Direct Effect of Temperature on the Catalytic Activity of Nitric Oxide Synthases Types I, II, and III

Nitric Oxide ◽  
1999 ◽  
Vol 3 (5) ◽  
pp. 375-382 ◽  
Author(s):  
Giorgio Venturini ◽  
Marco Colasanti ◽  
Emanuela Fioravanti ◽  
Andrea Bianchini ◽  
Paolo Ascenzi
Keyword(s):  
Nitric Oxide ◽  
Catalytic Activity ◽  
Direct Effect ◽  
Nitric Oxide Synthases ◽  
Effect Of Temperature

scholarly journals Electron Transfer and Catalytic Activity of Nitric Oxide Synthases

1998 ◽  
Vol 273 (10) ◽  
pp. 5566-5571 ◽  
Author(s):  
Clinton R. Nishida ◽  
Paul R. Ortiz de Montellano
Keyword(s):  
Nitric Oxide ◽  
Electron Transfer ◽  
Catalytic Activity ◽  
Nitric Oxide Synthases

Expression of Nitric Oxide Synthases (NOS) in rat uterus and cervix after LPS administration to pregnant and nonpregnant rats

1998 ◽  
Vol 5 (1) ◽  
pp. 145A-145A
Author(s):  
M ALI ◽  
I BUHIMSCHI ◽  
P ORISE ◽  
V JAIN ◽  
G SAADE ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthases ◽  
Rat Uterus

Retinal Cell Death Induced by TRPV1 Activation Involves NMDA Signaling and Upregulation of Nitric Oxide Synthases

2013 ◽  
Vol 33 (3) ◽  
pp. 379-392 ◽  
Author(s):  
Mauro Leonelli ◽  
Daniel O. Martins ◽  
Luiz R. G. Britto
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Nitric Oxide Synthases ◽  
Retinal Cell

Bacterial Nitric Oxide Synthases

2010 ◽  
Vol 79 (1) ◽  
pp. 445-470 ◽  
Author(s):  
Brian R. Crane ◽  
Jawahar Sudhamsu ◽  
Bhumit A. Patel
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthases

scholarly journals Nitric oxide inhibits, and carbon monoxide activates, islet acid α-glucoside hydrolase activities in parallel with glucose-stimulated insulin secretion

2006 ◽  
Vol 190 (3) ◽  
pp. 681-693 ◽  
Author(s):  
Henrik Mosén ◽  
Albert Salehi ◽  
Ragnar Henningsson ◽  
Ingmar Lundquist
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Insulin Secretion ◽  
Insulin Release ◽  
Islets Of Langerhans ◽  
Direct Effect ◽  
Appreciable Effect ◽  
Intact Mouse ◽  
Glucose Stimulated Insulin Secretion ◽  
Glucoside Hydrolases

We have studied the influence of nitric oxide (NO) and carbon monoxide (CO), putative messenger molecules in the brain as well as in the islets of Langerhans, on glucose-stimulated insulin secretion and on the activities of the acid α-glucoside hydrolases, enzymes which we previously have shown to be implicated in the insulin release process. We have shown here that exogenous NO gas inhibits, while CO gas amplifies glucose-stimulated insulin secretion in intact mouse islets concomitant with a marked inhibition (NO) and a marked activation (CO) of the activities of the lysosomal/vacuolar enzymes acid glucan-1,4-α-glucosidase and acid α-glucosidase (acid α-glucoside hydrolases). Furthermore, CO dose-dependently potentiated glucose-stimulated insulin secretion in the range 0.1–1000 μM. In intact islets, the heme oxygenase substrate hemin markedly amplified glucose-stimulated insulin release, an effect which was accompanied by an increased activity of the acid α-glucoside hydrolases. These effects were partially suppressed by the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one. Hemin also inhibited inducible NO synthase (iNOS)-derived NO production probably through a direct effect of CO on the NOS enzyme. Further, exogenous CO raised the content of both cGMP and cAMP in parallel with a marked amplification of glucose-stimulated insulin release, while exogenous NO suppressed insulin release and cAMP, leaving cGMP unaffected. Emiglitate, a selective inhibitor of α-glucoside hydrolase activities, was able to markedly inhibit the stimulatory effect of exogenous CO on both glucose-stimulated insulin secretion and the activityof acid glucan-1,4-α-glucosidase and acid α-glucosidase, while no appreciable effect on the activities of other lysosomal enzyme activities measured was found. We propose that CO and NO, both produced in significant quantities in the islets of Langerhans, have interacting regulatory roles on glucose-stimulated insulin secretion. This regulation is, at least in part, transduced through the activity of cGMP and the lysosomal/vacuolar system and the associated acid α-glucoside hydrolases, but probably also through a direct effect on the cAMP system.

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