BioNyt - Videnskabens Verden
Bog fra okt. 2015 om cyanidforgiftninger. Google viser kap. 15.4.4. start og nogle sider forud. Her anføres at cyanider fremkalder oxidativt stress via mange mekanismer, og at hjernen selv også kan danne cyanider, og at cyanid-dannelse fremkaldes af opioid-agonister, men ikke hvis der er opioid-antagonister til stede.
Amerikansk side om cyanid-forgiftning.
wIKIPEDIA-SIDE om bl.a. hydrogencyanid i sammenhæng med nerveceller.
Some authors have been shown that neurons can produce hydrogen cyanide upon activation of their opioid receptors by endogenous or exogenous opioids. They also shown that neuronal production of HCN activates NMDA receptors and plays a role in signal transduction between neuronal cells (neurotransmission). Moreover, increased endogenous neuronal HCN production under opioids was seemingly needed for adequate opioid analgesia, as analgesic action of opioids was attenuated by HCN scavengers. They considered endogenous HCN to be a neuromodulator.[[WIKISIDEN HENVISER TIL: Borowitz JL, Gunasekar PG, Isom GE. (12 Sep 1997). "Hydrogen cyanide generation by mu-opiate receptor activation: possible neuromodulatory role of endogenous cyanide.". Brain Res. 768 (1-2): 294–300. doi:10.1016/S0006-8993(97)00659-8. PMID 9369328.]]
It was also shown that, while stimulating muscarinic cholinergic receptors in cultured pheochromocytoma cells increases HCN production, in a living organism (in vivo) muscarinic cholinergic stimulation actually decreases HCN production.[[WIKISIDEN HENVISER TIL: Gunasekar PG, Prabhakaran K, Li L, Zhang L, Isom GE, Borowitz JL. (May 2004). "Receptor mechanisms mediating cyanide generation in PC12 cells and rat brain.". Neurosci Res. 49 (1): 13–18. doi:10.1016/j.neures.2004.01.006. PMID 15099699.]]
Leukocytes generate HCN during phagocytosis.[[WIKISIDEN HENVISER TIL: Borowitz JL, Gunasekar PG, Isom GE. (12 Sep 1997). "Hydrogen cyanide generation by mu-opiate receptor activation: possible neuromodulatory role of endogenous cyanide.". Brain Res. 768 (1-2): 294–300. doi:10.1016/S0006-8993(97)00659-8. PMID 9369328.]]
The vasodilatation, caused by sodium nitroprusside, has been shown to be mediated not only by NO generation, but also by endogenous cyanide generation, which adds not only toxicity, but also some additional antihypertensive efficacy compared to nitroglycerine and other non-cyanogenic nitrates which do not cause blood cyanide levels to rise.[[WIKISIDEN HENVISER TIL: Smith RP, Kruszyna H. (Jan 1976). "Toxicology of some inorganic antihypertensive anions.". Fed Proc. 35 (1): 69–72. PMID 1245233.]]
HER ER ABSTRACT FRA EN (TILFÆLDIG) KILDE FUNDET PÅ PUBMED OM CYANIDE + NERVECELLER: Activation of NMDA receptors plays an important role in cyanide neurotoxicity. Cyanide indirectly activates the receptor by inducing neuronal release of glutamate and also enhances receptor-mediated responses by a direct interaction with the receptor complex. This study investigated the mechanism in cerebellar granule cells by which cyanide enhances NMDA-induced Ca2+ influx. Cyanide (50 microM) increased the influx of Ca2+ over the NMDA concentration range of 0.5-500 microM. Experiments showed that cyanide does not interact with the receptor's glycine or PKC mediated phosphorylation regulatory sites. N-ethylmaleimide, a thiol alkylating agent which inactivates the redox regulatory sites of the receptor, blocked the enhancing effect of cyanide. Pretreatment of cells with 5,5-dithio-bis-2-nitrobenzoic acid (DTNB), a compound that oxidizes the receptor redox sites, had no effect on the response to cyanide. On the other hand, the nonpermeant reducing agents, dithiothreitol or cysteine, further increased the cyanide effect. These observations can be explained by cyanide interacting with redox sensitive disulfide groups that are not accessible to the non-permeant reducing agents. It is proposed that cyanide interacts with a redox site(s) located either on the intracellular receptor domain or in the transmembrane hydrophobic domain. Furthermore the enhancement by cyanide of the excitotoxic actions of NMDA involves receptor sites that are sensitive to oxidation/reduction and this interaction contributes to the neurotoxic action of cyanide. KILDE: http://www.ncbi.nlm.nih.gov/pubmed/10402559
HER ER ABSTRACT FRA EN ANDEN (TILFÆLDIG) KILDE FUNDET PÅ PUBMED OM CYANIDE + NERVECELLER: Hydrogen cyanide, a gaseous molecule, is produced by white blood cells during phagocytosis. The present study examined the possibility that neuronal-like cells may also produce cyanide following activation. Rat pheochromocytoma (PC12) cells exhibited a low level of cyanide generation that was significantly increased by mu-opiate agonists (hydromorphone, morphine) and blocked by naloxone. A variety of other agonists including bradykinin, nicotine and glutamate did not generate cyanide in PC12 cells. Systemic administration of hydromorphone to rats increased brain cyanide levels by 61% after 15 min. Using microdialysis probes implanted in the cortical-hippocampal areas of the anesthetized rat or in the hypothalamus of the conscious hamster, a 2- to 5-fold increase in cyanide generation was seen after hydromorphone administration and this increase was blocked by naloxone. To determine whether cyanide release by hydromorphone has functional significance in a neuronal system, cyanide enhancement of N-methyl-D-aspartate (NMDA)-induced increased [Ca2+]i was measured in rat cerebellar granule cells. Hydromorphone enhanced the response to NMDA similar to cyanide and the hydromorphone effect was blocked by cyanide scavengers. These data show that cyanide generation is increased in neuronal tissue by a mu-opiate receptor agonist and it is proposed that endogenous cyanide may modulate the NMDA receptor response. KILDE: http://www.ncbi.nlm.nih.gov/pubmed/9369328
DET SKAL BEMÆRKES, AT SØGEORDET "HCN" IKKE ALTID VIL GIVE ARTIKLER OM HYDROGENCYANID, IDET "HCN" BRUGES SOM FORKORTELSER, F.EKS:
hyperpolarization-activated cyclic nucleotide (HCN)-gated channels
hippocampal neurons (HCN)
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