Poison in cellular respiration.

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Discussion Overview

The discussion revolves around the effects of cyanide as a poison in cellular respiration, specifically its impact on the electron transport chain and subsequent metabolic processes such as glycolysis and the Krebs cycle. Participants explore various explanations for why these processes cease when cyanide is present, examining both biochemical mechanisms and the characteristics of cyanide as a compound.

Discussion Character

  • Technical explanation
  • Debate/contested

Main Points Raised

  • Some participants propose that the cessation of glycolysis and the Krebs cycle is primarily due to the lack of NAD+ and FAD, as suggested in option c).
  • Others argue that both a) and c) are correct, emphasizing that the buildup of NADH and FADH2 occurs when the electron transport chain is blocked, preventing the regeneration of NAD+ and FAD.
  • One participant suggests that option b) is the best explanation, noting that cyanide acts as a competitive inhibitor to oxygen, affecting its uptake.
  • A later reply clarifies that while option b) is true, it may not be the most direct cause of the halted metabolic processes, as cells can still run glycolysis under anaerobic conditions if they manage NADH levels.
  • Another participant discusses the mechanism of cyanide's entry into cells, detailing how it can be inhaled or ingested and its rapid binding to cytochrome oxidase in the electron transport chain.
  • Further contributions address the properties of cyanide, including its ability to dissolve in the bloodstream and its molecular characteristics that facilitate diffusion through cell membranes.

Areas of Agreement / Disagreement

Participants express differing views on the primary reason for the cessation of glycolysis and the Krebs cycle, with no consensus reached on which explanation is the most accurate. Multiple competing explanations are presented, indicating an unresolved discussion.

Contextual Notes

Some statements rely on specific biochemical assumptions, such as the role of NAD+ and FAD in metabolic processes, and the discussion does not resolve the implications of cyanide's competitive inhibition or its molecular behavior in biological systems.

alexwaylo2008
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When a poison such as cyanide blocks the electron transport chain during cellular respiration, glycolysis and the krebs cycle soon grind to halt as well. Which of the following is the best explanation for this?

a) A high level of NADH is present in the cell.
b) the uptake of oxygen stops because electrobn transport was inhibited.
c) NAD+ and FAD are not available for glycolysis and the krebs cycle does not continue.
d) electrons are no longer available from the electron transport chain to power glycolysis and the Krebs cycle.
e) they run out of ATP

I think it would be C, but I'm not very sure. Could someone confirm me my answer please?
 
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Both a) and c) are correct, though I think c) is more likely to be the right answer. If the electron transport chain is blocked, then the electron carriers NADH and FADH2 cannot unload their electrons into it, which means NAD+ and FAD are not regenerated. Since glycolysis and the Krebs cycle both require NAD+ (and the Krebs cycle requires FAD), both of these processes stop running.
 
I think it is B. Cyanide is a compettive inhibitor to oxygen. It binds to Hemoglobin far more effeciently than Oxygen molecules do.
 
Statement b) is true too (though the toxicity of cyanide results from its binding to cytochrome oxidase in the electron transport chain as stated in the problem, not to haemoglobin), but it's not the most direct cause of stopped glycolysis/Krebs cycle. A cell that could eliminate its buildup of NADH/FADH2 could still run glycolysis even under oxygen starvation - this is what your muscle cells do during anaerobic exercise.
 
How does cyanide get to the cells so effectively then?
 
Depends on how it's introduced. If it's inhaled, then it enters the bloodstream via the lungs, proceeds directly to the heart, and kills quickly. Oral toxicity is more gradual, but also passes through the bloodstream. In either case, if too much cyanide gets into the heart or CNS tissue, it binds irreversibly to cytochrome oxidase and kills the cell.
 
Kalirren said:
Depends on how it's introduced. If it's inhaled, then it enters the bloodstream via the lungs, proceeds directly to the heart, and kills quickly. Oral toxicity is more gradual, but also passes through the bloodstream. In either case, if too much cyanide gets into the heart or CNS tissue, it binds irreversibly to cytochrome oxidase and kills the cell.

Let me rephrase my question. How does cyanide dissolve so well in the blood stream. I realize what it does metabolically, what I was trying to point out though is a characteristic of poisons.
 
Cyanide competes with oxygen for binding at respiratory complex 4, Cytochrome C Oxidase. NADH is still able to feed electrons into the chain, they just never reach their final destination. That should help answer your question.
 
t-money said:
How does cyanide get to the cells so effectively then?

Small, uncharged polar molecules such as water diffuse reasonably well through cell membranes. Cyanide (HCN) may be slightly larger than water but it is also less polar. Remember the Hydrogen is bonded to carbon which is a mostly non polar bond.
 

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