Disruption of mitochondrial function and mitochondria-mediated toxicity
10 important questions on Disruption of mitochondrial function and mitochondria-mediated toxicity
In what ways chemicals can interrupt in the ETC?
2) Energy supply for the driven proton pumps can be impaired
3) They can open the mitochondrial permeability pore, triggering apoptosis (release of cyt C)
4) blocking of the citrate cycle
5) inhibition of substrate uptake
6) inhibition of fatty acid acyl beta oxidation
7) inhibition of ATP synthetase activity.
Which organs are highly sensitive to mitochondrial stress?
What are the molecular mechanisms of pentachlorophenol toxicity?
- consequences are increased oxygen consumption and increased loss of energy in the form of heat.
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What are the mechanisms behind valproic toxicity?
2 possible mechanisms
1) VPA decreases the cellular levels of free CoA and of carnitine. Therefore beta oxidation of short, medium and long fatty acids is depleted.
2) Direct inhibition of enzymes involved in the beta oxidation.
In some organs inhibition of energy generation can lead to severe energy crisis (liver heart)
Another side effect is accumulation of fatty acids. This can lead to microvesicular steatosis. This also causes an increase risk for lipid peroxidation.
What are the mechanisms behind fluoracetate toxicity?
- normally acetate is coupled to CoA to form in the end citrate. In the next step citrate becomes isocitrate. which is further oxidized to alpha-ketoglutarate, thereby reducing NAD+ and forming NADH and H+
- The crucial step during the isomerization of citrate to isocitrate is catalyzed by aconitase which is an enzyme that contains a 4Fe-4S cluster. The negatively charged oxygen of citrate binds to the specific iron in this cluster.
- fluoracetate can also couple to coA and can also become condensated, however the isomerization step is not possible because it inhibits aconitase.
What are the mechanisms behind cadmium-induced mitochondrial ROS production?
What are the mechanisms behind cyanide toxicity?
What is the mPT pore?
What are the mechanisms behind inhibition of the mPT pore?
What are the mechanisms behind tacrine-induced mitochondrial toxicity?
- Therefore it is in liver cells rapidly protonated.
- It is therefore rapidly transported into the inner mitochondrial membrane into the matrix.
- accumulation occurs.
- mitochondrial electron transport becomes uncoupled
- tacrine undergoes intercalative activity in the mtDNA. As a result it can inhibit topoisomerases.
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