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Sagot :
To determine the poison given to Jared, we need to analyze the data provided and understand how these different components relate to various stages of cell respiration. Let's go through the steps methodically.
### Analysis of the Data:
1. Pyruvate Levels:
- In healthy muscle cells, the pyruvate level is 0.12 mM.
- In Jared's muscle cells, the pyruvate level is 0.12 mM.
- Since the levels of pyruvate are the same in both healthy and Jared's muscle cells, we can infer that glycolysis is not affected. This rules out Deoxyglucose as the poison, because Deoxyglucose would affect glycolysis, leading to a decrease in pyruvate levels in Jared's cells compared to healthy cells.
2. NADH Levels:
- In healthy muscle cells, the NADH level is 0.30 mM.
- In Jared's muscle cells, the NADH level is elevated at 0.50 mM.
- An increased level of NADH suggests that the cells are not successfully utilizing NADH in subsequent steps of cell respiration, which are the Krebs cycle and the Electron Transport Chain (ETC).
3. Intermembrane H+ Levels:
- In healthy muscle cells, the intermembrane hydrogen ion concentration is 0.32 mM.
- In Jared’s muscle cells, this concentration is significantly reduced to 0.05 mM.
- A low concentration of intermembrane H+ indicates that the proton gradient usually generated by the ETC is disrupted.
### Hypothesis for Poison Effect:
1. Deoxyglucose:
- Affects glycolysis by inhibiting hexokinase.
- Since pyruvate levels are the same, glycolysis is not inhibited, ruling out Deoxyglucose.
2. Arsenic:
- Affects the Krebs cycle by disrupting the conversion of pyruvate to Acetyl-CoA.
- However, since pyruvate levels are consistent and not building up, the Krebs cycle itself may not be directly affected by Arsenic. This makes Arsenic an unlikely candidate.
3. Cyanide:
- Inhibits cytochrome c oxidase in the electron transport chain (ETC).
- This results in the accumulation of NADH, as electrons cannot be transferred efficiently to oxygen.
- This aligns with the observed data of higher NADH levels in Jared's cells and the drastic decrease in intermembrane H+ concentration, since the ETC is crucial for pumping protons to create the gradient used by ATP synthase.
4. Oligomycin (referred to as 'sily'):
- Inhibits ATP synthase, preventing ATP production.
- This would not directly explain the increase in NADH or the low intermembrane H+ concentration since it does not block the ETC itself but rather the final step in ATP production.
### Conclusion:
Based on the data:
- Same pyruvate levels indicate unaffected glycolysis.
- Higher NADH levels suggest a blockage in the electron transport chain.
- Lower intermembrane H+ concentration further supports disruption in the ETC.
The data supports the hypothesis that Cyanide was given to Jared. Cyanide inhibits cytochrome c oxidase in the electron transport chain, preventing the transfer of electrons to oxygen. This causes NADH to accumulate and reduces the creation of the proton gradient across the inner mitochondrial membrane.
Therefore, the most likely candidate for the poison given to Jared is Cyanide.
The detailed explanation supporting this conclusion is as follows:
Cyanide inhibits cytochrome c oxidase in the electron transport chain. This inhibition prevents the transfer of electrons to oxygen, leading to an accumulation of NADH, as seen in the higher levels of NADH in Jared's cells. Additionally, the lack of electron flow prevents the proton pumps from functioning, resulting in a low intermembrane hydrogen ion concentration, which is observed in Jared's cells. These disruptions in the ETC explain the patterns seen in the data provided, consistent with Cyanide poisoning.
### Analysis of the Data:
1. Pyruvate Levels:
- In healthy muscle cells, the pyruvate level is 0.12 mM.
- In Jared's muscle cells, the pyruvate level is 0.12 mM.
- Since the levels of pyruvate are the same in both healthy and Jared's muscle cells, we can infer that glycolysis is not affected. This rules out Deoxyglucose as the poison, because Deoxyglucose would affect glycolysis, leading to a decrease in pyruvate levels in Jared's cells compared to healthy cells.
2. NADH Levels:
- In healthy muscle cells, the NADH level is 0.30 mM.
- In Jared's muscle cells, the NADH level is elevated at 0.50 mM.
- An increased level of NADH suggests that the cells are not successfully utilizing NADH in subsequent steps of cell respiration, which are the Krebs cycle and the Electron Transport Chain (ETC).
3. Intermembrane H+ Levels:
- In healthy muscle cells, the intermembrane hydrogen ion concentration is 0.32 mM.
- In Jared’s muscle cells, this concentration is significantly reduced to 0.05 mM.
- A low concentration of intermembrane H+ indicates that the proton gradient usually generated by the ETC is disrupted.
### Hypothesis for Poison Effect:
1. Deoxyglucose:
- Affects glycolysis by inhibiting hexokinase.
- Since pyruvate levels are the same, glycolysis is not inhibited, ruling out Deoxyglucose.
2. Arsenic:
- Affects the Krebs cycle by disrupting the conversion of pyruvate to Acetyl-CoA.
- However, since pyruvate levels are consistent and not building up, the Krebs cycle itself may not be directly affected by Arsenic. This makes Arsenic an unlikely candidate.
3. Cyanide:
- Inhibits cytochrome c oxidase in the electron transport chain (ETC).
- This results in the accumulation of NADH, as electrons cannot be transferred efficiently to oxygen.
- This aligns with the observed data of higher NADH levels in Jared's cells and the drastic decrease in intermembrane H+ concentration, since the ETC is crucial for pumping protons to create the gradient used by ATP synthase.
4. Oligomycin (referred to as 'sily'):
- Inhibits ATP synthase, preventing ATP production.
- This would not directly explain the increase in NADH or the low intermembrane H+ concentration since it does not block the ETC itself but rather the final step in ATP production.
### Conclusion:
Based on the data:
- Same pyruvate levels indicate unaffected glycolysis.
- Higher NADH levels suggest a blockage in the electron transport chain.
- Lower intermembrane H+ concentration further supports disruption in the ETC.
The data supports the hypothesis that Cyanide was given to Jared. Cyanide inhibits cytochrome c oxidase in the electron transport chain, preventing the transfer of electrons to oxygen. This causes NADH to accumulate and reduces the creation of the proton gradient across the inner mitochondrial membrane.
Therefore, the most likely candidate for the poison given to Jared is Cyanide.
The detailed explanation supporting this conclusion is as follows:
Cyanide inhibits cytochrome c oxidase in the electron transport chain. This inhibition prevents the transfer of electrons to oxygen, leading to an accumulation of NADH, as seen in the higher levels of NADH in Jared's cells. Additionally, the lack of electron flow prevents the proton pumps from functioning, resulting in a low intermembrane hydrogen ion concentration, which is observed in Jared's cells. These disruptions in the ETC explain the patterns seen in the data provided, consistent with Cyanide poisoning.
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