What happen to our mitochondria when we take antibiotic like tetracyclines?

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Discussion Overview

The discussion revolves around the effects of antibiotics, specifically tetracyclines, on mitochondria, which share similarities with bacteria. Participants explore the mechanisms by which these antibiotics inhibit bacterial protein synthesis and the implications for mitochondrial function.

Discussion Character

  • Exploratory
  • Technical explanation
  • Debate/contested

Main Points Raised

  • Some participants propose that antibiotics like tetracyclines inhibit bacterial protein synthesis by targeting prokaryotic ribosomes, which are similar to those in mitochondria, potentially impairing mitochondrial function.
  • Others suggest that the double membrane of mitochondria may prevent antibiotics from entering, thereby protecting them from the effects of these drugs.
  • It is noted that while tetracyclines can affect mitochondrial protein synthesis at higher concentrations, the clinical significance of this at recommended doses remains unclear.
  • Some participants mention that antibiotics generally block bacterial growth, allowing the immune system to manage the infection, and that the effects on mitochondria may not be as critical due to existing mitochondrial populations.
  • Concerns are raised about the adverse effects of tetracyclines, particularly in children, due to their impact on tooth development.

Areas of Agreement / Disagreement

Participants express a range of views on the effects of tetracyclines on mitochondria, with some suggesting protective mechanisms while others highlight potential risks. There is no consensus on the clinical significance of mitochondrial inhibition by these antibiotics.

Contextual Notes

Limitations include the lack of specific studies addressing the effects of tetracyclines on mitochondria at therapeutic doses and the dependence on various assumptions regarding antibiotic action and mitochondrial biology.

Ahmed Abdullah
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Some antibiotic kills bacteria by inhibiting their protein synthesis. The idea is that, prokaryotic and eukaryotic protein synthesis machinery is not the same, so we can selectively use antibiotic that inhibit bacterial protein synthesis but not ours. Mitochondrion also known as the powerhouse of the cell, is of prokaryotic origin and is similar to bacteria in a many aspect most importantly both have 70S ribosome - their protein synthetic machinery. So what inhibit bacterial protein synthesis (unspecifically) should also inhibit mitochondrial protein synthesis.

Antibiotic like aminoglycosides, macrolides, and tetracyclines works by inhibiting bacterial protein synthesis. So they should also inhibit mitochondrial protein synthesis ---> impair their function .---> and possibly kill them.
Obviously this should not be right, otherwise these antibiotic would not be here. So my question is how they manage, not to kill the mitochondria or be benevolent on them?
 
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A general answer could be that the mitochondria have a double membrane that does not easily permit the antibiotics to enter the organelle.
 
I'd add, the drugs generally out there target specific surface proteins that our cells don't rely on as heavily, but there can be some cell-death.

It's hard to answer this without speaking to a specific antiobiotic... Mkorr's answer works for me.
 
Tetracylines reversibly block protein synthesis in bacteria and at somewhat higher concentrations in human mitochondria, particularly doxycycline. The clinical significance of this at recommended doses is unknown. Tetracylines have a number of important adverse effects and should not be used in children because of their effect on tooth development. They should only be used for limited periods of time, typically a week. They are first line drugs only for rickettsial diseases like Rocky Mountain spotted fever, and in situations where other agents may not be effective. In fact they have been considered for use at higher doses as chemotherapy in aggressive cancers.

The following link has been cited in other papers although its primary focus was not on tetracyclines. Click on manual download, http://aac.asm.org/cgi/reprint/34/1/167?ijkey=51ec1511576efc40773f34181d7607cb31425ef1
 
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Sorry I can't give an expert answer but just vague memory and biological instinct. But I thought many or most of the antibiotics blocked the growth of bacteria, following which they either self-destruct or the immune system has time to deal with them. For mitochondria, apart from permeability barriers etc. you can get by with the ones you already have - but it is not surprising that it is growing children the most sensitive to unwanted side-effects.
 
epenguin said:
Sorry I can't give an expert answer but just vague memory and biological instinct. But I thought many or most of the antibiotics blocked the growth of bacteria, following which they either self-destruct or the immune system has time to deal with them. For mitochondria, apart from permeability barriers etc. you can get by with the ones you already have - but it is not surprising that it is growing children the most sensitive to unwanted side-effects.

That is the usual way, and SW VandeCarr described just that; blocking protein synthesis = no new bacteria, or less, so that the immune system can take over. So, yep... the fate of anyone bacterium isn't the issue, but the growth and reduction of colonies.
 

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