Signaling pathways in the nitric oxide and iron-induced dopamine release in the striatum of freely moving rats: Role of extracellular Ca2+ and L-type Ca2+ channels

2005 ◽  
Vol 1047 (1) ◽  
pp. 18-29 ◽  
Author(s):  
Gaia Rocchitta ◽  
Rossana Migheli ◽  
Maria P. Mura ◽  
Giuseppe Grella ◽  
Giovanni Esposito ◽  
...  
2001 ◽  
Vol 134 (2) ◽  
pp. 275-282 ◽  
Author(s):  
Pier Andrea Serra ◽  
Gaia Rocchitta ◽  
Giovanni Esposito ◽  
M Rosaria Delogu ◽  
Rossana Migheli ◽  
...  

2000 ◽  
Vol 131 (4) ◽  
pp. 836-842 ◽  
Author(s):  
Pier Andrea Serra ◽  
Giovanni Esposito ◽  
M Rosaria Delogu ◽  
Rossana Migheli ◽  
Gaia Rocchitta ◽  
...  

2001 ◽  
Vol 132 (4) ◽  
pp. 941-949 ◽  
Author(s):  
Pier Andrea Serra ◽  
Giovanni Esposito ◽  
M Rosaria Delogu ◽  
Rossana Migheli ◽  
Gaia Rocchitta ◽  
...  

2004 ◽  
Vol 357 (3) ◽  
pp. 179-182 ◽  
Author(s):  
Jo Watts ◽  
Joanna Segieth ◽  
Brian Pearce ◽  
Peter S. Whitton

2018 ◽  
Vol 16 (2) ◽  
pp. 194-199
Author(s):  
Wioletta Ratajczak-Wrona ◽  
Ewa Jablonska

Background: Polymorphonuclear neutrophils (PMNs) play a crucial role in the innate immune system’s response to microbial pathogens through the release of reactive nitrogen species, including Nitric Oxide (NO). </P><P> Methods: In neutrophils, NO is produced by the inducible Nitric Oxide Synthase (iNOS), which is regulated by various signaling pathways and transcription factors. N-nitrosodimethylamine (NDMA), a potential human carcinogen, affects immune cells. NDMA plays a major part in the growing incidence of cancers. Thanks to the increasing knowledge on the toxicological role of NDMA, the environmental factors that condition the exposure to this compound, especially its precursors- nitrates arouse wide concern. Results: In this article, we present a detailed summary of the molecular mechanisms of NDMA’s effect on the iNOS-dependent NO production in human neutrophils. Conclusion: This research contributes to a more complete understanding of the mechanisms that explain the changes that occur during nonspecific cellular responses to NDMA toxicity.


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