scholarly journals Effects of nitric oxide synthase inhibition on goat oocyte meiotic maturation

2013 ◽  
Vol 56 (1) ◽  
pp. 255-263
Author(s):  
M. H. Amale ◽  
A. Z. Shahneh ◽  
S. Nasrollahi
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inhibitory Effect ◽  
Nitric Oxide Donor ◽  
Meiotic Maturation ◽  
Dependent Manner ◽  
Cumulus Expansion ◽  
Maturation Medium ◽  
First Polar Body ◽  
Oxide Synthase

Abstract. Nitric oxide is a biological signalling molecule that plays a crucial role in oocyte maturation of mammalians. It is generated by the nitric oxide synthase enzyme from L-arginine. In this study we assessed the effect of nitric oxide synthase inhibition by Nω-nitro-L-arginine methyl ester (L-NAME) on meiotic maturation of goat oocytes. So, different concentrations of L-NAME (0.1, 1, 10 mM) were added to the maturation medium to evaluate the effect of inhibiting nitric oxide synthase on cumulus expansion and meiotic resumption of goat oocytes. The results showed that none of the concentrations affected cumulus expansion but the formation of the first polar body of the oocytes was suppressed in a dose dependent manner. The highest inhibitory effect was observed with 10 mM L-NAME. Moreover, to confirm the results and to evaluate whether this effect is reversible, 0.1 mM sodium nitroprusside (a nitric oxide donor) was added only to the maturation medium which had the highest concentration of L-NAME (10 mM). The concomitant addition of nitric oxide synthase inhibitor with nitric oxide donor reversed the inhibitory effect of L-NAME on meiotic maturation. These results indicated that the nitric oxide / nitric oxide synthase system is involved in the maturation of goat oocytes and that nitric oxide requirement for nuclear maturation is higher than that for cumulus expansion.

Effects of nitric oxide synthase inhibitors on porcine oocyte meiotic maturation

Zygote ◽  
2005 ◽  
Vol 13 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Yong Tao ◽  
Huirong Xie ◽  
Haiyan Hong ◽  
Xiufen Chen ◽  
Jie Jang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Dna Fragmentation ◽  
Cumulus Cell ◽  
Cumulus Cells ◽  
Meiotic Maturation ◽  
Cumulus Expansion ◽  
Wide Range ◽  
Oxide Synthase ◽  
Oocyte Meiotic Maturation

As an important biological messenger, nitric oxide (NO) exhibits a wide range of effects during physiological and pathophysiological processes, including mammalian oocyte meiotic maturation. The present study investigated whether NO derived from two nitric oxide synthase (NOS) isoforms, inducible NOS (iNOS) or endothelial NOS (eNOS), is involved in the meiotic maturation of porcine oocytes. Meanwhile, the cumulus cells' function in meiotic maturation and their interaction with oocyte development and degeneration were also investigated using cumulus-enclosed oocytes (CEOs) and denuded oocytes (DOs). Different inhibitors for NOS were supplemented to the medium. Cumulus expansion, cumulus cell DNA fragmentation and oocyte meiotic resumption were evaluated 48 h after incubation. Aminoguanidine (AG), a selective inhibitor for iNOS, suppressed cumulus expansion and inhibited CEOs to resume meiosis (p<0.05), but did not inhibit cumulus cell DNA fragmentation. Both Nω-nitro-L-arginine (L-NNA) and Nω-nitro-L-arginine methyl ester (L-NAME), inhibitors for both iNOS and eNOS, delayed cumulus expansion, inhibited cumulus cell DNA fragmentation and inhibited CEOs to resume meiosis. Such effects were not seen in DOs. These results indicate that iNOS-derived NO is necessary for cumulus expansion and meiotic maturation by mediating the function of the surrounding cumulus cells, and eNOS-derived NO is also involved in porcine meiotic maturation.

scholarly journals Effects of inhibiting nitric oxide synthase on cumulus expansion and nuclear maturation of sheep oocytes

2011 ◽  
Vol 56 (No. 6) ◽  
pp. 284-291 ◽  
Author(s):  
Heidari Amale M ◽  
Zare Shahne A ◽  
A. Abavisani ◽  
S. Nasrollahi
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oocyte Maturation ◽  
In Vitro Maturation ◽  
No Donor ◽  
Cumulus Expansion ◽  
Maturation Medium ◽  
Nos Inhibitor ◽  
Oxide Synthase

Nitric oxide (NO) is a biological signaling molecule that plays a crucial role in oocyte maturation of mammalians. It is generated by the nitric oxide synthase (NOS) enzyme from l-arginine. Although the effect of NO has been shown in oocyte maturation of some species, there is no report about its effect on the in vitro maturation of sheep oocyte. So, this study aimed to investigate the importance of NO/NOS system in the in vitro maturation of ovine oocytes. Different concentrations of L-NAME (a NOS inhibitor) (0.1, 1 and 10mM) were added to maturation medium to evaluate the effect of inhibiting NOS on cumulus expansion and meiotic resumption of sheep oocytes. After 26 h culture, low and medium concentrations of L-NAME (0.1 and 1mM) had no significant effect on cumulus expansion, however, its higher concentration (10mM) decreased percentage of oocytes with total cumulus expansion as compared to control (P &lt; 0.05). The extrusion of the first polar body was also suppressed in a dose-dependent manner, so that the addition of 10mM L-NAME to maturation medium significantly stopped oocytes in GV stage (P &lt; 0.05). Moreover, to confirm the results and to evaluate if this effect is reversible, 0.1mM sodium nitroprusside (SNP, a NO donor) was added only to the maturation medium which had the highest concentration of L-NAME (10mM). The concomitant addition of NOS inhibitor with NO donor reversed the inhibitory effect of L-NAME on cumulus expansion and meiotic maturation. These results indicated that NO/NOS system is involved in the maturation of sheep oocytes.

scholarly journals Interleukin-13 inhibits inducible nitric oxide synthase expression in human mesangial cells

1996 ◽  
Vol 313 (2) ◽  
pp. 641-646 ◽  
Author(s):  
Marta SAURA ◽  
Rosa MARTÍNEZ-DALMAU ◽  
Adrian MINTY ◽  
Dolores PÉREZ-SALA ◽  
Santiago LAMAS
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mesangial Cells ◽  
Inhibitory Effect ◽  
Northern Analysis ◽  
Inos Mrna ◽  
Dependent Manner ◽  
Human Mesangial Cells ◽  
Oxide Synthase ◽  
Stimulation Of

The synthesis of nitric oxide in inflammatory situations requires the expression of an inducible isoform of nitric oxide synthase (iNOS). Human mesangial cells (HMC) express an iNOS enzyme after exposure to multiple co-stimuli. In this study we have observed that while tumour necrosis factor-α, interleukin (IL)-1β, interferon-γ and bacterial lipopolysaccharide (LPS) were unable to significantly induce NO synthesis when used alone, they induced an evident stimulation of NO synthesis when used in various combinations. A mixture of the three cytokines (CM) and LPS resulted in a 10-15-fold stimulation of NO synthesis over control values which started to be significant after 16 h. The addition of IL-13, a cytokine with anti-inflammatory properties, inhibited CM/LPS-induced NO synthesis in a concentration-dependent manner. A marked inhibitory effect (60-65%) could be observed when HMC were treated with IL-13 (10 ng/ml) 24 h before, at the same time as, or even 4 h after the addition of CM/LPS. This inhibitory effect was still significant (25%) when IL-13 was added 16 h after CM/LPS. Northern analysis showed that IL-13-mediated iNOS inhibition was closely correlated with the suppression of iNOS mRNA expression. These results identify IL-13 as a powerful regulatory tool for the inhibition of NO synthesis in human cells, a property which may be pathophysiologically relevant in NO-related inflammatory processes.

Inhibitory effect of melatonin on nitric oxide synthase in rat enteric nervous system

2001 ◽  
Vol 120 (5) ◽  
pp. A176-A176
Author(s):  
P KOPPITZ ◽  
M STORR ◽  
D SAUR ◽  
M KURJAK ◽  
H ALLESCHER
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nitric Oxide Synthase ◽  
Enteric Nervous System ◽  
Inhibitory Effect ◽  
Oxide Synthase

scholarly journals Activation of Nuclear Factor κB and Induction of Inducible Nitric Oxide Synthase by Ureaplasma urealyticumin Macrophages

2000 ◽  
Vol 68 (12) ◽  
pp. 7087-7093 ◽  
Author(s):  
Y.-H. Li ◽  
Z.-Q. Yan ◽  
J. Skov Jensen ◽  
K. Tullus ◽  
A. Brauner
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Alveolar Macrophages ◽  
Nuclear Factor Κb ◽  
Inos Expression ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

ABSTRACT Chronic lung disease (CLD) of prematurity is an inflammatory disease with a multifactorial etiology. The importance ofUreaplasma urealyticum in the development of CLD is debated, and steroids produce some improvement in neonates with this disease. In the present study, the capability of U. urealyticum to stimulate rat alveolar macrophages to produce nitric oxide (NO), express inducible nitric oxide synthase (iNOS), and activate nuclear factor κB (NF-κB) in vitro was characterized. The effect of NO on the growth of U. urealyticum was also investigated. In addition, the impact of dexamethasone and budesonide on these processes was examined. We found that U. urealyticum antigen (≥4 × 107 color-changing units/ml) stimulated alveolar macrophages to produce NO in a dose- and time-dependent manner (P < 0.05). This effect was further enhanced by gamma interferon (100 IU/ml; P < 0.05) but was attenuated by budesonide and dexamethasone (10−4 to 10−6 M) (P < 0.05). The mRNA and protein levels of iNOS were also induced in response to U. urealyticum and inhibited by steroids.U. urealyticum antigen triggered NF-κB activation, a possible mechanism for the induced iNOS expression, which also was inhibited by steroids. NO induced by U. urealyticum caused a sixfold reduction of its own growth after infection for 10 h. Our findings imply that U. urealyticum may be an important factor in the development of CLD. The host defense response againstU. urealyticum infection may also be influenced by NO. The down-regulatory effect of steroids on NF-κB activation, iNOS expression, and NO production might partly explain the beneficial effect of steroids in neonates with CLD.

Inhibition of tetrahydrobiopterin biosynthesis impairs endothelium-dependent relaxations in canine basilar artery

1997 ◽  
Vol 273 (2) ◽  
pp. H718-H724 ◽  
Author(s):  
H. Kinoshita ◽  
S. Milstien ◽  
C. Wambi ◽  
Z. S. Katusic
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Nitric Oxide Synthase ◽  
Endothelial Function ◽  
Isometric Force ◽  
Cerebral Arteries ◽  
Calcium Ionophore ◽  
Nitric Oxide Donor ◽  
Ionophore A23187 ◽  
Oxide Synthase

Tetrahydrobiopterin is an essential cofactor in biosynthesis of nitric oxide. The present study was designed to determine the effect of decreased intracellular tetrahydrobiopterin levels on endothelial function of isolated cerebral arteries. Blood vessels were incubated for 6 h in minimum essential medium (MEM) in the presence or absence of a GTP cyclohydrolase I inhibitor, 2,4-diamino-6-hydroxypyrimidine (DAHP, 10(-2) M). Rings with and without endothelium were suspended for isometric force recording in the presence of a cyclooxygenase inhibitor, indomethacin (10(-5) M). In arteries with endothelium, DAHP significantly reduced intracellular levels of tetrahydrobiopterin. DAHP in combination with a precursor of the salvage pathway of tetrahydrobiopterin biosynthesis, sepiapterin (10(-4) M), not only restored but increased levels of tetrahydrobiopterin above control values. In DAHP-treated arteries, endothelium-dependent relaxations to bradykinin (10(-10)-10(-6) M) or calcium ionophore A23187 (10(-9)-10(-6) M) were significantly reduced, whereas endothelium-independent relaxations to a nitric oxide donor, 3-morpholinosydnonimine (10(-9)-10(-4) M), were not affected. When DAHP-treated arteries with endothelium were incubated with sepiapterin (10(-4) M) or superoxide dismutase (150 U/ml), relaxations to bradykinin and A23187 were restored to control levels. In contrast, superoxide dismutase did not affect endothelium-dependent relaxations in arteries incubated in MEM. A nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (10(-4) M), abolished relaxations to bradykinin or A23187 in control arteries and in DAHP-treated arteries. These studies demonstrate that in cerebral arteries, decreased intracellular levels of tetrahydrobiopterin can reduce endothelium-dependent relaxations. Production of superoxide anions during activation of dysfunctional endothelial nitric oxide synthase appears to be responsible for the impairment of endothelial function.

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