scholarly journals Nitric oxide mediates the fungal-elicitor-enhanced biosynthesis of antioxidant polyphenols in submerged cultures of Inonotus obliquus

Microbiology ◽  
2009 ◽  
Vol 155 (10) ◽  
pp. 3440-3448 ◽  
Author(s):  
Weifa Zheng ◽  
Kangjie Miao ◽  
Yanxia Zhang ◽  
Shenyuan Pan ◽  
Meimei Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Higher Plants ◽  
Antioxidant Activities ◽  
Fungal Elicitor ◽  
Submerged Cultures ◽  
No Donor ◽  
Inonotus Obliquus ◽  
Pal Activity ◽  
Exogenous Addition ◽  
Nos Inhibitor

A fungal elicitor prepared from the cell debris of the plant-pathogenic ascomycete Alternaria alternata induces multiple responses by Inonotus obliquus cells, including an increase in generation of nitric oxide (NO), activity of phenylalanine ammonia lyase (PAL) and accumulation of total mycelial phenolic compounds (TMP), but does not trigger production of oxylipins or jasmonic acid (JA). The role of NO in TMP production was investigated via the effects of the NO-specific scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPITO) and the nitric oxide synthase (NOS) inhibitor aminoguanidine (AG). TMP profiles were assayed using 1H NMR spectroscopy combining multivariate pattern recognition strategies. Pretreatment of I. obliquus mycelia with cPITO or AG suppressed not only elicitor-enhanced NO generation and PAL activity, but also the elicitor-induced increase in TMP production. This TMP reduction by either a NO scavenger or a NOS inhibitor was reversed by exogenous addition of either a NO donor, sodium nitroprusside, or JA separately. NMR-based metabonomic analysis of TMP profiles showed that the induced TMP were hispidin analogues including inoscavins, phelligridins, davallialactone and methyldavallialactone, which possess high antioxidant activities. Thus, NO mediates an elicitor-induced increase in production of antioxidant polyphenols in I. obliquus via a signalling pathway independent of oxylipins or JA, a mechanism which differs from those in some higher plants.

Influence of Nitric Oxide on the Secretory Function of the Bovine Corpus Luteum: Dependence on Cell Composition and Cell-to-Cell Communication

2003 ◽  
Vol 228 (6) ◽  
pp. 741-748 ◽  
Author(s):  
Jerzy J. Jaroszewski ◽  
Dariusz J. Skarzynski ◽  
Robert M. Blair ◽  
William Hansel
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Corpus Luteum ◽  
Cell Contact ◽  
Secretory Function ◽  
No Donor ◽  
Luteal Cells ◽  
Cell Composition ◽  
Bovine Corpus Luteum ◽  
Nos Inhibitor

The objective of the present study was to investigate the role of cell-to-cell contact in the influence of nitric oxide (NO) on the secretory function of the bovine corpus luteum (CL). In Experiment 1, separate small luteal cells (SLC) or large (LLC) luteal cells were perfused with 100 μ M spermineNONOate, a NO donor, or with 100 μ M Nω-nitro-L-arginine methyl ester (L-NAME), a NO synthase (NOS) inhibitor; in Experiment 2, a mixture of LLC and SLC and endothelial cells was cultured and incubated with spermineNONOate or L-NAME; in Experiment 3, spermineNONOate was perfused into the CL (100 mg/4 hr) by a microdialysis system in vivo. Perfusion of isolated SLC and LLC with the NO donor or NOS inhibitor (Experiment 1) did not affect ( P > 0.05) secretion of progesterone (P4) or oxytocin (OT). L-NAME perfusion increased ( P < 0.05) leukotriene C4 (LTC4) secretion by both SLC and LLC cells. Treatment of mixtures of luteal cells with an NO donor (Experiment 2) significantly decreased ( P < 0.001) secretion of P4 and OT and increased ( P < 0.001) production of prostaglandin F2α (PGF2α) and LTC4. L-NAME stimulated ( P < 0.001) P4 secretion, but did not influence ( P > 0.05) OT, PGF2α or LTC4 production. Intraluteal administration (Experiment 3) of spermineNONOate increased ( P < 0.001) LTC4 and PGF2α, decreased OT, but did not change P4 levels in perfusate samples. These data indicate that cell-to-cell contact and cell composition play important roles in the response of bovine CL to treatment with NO donors or NOS inhibitors, and that paracrine mechanisms are required for the full secretory response of the CL in NO action. Endothelial cells appear to be required for the full secretory response of the CL to NO.

scholarly journals The role of nitric oxide on matrix metalloproteinase 2 (MMP2) and MMP9 in placenta and fetus from diabetic rats

Reproduction ◽  
2007 ◽  
Vol 134 (4) ◽  
pp. 605-613 ◽  
Author(s):  
M C Pustovrh ◽  
A Jawerbaum ◽  
V White ◽  
E Capobianco ◽  
R Higa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Structural Changes ◽  
Diabetic Rats ◽  
Matrix Metalloproteinase 2 ◽  
No Donor ◽  
Diaphorase Activity ◽  
Nos Inhibitor ◽  
And Function ◽  
Fetal Organs

Matrix metalloproteinases (MMPs) play an important role in tissue remodeling that accompanies the rapid growth, differentiation, and structural changes of the placenta and several fetal organs. In the present study, we investigated whether the diabetic maternal environment may alter the regulatory homeostasis exerted by nitric oxide (NO) on MMPs activity in the feto-placental unit from rats at midgestation. We found that NADPH-diaphorase activity, which reflects the distribution and activity of NO synthases (NOS), was increased in both placenta and fetuses from diabetic rats when compared with controls. In addition, while a NO donor enhanced MMP2 and MMP9 activities, a NOS inhibitor reduced these activities in the maternal side of the placenta from control rats. This regulatory effect of NO was only observed on MMP9 in the diabetic group. On the other hand, the NO donor did not modify MMP2 and MMP9 activities, while the NOS inhibitor reduced MMP9 activity in the fetal side of both control and diabetic placentas. In the fetuses, MMP2 was enhanced by the NO donor and reduced by the NO inhibitor in both fetuses from control and diabetic rats. Overall, this study demonstrates that NO is able to modulate the activation of MMPs in the feto-placental unit, and provides supportive evidence that increased NOS activity leads to NO overproduction in the feto-placental unit from diabetic rats, an alteration closely related to the observed MMPs dysregulation that may have profound implications in the formation and function of the placenta and the fetal organs.

scholarly journals The Effect of Mitochondrial Complex I-Linked Respiration by Isoflurane Is Independent of Mitochondrial Nitric Oxide Production

2018 ◽  
Vol 8 (2) ◽  
pp. 113-122 ◽  
Author(s):  
Fuqi Xu ◽  
Shigang Qiao ◽  
Hua Li ◽  
Yanjun Deng ◽  
Chen Wang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mitochondrial Respiration ◽  
Complex I ◽  
Adenosine Diphosphate ◽  
Sprague Dawley ◽  
No Donor ◽  
Anesthetic Preconditioning ◽  
Rat Hearts ◽  
Nos Inhibitor

Background: Anesthetic preconditioning (APC) of the myocardium is mediated in part by reversible alteration of mitochondrial function. Nitric oxide (NO) inhibits mitochondrial respiration and may mediate APC-induced cardioprotection. In this study, the effects of isoflurane on different states of mitochondrial respiration during the oxidation of complex I-linked substrates and the role of NO were investigated. Methods: Mitochondria were isolated from Sprague-Dawley rat hearts. Respiration rates were measured polarographically at 28ºC with a computer-controlled Clark-type O2 electrode in the mitochondria (0.5 mg/mL) with complex I substrates glutamate/malate (5 mM). Isoflurane (0.25 mM) was administered before or after adenosine diphosphate (ADP)-initiated state 3 respiration. The NO synthase (NOS) inhibitor L-N5-(1-iminoethyl)-ornithine (L-NIO, 10 μM) and the NO donor S-nitroso-N-acetylpenicillamine (SNAP, 1 μM) were added before or after the addition of ADP. Results: Isoflurane administered in state 2 increased state 2 respiration and decreased state 3 respiration. This attenuation of state 3 respiration by isoflurane was similar when it was given during state 3. L-NIO did not alter mitochondrial respiration or the effect of isoflurane. SNAP only, added in state 3, decreased state 3 respiration and enhanced the isoflurane-induced attenuation of state 3 respiration. Conclusion: Isoflurane has clearly distinguishable effects on different states of mitochondrial respiration during the oxidation of complex I substrates. The uncoupling effect during state 2 respiration and the attenuation of state 3 respiration may contribute to the mechanism of APC-induced cardioprotection. These effects of isoflurane do not depend on endogenous mitochondrial NO, as the NOS inhibitor L-NIO did not alter the effects of isoflurane on mitochondrial respiration.

scholarly journals Nitric oxide synthase acutely regulates progesterone production by in vitro cultured rabbit corpora lutea

1999 ◽  
Vol 160 (2) ◽  
pp. 275-283 ◽  
Author(s):  
A Gobbetti ◽  
C Boiti ◽  
C Canali ◽  
M Zerani
Keyword(s):  
Nitric Oxide ◽  
In Vitro Release ◽  
Inhibitory Effect ◽  
Corpora Lutea ◽  
No Donor ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Vitro Release

We examined the presence and the regulation of nitric oxide (NO) synthase (NOS) using in vitro cultured corpora lutea (CL) obtained from rabbits at days 4 and 9 of pseudopregnancy. The role of NO and NOS on steroidogenesis was also investigated using the same CL preparations after short-term incubations (30 min and 2 h) with the NO donor, sodium nitroprusside (NP), the NOS inhibitor, Nomega-nitro-l-arginine methyl ester (l-NAME) and prostaglandin (PG) F-2alpha. The basal NOS activity was greater in CL at day 4 than at day 9, and was also differently modulated by PGF-2alpha, depending on the age of the CL. The addition of PGF-2alpha to day 4 CL had no effect, but PGF-2alpha on day 9 caused a threefold increase in NOS activity. NP caused a two- to fivefold decrease in release of progesterone from CL of both ages, and this inhibitory effect on steroidogenesis was reversed by l-NAME. All treatments failed to modify basal androgens and 17beta-oestradiol was not detectable in either control or treated CL. These results suggest that NO is effectively involved in the regulation process of steroidogenesis, independently of 17beta-oestradiol. PGF-2alpha had no effect on day 4, but induced luteolysis on day 9, by reducing progesterone (P</=0. 01) to about 18% of control. The luteolytic action of PGF-2alpha was completely reversed by co-incubation with l-NAME, thus supporting the hypothesis that luteolysis is mediated by NO. The addition of NP or l-NAME did not modify the in vitro release of PGF-2alpha. We hypothesised that PGF-2alpha upregulates NOS activity and, consequently, the production of NO, which acutely inhibits progesterone release from day 9 CL of pseudopregnant rabbits.

Chronic Nitric Oxide Deficiency is Associated with Altered Leutinizing Hormone and Follicle-Stimulating Hormone Release in Ovariectomized Rats1

2002 ◽  
Vol 227 (9) ◽  
pp. 817-822 ◽  
Author(s):  
Maria J. Barnes ◽  
Karen Lapanowski ◽  
Jose A. Rafols ◽  
David M. Lawson ◽  
Joseph C. Dunbar
Keyword(s):  
Nitric Oxide ◽  
Follicle Stimulating Hormone ◽  
Independent Effect ◽  
Control Group ◽  
Gonadotropin Secretion ◽  
No Donor ◽  
Ovx Rats ◽  
Nos Inhibitor ◽  
Stimulating Hormone

Nitric oxide (NO) synthase (NOS) has been found in the gonadotrophs and folliculo-stellate cells of the anterior pituitary. Previous observations from our laboratory suggest that NO may play a role in regulating gonadotropin secretion. Because estrogen secretion by the ovary can influence gonadotropin secretion, we investigated the hypothesis that chronic in vivo NO deficiency has a direct estrogen-independent effect on luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. Chronic NO deficiency was induced by adding an NOS inhibitor, N-nitro-L-arginine (L-NNA, 0.6 g/l) to the drinking water of ovariectomized (OVX) rats. The control OVX rats were untreated. After 6–8 weeks, the animals were sacrificed, and the pituitaries were removed and perfused continuously for 4 hr in the presence of pulsatile gonadotropin-releasing hormone (GnRH, 500 ng/pulse) every 30 min. S-Nitroso-l-acetyl penicillamine (SNAP, an NO donor, 0.1 mM) or l-nitro-arginine methyl ester (L-NAME, an NOS inhibitor, 0.1 mM) was added to the media and perfusate samples were collected at 10-min intervals. GnRH-stimulated LH and FSH levels were significantly lower in pituitaries from OVX/NO-deficient pituitaries compared with pituitaries from the OVX control group. The addition of SNAP significantly decreased LH and FSH secretion by pituitaries from OVX control animals, but significantly increased their secretion by pituitaries from the OVX/NO-deficient animals. L-NAME also suppressed LH and FSH secretion by pituitaries from the OVX control animals and stimulated their release by pituitaries from the NO-deficient/OVX animals. Immunohisto-chemistry of frontal sections through the hypothalamus demonstrated that OVX/NO deficiency is associated with increased GnRH in the median eminence. We conclude that NO has a chronic stimulatory effect on LH and FSH release and the subsequent altered secretory responsiveness to NO agonist or antagonist is the result of chronic NO suppression.

Evidence that nitric oxide increases glucose transport in skeletal muscle

1997 ◽  
Vol 82 (1) ◽  
pp. 359-363 ◽  
Author(s):  
Thomas W. Balon ◽  
Jerry L. Nadler ◽  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Glucose Transport ◽  
Type I ◽  
Stimulation Protocol ◽  
No Donor ◽  
Nos Inhibitor ◽  
Exercise Induced ◽  
Oxide Synthase

Balon, Thomas W., and Jerry L. Nadler. Evidence that nitric oxide increases glucose transport in skeletal muscle. J. Appl. Physiol. 82(1): 359–363, 1997.—Nitric oxide synthase (NOS) is expressed in skeletal muscle. However, the role of nitric oxide (NO) in glucose transport in this tissue remains unclear. To determine the role of NO in modulating glucose transport, 2-deoxyglucose (2-DG) transport was measured in rat extensor digitorum longus (EDL) muscles that were exposed to either a maximally stimulating concentration of insulin or to an electrical stimulation protocol, in the presence of N G-monomethyl-l-arginine, a NOS inhibitor. In addition, EDL preparations were exposed to sodium nitroprusside (SNP), an NO donor, in the presence of submaximal and maximally stimulating concentrations of insulin. NOS inhibition reduced both basal and exercise-enhanced 2-DG transport but had no effect on insulin-stimulated 2-DG transport. Furthermore, SNP increased 2-DG transport in a dose-responsive manner. The effects of SNP and insulin on 2-DG transport were additive when insulin was present in physiological but not in pharmacological concentrations. Chronic treadmill training increased protein expression of both type I and type III NOS in soleus muscle homogenates. Our results suggest that NO may be a potential mediator of exercise-induced glucose transport.

scholarly journals Comparative transcriptome combined with metabolome analyses revealed key factors involved in nitric oxide (NO)-regulated cadmium stress adaptation in tall fescue

2020 ◽  
Author(s):  
Liang Chen ◽  
Huihui Zhu ◽  
Honglian Ai ◽  
Zhengrong Hu ◽  
Dongyun Du ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Stress Response ◽  
Secondary Metabolites ◽  
Tall Fescue ◽  
Molecular Mechanisms ◽  
Antioxidant Activities ◽  
Cadmium Stress ◽  
Glutathione Metabolism ◽  
Cd Stress ◽  
No Donor

Abstract Background It has been reported that nitric oxide (NO) could ameliorate cadmium (Cd) toxicity in tall fescue; however, the underlying mechanisms of NO mediated Cd detoxification are largely unknown. In this study, we investigated the possible molecular mechanisms of Cd detoxification process by comparative transcriptomic and metabolomic approaches. Results The application of Sodium nitroprusside (SNP) as NO donor decreased the Cd content of tall fescue by 11% under Cd stress (T1 treatment), but the Cd content was increased by 24% when treated with c-PTIO together with L-NAME (T2 treatment). RNA-seq analysis revealed that 904 (414 up- and 490 down-regulated) and 118 (74 up- and 44 down-regulated) DEGs were identified in the T1 vs Cd and T2 vs Cd comparisons, respectively. Moreover, metabolite profile analysis showed that 99 (65 up- and 34-down- regulated) and 131 (45 up- and 86 down-regulated) metabolites were altered in the T1 vs Cd and T2 vs Cd comparisons, respectively. The integrated analyses of transcriptomic and metabolic data showed that 81 DEGs and 15 differentially expressed metabolites were involved in 20 NO-induced pathways. The dominant pathways were involved in antioxidant activities such as glutathione metabolism, arginine and proline metabolism, secondary metabolites such as flavone and flavonol biosynthesis and phenylpropanoid biosynthesis, ABC transporters, and nitrogen metabolism. Conclusions In general, the results revealed that there are three major mechanisms regulated by NO in Cd stress response in tall fescue: (a) antioxidant capacity enhancement; (b) accumulation of secondary metabolites related to cadmium chelation and sequestration; and (c) regulation of cadmium ion transportation, such as ABC transporter activation. In conclusion, this study provides new insights into the NO-mediated cadmium stress response.

scholarly journals Comparative transcriptome combined with metabolome analyses revealed key factors involved in nitric oxide (NO)-regulated cadmium stress adaptation in tall fescue

2020 ◽  
Author(s):  
Huihui Zhu ◽  
Honglian Ai ◽  
Zhengrong Hu ◽  
Dongyun Du ◽  
Jie Sun ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Secondary Metabolites ◽  
Tall Fescue ◽  
Molecular Mechanisms ◽  
Antioxidant Activities ◽  
Profile Analysis ◽  
Cadmium Stress ◽  
Metabolite Profile ◽  
Glutathione Metabolism ◽  
No Donor

Abstract Background: It has been reported that nitric oxide (NO) could ameliorate cadmium (Cd) toxicity in tall fescue; however, the underlying mechanisms of NO mediated Cd detoxification are largely unknown. In this study, we investigated the possible molecular mechanisms of Cd detoxification process by comparative transcriptomic and metabolomic approaches. Results: The application of Sodium nitroprusside (SNP) as NO donor decreased the Cd content of tall fescue by 11% under Cd stress (T1 treatment), but the Cd content was increased by 24% when treated with Carboxy-PTIO (c-PTIO) together with Nitro-L-arginine methyl ester (L-NAME) (T2 treatment). RNA-seq analysis revealed that 904 (414 up- and 490 down-regulated) and 118 (74 up- and 44 down-regulated) DEGs were identified in the T1 vs Cd (only Cd treatment) and T2 vs Cd comparisons, respectively. Moreover, metabolite profile analysis showed that 99 (65 up- and 34-down- regulated) and 131 (45 up- and 86 down-regulated) metabolites were altered in the T1 vs Cd and T2 vs Cd comparisons, respectively. The integrated analyses of transcriptomic and metabolic data showed that 81 DEGs and 15 differentially expressed metabolites were involved in 20 NO-induced pathways. The dominant pathways were antioxidant activities such as glutathione metabolism, arginine and proline metabolism, secondary metabolites such as flavone and flavonol biosynthesis and phenylpropanoid biosynthesis, ABC transporters, and nitrogen metabolism.Conclusions: In general, the results revealed that there are three major mechanisms involved in NO-mediated Cd detoxification in tall fescue, including (a) antioxidant capacity enhancement; (b) accumulation of secondary metabolites related to cadmium chelation and sequestration; and (c) regulation of cadmium ion transportation, such as ABC transporter activation. In conclusion, this study provides new insights into the NO-mediated cadmium stress response.

Effect of aging on nitric oxide-mediated penile erection in rats

1995 ◽  
Vol 268 (1) ◽  
pp. H467-H475 ◽  
Author(s):  
H. Garban ◽  
D. Vernet ◽  
A. Freedman ◽  
J. Rajfer ◽  
N. Gonzalez-Cadavid
Keyword(s):  
Nitric Oxide ◽  
Muscle Relaxation ◽  
Phosphodiesterase Inhibitor ◽  
Smooth Muscle Relaxation ◽  
Adult Rats ◽  
No Donor ◽  
Tissue Sections ◽  
Old Rats ◽  
Nos Inhibitor ◽  
Erectile Response

Aging is an important risk factor for impotence in men. Because nitric oxide (NO) appears to be the mediator of corpora cavernosal smooth muscle relaxation, we have examined in 5-, 20-, and 30-mo-old rats, designated “adult,” “old,” and “senescent,” respectively, whether aging causes a decrease of erectile response that may correlate with lower NO synthase (NOS) in the penis. Electric field stimulation (EFS) of the cavernosal nerve showed that the maximum intracavernosal pressure (MIP) declined in the old and senescent rats to 80 and 51% of the adult value, respectively. A low systemic dose of the NOS inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME; 2 mg/kg), reduced the MIP by only 38% in the adult rats but decreased it in the old and senescent rats by 72 and 80%, respectively. In the absence of EFS, intracavernosal papaverine (phosphodiesterase inhibitor), or nitroglycerin (NO donor), caused a lower erectile response in the old and senescent rats compared with the adult animals (MIP: 41 and 14%, respectively; duration of the erection 46 and 21%, respectively). Tissue sections from old and senescent penises showed increasing degrees of sclerotic degeneration. In comparison with the adult rats, the penile soluble NOS activity per gram of tissue that is sensitive to L-NAME decreased significantly by 63% in the senescent rats but was elevated in the old rats. These results indicate that aging causes an erectile failure due to factors initially independent from an impairment of penile NO synthesis but which are compounded in the very old rats by the decrease of penile NOS activity.

Peroxynitrite triggers a delayed resistance of coronary endothelial cells against ischemia-reperfusion injury

2002 ◽  
Vol 283 (4) ◽  
pp. H1418-H1423 ◽  
Author(s):  
Karine Laude ◽  
Christian Thuillez ◽  
Vincent Richard
Keyword(s):  
Nitric Oxide ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
No Synthase ◽  
No Donor ◽  
Rat Hearts ◽  
Nos Inhibitor ◽  
Coronary Endothelial Cells ◽  
Peroxynitrite Scavengers ◽  
Inducible Nos

Experiments were designed to test whether nitric oxide (NO) and peroxynitrite trigger delayed coronary endothelial protection induced by preconditioning (PC) in rats. Prolonged ischemia reperfusion markedly reduced the response of isolated coronary arteries to acetylcholine, and this was prevented by PC performed 24 h earlier. The NO synthase (NOS) inhibitor N G-nitro-l-arginine methyl ester (l-NAME) administered during PC abolished its delayed endothelial protective effect, whereas the inducible NOS inhibitor N-(3(aminomethyl)benzyl)acetaminide had no effect. Delayed endothelial PC was also abolished by the peroxynitrite scavengers selenomethionine or uric acid given during PC. In parallel, the NO/peroxynitrite donor S-morpholinosydnonimine and authentic peroxynitrite, administered 24 h before prolonged ischemia-reperfusion mimicked endothelial PC, whereas the NO donor S-nitroso- N-acetylpencillamine had no effect. This suggests that peroxynitrite is an essential trigger of the delayed coronary endothelial protection induced by PC in rat hearts.

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