Receptor mechanisms mediating cyanide generation in PC12 cells and rat brain

@article{Gunasekar2004ReceptorMM,
  title={Receptor mechanisms mediating cyanide generation in PC12 cells and rat brain},
  author={Palur G. Gunasekar and Krishnan Prabhakaran and Li Feng Li and L W Zhang and Joseph L. Borowitz},
  journal={Neuroscience Research},
  year={2004},
  volume={49},
  pages={13-18}
}
The two faces of cyanide: an environmental toxin and a potential novel mammalian gasotransmitter.
TLDR
Cyanide fulfills many of the general criteria as a 'classical' mammalian gasotransmitter and shares some common features with the current members of this class: nitric oxide, carbon monoxide and hydrogen sulfide.
Up-Regulation of Uncoupling Protein 2 by Cyanide Is Linked with Cytotoxicity in Mesencephalic Cells
TLDR
The findings indicate that UCP-2 can serve as a regulator of mitochondria-mediated necrotic cell death, in which enhanced expression can increase the vulnerability of primary MCs to injury due to complex IV-mediated inhibition by cyanide.
A Mitochondria-Specific Fluorescent Probe for Visualizing Endogenous Hydrogen Cyanide Fluctuations in Neurons.
TLDR
A mitochondria-specific coumarin pyrrolidinium-derived fluorescence probe (MRP1) that permits the real-time ratiometric imaging ofHCN in living cells and has proved effective in visualizing different concentrations of exogenous HCN in the mitochondria of HepG2 cells, as well as the imaging of endogenous HCN within neurons.
The inhibition of mitochondrial cytochrome oxidase by the gases carbon monoxide, nitric oxide, hydrogen cyanide and hydrogen sulfide: chemical mechanism and physiological significance
TLDR
The chemistry of this inhibition by NO and CO is dependent on oxygen concentration, but that of HCN and H2S is not, and the enzyme may act as a physiological detoxifier of these gases.
[Acute poisoning with carbon monoxide (CO) and cyanide (CN)].
  • F. Baud
  • Medicine
    Therapeutische Umschau. Revue therapeutique
  • 2009
TLDR
A critical analysis of acute CO and CN poisonings evidences that the lone toxicological similarity between CO andCN is their ability to avidly bind iron ions in the different hemoproteins, further supporting different mechanisms of action.
Gaseous Signaling Molecules in Cardiovascular Function: From Mechanisms to Clinical Translation.
TLDR
In this review, the basic aspects of CO, H2S, and NO, including their production and effects on enzymes, mitochondrial respiration and biogenesis, and ion channels are briefly addressed to provide insight into their biology with respect to the CVS.
Interactions of multiple gas-transducing systems: hallmarks and uncertainties of CO, NO, and H2S gas biology.
TLDR
This work takes an integrated approach to the interaction of gases by considering the physiological significance of CO, NO, CO, and H2S on mitochondrial cytochrome c oxidase, a key target and central mediator of mitochondrial respiration.
Endogenous opiates and behavior: 2004
TLDR
This paper is the 27th consecutive installment of the annual review of research concerning the endogenous opioid system, and summarizes papers published during 2004 that studied the behavioral effects of molecular, pharmacological and genetic manipulation of opioid peptides, opioid receptors, opioid agonists and opioid antagonists.
Mitochondrial β-Cyanoalanine Synthase Is Essential for Root Hair Formation in Arabidopsis thaliana[W]
TLDR
Transcriptional profiling of the cys-c1 mutant reveals that cyanide accumulation acts as a repressive signal for several genes encoding enzymes involved in cell wall rebuilding and the formation of the root hair tip as well as genes involved in ethylene signaling and metabolism.
Signaling by hydrogen sulfide and cyanide through posttranslational modification.
TLDR
The signaling roles of sulfide and most probably of cyanide are performed through the modification of specific cysteine residues, thus altering protein functions, and could play a protective function for thiols against oxidative damage.
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