonary surfactant system have been performed by biochemical techniques, using atmospheric pollutants in a much higher concentration than that found in polluted city air. A comparative study of the number of lamellar bodies (LB) (pulmonary surfactant precursors) from type II pneumocytes of pigeon lungs belonging to a contaminated city habitat and a noncontaminated countryside one has been carried out.Methods: Lungs of both pigeon groups were subjected to standard processing for light microscopy. A representative number of histological sections from each lung were stained by Gomori's methenamine-silver nitrate technique, which appears to be a good marker for pulmonary LB. Diverse areas of atrial and parabronchial epithelia from each section were photographed, and then quantification of the number of LB per type II pneumocyte section was performed. The data were statistically analyzed and compared on the basis of the levels of atmospheric pollutants.Results: Gomori's methenamine-silver nitrate technique is a useful staining method to study pneumocyte LB. The average of LB per cell section in city birds was about 33% less than in countryside specimens. Moreover, a great amount of macrophages in the lungs from city pigeons has been shown to be present, whereas this cell type is absent or very scarce in the lungs from country birds.Conclusions: Solid particles and high rates of nitrogen oxides in the polluted air, as well as the oxygen metabolites produced by the macrophages, would represent the main factors for the marked decrease in the amount of LB from type II pneumocytes. Anat.

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“…In vitro, it has been demonstrated that synthetic surfactants can act as an antioxidant; in vivo, surfactants have been shown to scavenge oxidants to protect against hyperoxic lung injury [85, 91]. The antioxidant function of alveolar surfactant is caused by the presence of lipophilic antioxidantia, such as vitamin E [270]. In a preliminary study in primates, however, porcine surfactant did not protect the lung against oxygen injury [138].…”

Section: Complications In Surfactant Therapymentioning

confidence: 99%

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

Creuwels

Golde

Haagsman

1997

Lung

283

188

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Abstract. This article starts with a brief account of the history of research on pulmonary surfactant. We will then discuss the morphological aspects and composition of the pulmonary surfactant system. We describe the hydrophilic surfactant proteins A and D and the hydrophobic surfactant proteins B and C, with focus on the crucial roles of these proteins in the dynamics, metabolism, and functions of pulmonary surfactant. Next we discuss the major disorders of the surfactant system. The final part of the review will be focused on the potentials and complications of surfactant therapy in the treatment of some of these disorders. It is our belief that increased knowledge of the surfactant system and its functions will lead to a more optimal composition of the exogenous surfactants and, perhaps, widen their applicability to treatment of surfactant disorders other than neonatal respiratory distress syndrome.Key words: Surfactant protein-Pulmonary surfactant-Respiratory distress syndrome. HistoryResearch on surfactant goes back to 1929 when von Neergaard published the first paper about the difference in pressure needed to inflate lungs with air or with liquid [333]. He found that the pressure necessary for filling the lungs with air was higher than when the lungs were filled with liquid. To explain this result he stated that the alveoli were stabilized by lowering the naturally high surface tension of the air/water interface. In 1946 Thannhauser and co-workers reported that lung tissue has a remarkably high content of the lipid dipalmityl lecithin (current name, dipalmitoylphosphatidylcholine)Offprint requests to: Henk P. Haagsman.

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Type II pneumocytes secrete vitamin E together with surfactant lipids

Cited by 38 publications

References 0 publications

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

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

Incidence of air pollution in the pulmonary surfactant system of the pigeon (Columba livia)

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

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