scholarly journals Nitric oxide radicals are emitted by wasp eggs to kill mold fungi

2018 ◽  
Author(s):  
Erhard Strohm ◽  
Gudrun Herzner ◽  
Joachim Ruther ◽  
Martin Kaltenpoth ◽  
Tobias Engl
Keyword(s):  
Nitric Oxide ◽  
Alternative Splicing ◽  
Free Radical ◽  
No Synthase ◽  
Regulatory Domain ◽  
External Application ◽  
Key Innovation ◽  
Nitrogen Radicals ◽  
High Doses ◽  
Solitary Digger Wasp

Detrimental microbes caused the evolution of a great diversity of antimicrobial defenses in plants and animals. Here we show that the eggs of a solitary digger wasp, the European beewolf Philanthus triangulum, emit large amounts of the gaseous free radical nitric oxide (NO.) to protect themselves and their provisions, paralyzed honeybees, against mold fungi. Despite the extraordinary concentrations of nitrogen radicals (NO. and its oxidation product NO2.) in the brood cells (~1500ppm), NO. is synthesized from L-arginine by an NO-synthase (NOS) as in other animals. The beewolf NOS gene revealed no conspicuous differences to related species. However, due to alternative splicing, the NOS-mRNA in beewolf eggs lacks a 144bp exon near the regulatory domain. This preventive external application of high doses of NO. by seemingly defenseless wasp eggs represents an evolutionary key innovation that adds a remarkable novel facet to the array of functions of the important biological effector NO..

scholarly journals Nitric oxide radicals are emitted by wasp eggs to kill mold fungi

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Erhard Strohm ◽  
Gudrun Herzner ◽  
Joachim Ruther ◽  
Martin Kaltenpoth ◽  
Tobias Engl
Keyword(s):  
Nitric Oxide ◽  
Alternative Splicing ◽  
No Synthase ◽  
Regulatory Domain ◽  
External Application ◽  
Key Innovation ◽  
Nitrogen Radicals ◽  
High Doses ◽  
Solitary Digger Wasp ◽  
Nos Gene

Detrimental microbes caused the evolution of a great diversity of antimicrobial defenses in plants and animals. Insects developing underground seem particularly threatened. Here we show that the eggs of a solitary digger wasp, the European beewolf Philanthus triangulum, emit large amounts of gaseous nitric oxide (NO⋅) to protect themselves and their provisions, paralyzed honeybees, against mold fungi. We provide evidence that a NO-synthase (NOS) is involved in the generation of the extraordinary concentrations of nitrogen radicals in brood cells (~1500 ppm NO⋅ and its oxidation product NO2⋅). Sequencing of the beewolf NOS gene revealed no conspicuous differences to related species. However, due to alternative splicing, the NOS-mRNA in beewolf eggs lacks an exon near the regulatory domain. This preventive external application of high doses of NO⋅ by wasp eggs represents an evolutionary key innovation that adds a remarkable novel facet to the array of functions of the important biological effector NO⋅.

scholarly journals NITRIC OXIDE AND ALLYL ALCOHOL INDUCED HEPATOTOXICITY

2014 ◽  
Vol 1 (1) ◽  
Author(s):  
M. M. Korda
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Blood Serum ◽  
Allyl Alcohol ◽  
Calcium Ionophore ◽  
Free Radical Oxidation ◽  
No Synthase ◽  
Nitrate Content ◽  
Radical Oxidation ◽  
Nos Inhibitors

<p><strong>Background.</strong> Nitric oxide (NO) is an important mediator of hepatotoxicity. NO in liver can be derived from two sources: (1) constitutive NO synthase (eNOS) in endothelial cells, and (2) inducible NO synthase (iNOS) in hepatocytes and Kupffer cells.<br /><strong>Objectives.</strong> The present study was aimed to examine the effect of nonselective NOS inhibitor (L-NAME) and selective iNOS inhibitor (1400W) on the development of allyl alcohol (AA) induced hepatitis in rats.<br /><strong>Methods.</strong> Male Wistar rats were treated with intraperitoneal injection of saline or AA and L-NAME or 1400W. NO in liver was measured by electrochemical method after eNOS stimulation by calcium ionophore. Total NOS activity and nitrite/nitrate content were measured in liver and blood serum. The activity of free radical oxidation in liver was measured by chemiluminescent method. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were assayed in blood serum<br /><strong>Results.</strong> AA increased the activity of free radical processes in liver and markers of cytolysis in serum, as well as decreased eNOS and increased iNOS activities. L-NAME considerably inhibited eNOS and augmented the necrosogenic properties of AA, whereas 1400W partially prevented liver damage.<br /><strong>Conclusion.</strong> It has been concluded that in AA intoxication NO produced from eNOS is beneficial to the liver, but NO derived from the upregulated iNOS has deleterious effect.</p><p><strong>KEY WORDS:</strong> nitric oxide, toxic hepatitis, NOS inhibitors.<br /><br /></p>

CHANGES OF NITRIC OXIDE SYNTHASE AND HYDROGEN SULFIDE IN BLOOD LYMPHOCYTES IN THE ACUTE PERIOD OF POLYTRAUMA

2019 ◽  
Vol 72 (8) ◽  
pp. 1473-1476
Author(s):  
Nataliya Matolinets ◽  
Helen Sklyarova ◽  
Eugene Sklyarov ◽  
Andrii Netliukh
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Tissue Injury ◽  
Traumatic Injury ◽  
Cell Types ◽  
No Synthase ◽  
Septic Complications ◽  
Acute Period ◽  
Gaseous Transmitters ◽  
The Moment

Introduction: Polytrauma patients have high risk of shock, septic complications and death during few years of follow-up. In recent years a lot of attention is paid to gaseous transmitters, among which are nitrogen oxide (NO) and hydrogen sulfide (H2S). It is known that the rise of NO and its metabolites levels occurs during the acute period of polytrauma. Nitric oxide and hydrogen sulfide are produced in different cell types, among which are lymphocytes. The aim: To investigate the levels of NO, NOS, iNOS, еNOS, H2S in lymphocytes lysate in patients at the moment of hospitalization and 24 hours after trauma. Materials and methods: We investigated the levels of NO, NO-synthase, inducible NO-synthase, endothelial NO-synthase, H2S in lymphocytes lysate in patients at the moment of hospitalization and 24 hours after trauma. Results: The study included 20 patients with polytrauma who were treated in the intensive care unit (ICU) of the Lviv Emergency Hospital. Tissue injury was associated with an increased production of NO, NOS, iNOS, еNOS during the acute period of polytrauma. At the same time, the level of H2S decreased by the end of the first day of traumatic injury. Conclusions: In acute period of polytrauma, significant increasing of iNOS and eNOS occurs with percentage prevalence of iNOS over eNOS on the background of H2S decreasing.

SOME ASPECTS OF MECHANISM OF SUCCINAMIDES INFLUENCE ON METABOLIC HOMEOSTASIS OF THE ORGANISM

2018 ◽  
pp. 27-31
Author(s):  
I. A. Palagina
Keyword(s):  
Nitric Oxide ◽  
Biological Activity ◽  
Antioxidant System ◽  
No Synthase ◽  
Antioxidant Potential ◽  
Metabolic Homeostasis ◽  
Energetic Metabolism ◽  
Complex Action ◽  
Energy Processes ◽  
Stimulation Of

Succinate containing compounds possess many types of biological activity and are used for the development of drugs with the target and complex action. This paper is devoted to some aspects of the mechanism of succinamides’ action in a dose of 100 mg/kg. We studied the influence of the compound with antidiabetic properties, -phenylethylamide of 2-oxysuccinanyl acid ( -PhEA-OSAA), and its metabolites such as 2-hydroxyphenylsuccinamide (2-HPhSA) and β-phenylethylsuccinamide ( -PhESA) on the marker indicators of energetic metabolism (EM), antioxidant system (AOS) and nitric oxide (NO) metabolism in subacute experiment on rats. Studies have shown that the action of -FEA-OSAKA on metabolic homeostasis is realized through stimulation of EM, reduction of intensity of NO-synthase metabolism and weakening of the AOS. The nature of the action of -FES and 2-GFS, taking into account the indicators of the state of homeostasis, largely coincides with β-FEA-OSAKA. It was found that the key links in the mechanism of toxic action of succinamides are the effect on antioxidant potential, NO metabolism and energy processes.

Decrease in ambient [Cl-] stimulates nitric oxide release from cultured rat mesangial cells

1994 ◽  
Vol 267 (1) ◽  
pp. F190-F195 ◽  
Author(s):  
H. Tsukahara ◽  
Y. Krivenko ◽  
L. C. Moore ◽  
M. S. Goligorsky
Keyword(s):  
Nitric Oxide ◽  
Mesangial Cells ◽  
Ionic Composition ◽  
Juxtaglomerular Apparatus ◽  
Cytosolic Calcium ◽  
No Synthase ◽  
Tubuloglomerular Feedback ◽  
No Production ◽  
Rapid Reduction ◽  
No Release

It has been hypothesized that fluctuations of the ionic composition in the interstitium of juxtaglomerular apparatus (JGA) modulate the function of extraglomerular mesangial cells (MC), thereby participating in tubuloglomerular feedback (TGF) signal transmission. We examined the effects of isosmotic reductions in ambient sodium concentration ([Na+]) and [Cl-] on cytosolic calcium concentration ([Ca2+]i) in cultured rat MC. Rapid reduction of [Na+] or [Cl-] in the bath induced a concentration-dependent rise in [Ca2+]i. MC are much more sensitive to decreases in ambient [Cl-] than to [Na+]; a decrease in [Cl-] as small as 14 mM was sufficient to elicit a detectable [Ca2]i response. These observations suggest that MC can be readily stimulated by modest perturbations of extracellular [Cl-]. Next, we examined whether activation of MC by lowered ambient [Cl-] influences cellular nitric oxide (NO) production. Using an amperometric NO sensor, we found that a 13 mM decrease in ambient [Cl-] caused a rapid, Ca2+/calmodulin-dependent rise in NO release from MC. This response was not inhibitable by dexamethasone, indicating the involvement of the constitutive rather than the inducible type of NO synthase in MC. In addition, the NO release was blunted by indomethacin pretreatment, suggesting that a metabolite(s) of cyclooxygenase regulates the activation of NO synthase in MC. Our findings that small perturbations in external [Cl-] stimulate MC to release NO, a highly diffusible and rapidly acting vasodilator, provide a possible mechanism to explain the transmission of the signal for the TGF response within the JGA.

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

Arginase inhibition increases nitric oxide production in bovine pulmonary arterial endothelial cells

2004 ◽  
Vol 287 (1) ◽  
pp. L60-L68 ◽  
Author(s):  
Louis G. Chicoine ◽  
Michael L. Paffett ◽  
Tamara L. Young ◽  
Leif D. Nelin
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
No Synthase ◽  
No Production ◽  
Urea Production ◽  
Pulmonary Arterial ◽  
Factor Α ◽  
Arterial Endothelial Cells ◽  
Regular Medium ◽  
Necrosis Factor

Nitric oxide (NO) is produced by NO synthase (NOS) from l-arginine (l-Arg). Alternatively, l-Arg can be metabolized by arginase to produce l-ornithine and urea. Arginase (AR) exists in two isoforms, ARI and ARII. We hypothesized that inhibiting AR with l-valine (l-Val) would increase NO production in bovine pulmonary arterial endothelial cells (bPAEC). bPAEC were grown to confluence in either regular medium (EGM; control) or EGM with lipopolysaccharide and tumor necrosis factor-α (L/T) added. Treatment of bPAEC with L/T resulted in greater ARI protein expression and ARII mRNA expression than in control bPAEC. Addition of l-Val to the medium led to a concentration-dependent decrease in urea production and a concentration-dependent increase in NO production in both control and L/T-treated bPAEC. In a second set of experiments, control and L/T bPAEC were grown in EGM, EGM with 30 mM l-Val, EGM with 10 mM l-Arg, or EGM with both 10 mM l-Arg and 30 mM l-Val. In both control and L/T bPAEC, treatment with l-Val decreased urea production and increased NO production. Treatment with l-Arg increased both urea and NO production. The addition of the combination l-Arg and l-Val decreased urea production compared with the addition of l-Arg alone and increased NO production compared with l-Val alone. These data suggest that competition for intracellular l-Arg by AR may be involved in the regulation of NOS activity in control bPAEC and in response to L/T treatment.

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