Interaction of surfactant mixtures with reactive oxygen and nitrogen species

Increased concentrations of partially reduced oxygen and nitrogen reactive species damage the alveolar epithelium and either cause or exacerbate surfactant deficiency. For this reason, there is a quest to identify surfactant replacement mixtures, which in addition to repleting depleted surfactant stores can also reduce the steady-state concentrations of reactive species in the alveolar space. Herein, we evaluated the ability of natural lung surfactant (NLS) and two mixtures (Exosurf and Survanta) used clinically for the correction of surfactant deficiency to scavenge hydroxyl radical-type species (.OH), generated either by the decomposition of peroxynitrite or by Fenton reagents (FeCl3 + H2O2). Exosurf or Survanta decreased .OH only when present at high lipid concentrations (6.5 mM). On the other hand, 40 microM of NLS decreased .OH concentrations from 75 +/- 2 to 53 +/- 2 microM (P < 0.05), most likely because of the interaction of .OH with protein sulfhydryl groups. Similarly, 40 microM of NLS incubated with a bolus of H2O2 (400 microM) decreased the H2O2 concentration in the supernatant by approximately 50%, due to the presence of catalase-type activity. In contrast to NLS, neither Exosurf nor Survanta scavenged H2O2, even when present at millimolar lipid concentrations. We concluded that Exosurf and Survanta contain limited antioxidant activity compared with NLS.

Download Full-text

Relevance of mitochondrial dysfunction during Sorafenib-induced cell death in liver cancer cells. Role of oxidative and nitrogen reactive species

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2020.12.418 ◽

2021 ◽

Vol 165 ◽

pp. 54

Author(s):

Patricia de la Cruz-Ojeda ◽

M. Ángeles Rodríguez-Hernández ◽

Elena Navarro-Villarán ◽

Paloma Gallego ◽

Pavla Staňková ◽

...

Keyword(s):

Cell Death ◽

Liver Cancer ◽

Mitochondrial Dysfunction ◽

Cancer Cells ◽

Reactive Species ◽

Liver Cancer Cells ◽

Nitrogen Reactive Species

Download Full-text

A reaction involving protein sulfhydryl groups, a bound spin-label, and K3Fe(CN)6 as a probe of sulfhydryl proximity in myosin

Biochemistry ◽

10.1021/bi00542a006 ◽

1980 ◽

Vol 19 (1) ◽

pp. 33-39 ◽

Cited By ~ 30

Author(s):

Philip Graceffa ◽

John C. Seidel

Keyword(s):

Spin Label ◽

Sulfhydryl Groups ◽

Protein Sulfhydryl ◽

Protein Sulfhydryl Groups

Download Full-text

Diseases of Lung Surfactant Deficiency or Dysfunction

Lung Surfactants ◽

10.1201/9781482270426-21 ◽

2000 ◽

pp. 246-258

Keyword(s):

Lung Surfactant ◽

Surfactant Deficiency

Download Full-text

Clearance of intra-amniotic lung surfactant: uptake and utilization by the fetal rabbit lung

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1997.273.1.l55 ◽

1997 ◽

Vol 273 (1) ◽

pp. L55-L63 ◽

Cited By ~ 2

Author(s):

M. Hallman ◽

U. Lappalainen ◽

K. Bry

Keyword(s):

Amniotic Fluid ◽

Lung Surfactant ◽

Protein A ◽

Alveolar Epithelium ◽

Fetal Lung ◽

Surfactant Protein ◽

Lung Compliance ◽

Rabbit Lung ◽

Lower Lung ◽

Lung Surfactant Protein

To investigate the metabolism of intra-amniotic surfactant, surfactant containing double-labeled dipalmitoylphosphatidylcholine (DPPC) was injected in amniotic fluid on days 23-27 of gestation. Within 44 h, DPPC was distributed to the gastrointestinal tract (45.9%), fetal membranes and placenta (8.2%), fetal lung (6.6%), and liver (1.9%). DPPC uptake was higher in the upper than in the lower lung lobes. The mixture of phosphatidylglycerol and DPPC increased the uptake of DPPC that was not saturable (range 15-60 mg phospholipid). There was no detectable metabolism of DPPC taken up by the fetal lung. Surfactant protein A, originating from intra-amniotic heterplogous surfactant, was detected immunohistochemically in alveolar epithelium. Intra-amniotic surfactants did not affect the expression of surfactant protein mRNAs. Intra-amniotic surfactant (1,500-2,000 mg/kg on day 25.3) improved lung compliance of ventilated 27.0-day premature rabbits less than intratracheal surfactant at birth (75-100 mg/kg). Reutilization by the alveolar epithelium of surfactant secreted to future airspaces, airways, and amniotic fluid may be a mechanism that increases intracellular surfactant pool before birth.

Download Full-text

Ti4O7 Used as Electrode in Biomedicine and for Electrochemical Study of Scavenging Mechanism

Key Engineering Materials ◽

10.4028/www.scientific.net/kem.493-494.896 ◽

2011 ◽

Vol 493-494 ◽

pp. 896-901

Author(s):

María Canillas ◽

Ann Rajnicek ◽

C. Rosero ◽

Eva Chinarro ◽

Berta Moreno

Keyword(s):

Oxidation State ◽

Reactive Species ◽

Electrochemical Methods ◽

Electrochemical Study ◽

Scavenging Activity ◽

Reduction Reactions ◽

Oxidation Reduction ◽

Nitrogen Reactive Species

The biocompatibility of TiO2 is due to the activity that it shown in front of oxygen and nitrogen reactive species. Some authors suggest that the mechanism go through oxidation reduction reactions where changes of oxidation state in the Titanium and phases are involve. For this reason, Anderson-Magnelli phases could present scavenging activity. Moreover, these materials are use as electrodes and in that way are proposed as electrodes for study their scavenging mechanism by electrochemical methods.

Download Full-text

A simple method for stabilizing protein-sulfhydryl groups during SDS-gel electrophoresis

Analytical Biochemistry ◽

10.1016/0003-2697(78)90792-3 ◽

1978 ◽

Vol 86 (2) ◽

pp. 655-664 ◽

Cited By ~ 162

Author(s):

Leslie C. Lane

Keyword(s):

Gel Electrophoresis ◽

Sulfhydryl Groups ◽

Simple Method ◽

Protein Sulfhydryl ◽

Protein Sulfhydryl Groups

Download Full-text

Alveolar hyperoxic injury in rabbits receiving exogenous surfactant

Journal of Applied Physiology ◽

10.1152/jappl.1989.66.3.1087 ◽

1989 ◽

Vol 66 (3) ◽

pp. 1087-1092 ◽

Cited By ~ 44

Author(s):

G. M. Loewen ◽

B. A. Holm ◽

L. Milanowski ◽

L. M. Wild ◽

R. H. Notter ◽

...

Keyword(s):

Lung Injury ◽

Lung Surfactant ◽

Alveolar Epithelium ◽

Exposure Period ◽

Exogenous Surfactant ◽

Lung Pathology ◽

Sterile Saline ◽

Hyperoxic Exposure ◽

Minimum Surface Tension ◽

Hyperoxic Lung Injury

We have previously demonstrated that instillation of a calf lung surfactant extract (CLSE) in rabbits after exposure to 100% O2 for 64 h mitigates the progression of lung pathology after return to room air (J. Appl. Physiol. 62: 756–761, 1987). In the present study, we investigated whether we could prevent or reduce the onset and development of hyperoxic lung injury by sequential instillations of CLSE during the hyperoxic exposure. Rabbits were exposed to 100% O2. CLSE (125 mg, approximately 170 mumol of phospholipid) was suspended in 10 ml of sterile saline and instilled intratracheally into their lungs, starting at 24 h in O2, a time at which no physiological or biochemical injury was detected, and at 24-h intervals thereafter. Control rabbits breathed 100% O2 and received either equal volumes of saline or no instillations at all. CLSE-instilled rabbits had higher arterial PO2 (Pao2) values throughout the exposure period and survived longer when compared with saline controls [120 +/- 4 vs. 102 +/- 4 (SE) h; n greater than or equal to 10; P less than 0.05]. At 72 h in O2, CLSE-instilled rabbits had significantly higher lavageable alveolar phospholipid levels (12.5 +/- 1.5 vs. 5 +/- 1 mumol/kg) and total lung capacities (41 +/- 2 vs. 25 +/- 3.5 ml/kg) and lower levels of alveolar protein (24 +/- 3 vs. 52 +/- 8 mg/kg), minimum surface tension (2 +/- 1 vs. 26.1 dyn/cm), and lung wet-to-dry weights (5.9 +/- 0.2 vs. 6.5 +/- 0.3). After 72 h in O2, lungs from both CLSE- and saline-instilled rabbits showed evidence of diffuse hyperoxic injury. However, atelectasis was less prominent in the former. We concluded that instillation of CLSE limits the onset and development of hyperoxic lung injury to the alveolar epithelium of rabbits.

Download Full-text