Knowing the basics of the origin and evolution of the cells, I asked myself this question: "How do antibiotics affect human mitochondrial function?"
First, read this: Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. The Origin and Evolution of Cells.
Endosymbiosis: Symbiogenesis - Wikipedia
Endosymbiosis and The Origin of Eukaryotes
https://evolution.berkeley.edu/evoli...dosymbiosis_04
Indeed, mitochondria, the organelles responsible for energy production in the cell, have bacteria-like DNA and other molecules, suggesting that mitochondria are the product of an ancient endosymbiotic event, in which a bacterium was engulfed by another cell. The important implication of this, said Ronald DePinho, president of the MD Anderson Cancer Centre in Houston, Texas, who also did not participate in the research, is that “drugs targeted to [bacterial] physiology might also impinge on mitochondrial biology.”
and a comment [1] on this report:
In additon to the disruption of normal ROS signalling pathways mentioned in this paper many antibiotics have two other deleterious effects in human cells. They decrease respiratory competence and shift cell populations to aerobic glycolysis (the Warburg effect) resulting in localized lactic acidosis and a microenviroment favorable to tumor formation, tissue invasion and metastasis. In addition increased poduction of ROS is mutagenic to both nDNA and mtDNA destabilizing both genomes, decreasing mitochondrial survellance and clearing of tumorigenic karyotypes in the nucleus by the intrinsic apoptotic pathway, both hallmark features of cancer. I suggest (in agreement with many other investigators) that such antibiotics are carcinogenic and thus the findings reported here are very clinically relevant especially when administered for chronic infection. We need to find alternative antimicrobial therapies for non life threatening infections that do not harm these patients.
http://www.the-scientist.com/?articl...-Antibiotics-/
From:http://www.the-scientist.com/?articl...-Mitochondria/
Kalghatgi S, Spina CS, Costello JC, et al. Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells. Science translational medicine. 2013;5(192):192ra85. doi:10.1126/scitranslmed.3006055.
Bactericidal antibiotics induce mitochondrial dysfunction and oxidative damage in Mammalian cells. - PubMed - NCBI
(a MD's review of the above study)
Stefano GB, Samuel J, Kream RM. Antibiotics May Trigger Mitochondrial Dysfunction Inducing Psychiatric Disorders. Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2017;23:101-106. doi:10.12659/MSM.899478.
Antibiotics May Trigger Mitochondrial Dysfunction Inducing Psychiatric Disorders
Reactive Species Contribute to Antibiotic-Mediated Killing
Reactive Species Contribute to Antibiotic-Mediated Killing
Antibiotic and ROS linkage questioned
https://www.nature.com/articles/nbt.2574
Moullan N, Mouchiroud L, Wang X, Ryu D, Williams EG, Mottis A, Jovaisaite V, Frochaux MV, Quiros PM, Deplancke B, Houtkooper RH, Auwerx J (2015). "Tetracyclines Disturb Mitochondrial Function across Eukaryotic Models: A Call for Caution in Biomedical Research". Celll Reports. 10 (10): 1681–91. doi:10.1016/j.celrep.2015.02.034. PMID 25772356.
http://www.cell.com/cell-reports/pdf/S2211-1247(15)00180-1.pdf
Chatzispyrou IA, Held NM, Mouchiroud L, Auwerx J, Houtkooper RH (2015). "Tetracycline antibiotics impair mitochondrial function and its experimental use confounds research". Cancer Research. 75 (21): 4446–9. doi:10.1158/0008-5472.CAN-15-1626. PMID 26475870.
Wang X, Ryu D, Houtkooper RH, Auwerx J. Antibiotic use and abuse: A threat to mitochondria and chloroplasts with impact on research, health, and environment. Bioessays. 2015;37(10):1045-1053. doi:10.1002/bies.201500071.
Antibiotic use and abuse: A threat to mitochondria and chloroplasts with impact on research, health, and environment
Kohanski MA, Dwyer DJ, Hayete B, Lawrence CA, et al. 2007. A common mechanism of cellular death induced by bactericidal antibiotics. Cell 130: 797–810. [PubMed]
http://www.cell.com/cell/pdf/S0092-8674(07)00899-9.pdf
Ahler E, Sullivan WJ, Cass A, Braas D, York AG, et al. (2013) Doxycycline Alters Metabolism and Proliferation of Human Cell Lines. PLOS ONE 8(5): e64561. Doxycycline Alters Metabolism and Proliferation of Human Cell Lines
General info on bactericidal and bacteriostatic distinction in antibiotics: https://courses.lumenlearning.com/bo...obial-therapy/
Is there anything we can do to counter these harmful effects?
If the sole mechanism behind antibiotics’ disruption of mitochondrial function is through oxidative stress, then taking antioxidants like vitamin E, and doing things that support endogenous antioxidants during the antibiotic course could reduce the damage.
There is an “all positive” view of antibiotic usage in this community. My purpose in creating this thread is to open that view into discussion.
Regards
Logan
[1]: The comment below was added under the report by a reader. It appears the website has deleted the comments section from the web page. I had saved this comment when I first read this report a few months ago.
First, read this: Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. The Origin and Evolution of Cells.
Endosymbiosis: Symbiogenesis - Wikipedia
Endosymbiosis and The Origin of Eukaryotes
https://evolution.berkeley.edu/evoli...dosymbiosis_04
Indeed, mitochondria, the organelles responsible for energy production in the cell, have bacteria-like DNA and other molecules, suggesting that mitochondria are the product of an ancient endosymbiotic event, in which a bacterium was engulfed by another cell. The important implication of this, said Ronald DePinho, president of the MD Anderson Cancer Centre in Houston, Texas, who also did not participate in the research, is that “drugs targeted to [bacterial] physiology might also impinge on mitochondrial biology.”
and a comment [1] on this report:
In additon to the disruption of normal ROS signalling pathways mentioned in this paper many antibiotics have two other deleterious effects in human cells. They decrease respiratory competence and shift cell populations to aerobic glycolysis (the Warburg effect) resulting in localized lactic acidosis and a microenviroment favorable to tumor formation, tissue invasion and metastasis. In addition increased poduction of ROS is mutagenic to both nDNA and mtDNA destabilizing both genomes, decreasing mitochondrial survellance and clearing of tumorigenic karyotypes in the nucleus by the intrinsic apoptotic pathway, both hallmark features of cancer. I suggest (in agreement with many other investigators) that such antibiotics are carcinogenic and thus the findings reported here are very clinically relevant especially when administered for chronic infection. We need to find alternative antimicrobial therapies for non life threatening infections that do not harm these patients.
http://www.the-scientist.com/?articl...-Antibiotics-/
From:http://www.the-scientist.com/?articl...-Mitochondria/
Kalghatgi S, Spina CS, Costello JC, et al. Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells. Science translational medicine. 2013;5(192):192ra85. doi:10.1126/scitranslmed.3006055.
Bactericidal antibiotics induce mitochondrial dysfunction and oxidative damage in Mammalian cells. - PubMed - NCBI
(a MD's review of the above study)
Stefano GB, Samuel J, Kream RM. Antibiotics May Trigger Mitochondrial Dysfunction Inducing Psychiatric Disorders. Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2017;23:101-106. doi:10.12659/MSM.899478.
Antibiotics May Trigger Mitochondrial Dysfunction Inducing Psychiatric Disorders
Reactive Species Contribute to Antibiotic-Mediated Killing
Reactive Species Contribute to Antibiotic-Mediated Killing
Antibiotic and ROS linkage questioned
https://www.nature.com/articles/nbt.2574
Moullan N, Mouchiroud L, Wang X, Ryu D, Williams EG, Mottis A, Jovaisaite V, Frochaux MV, Quiros PM, Deplancke B, Houtkooper RH, Auwerx J (2015). "Tetracyclines Disturb Mitochondrial Function across Eukaryotic Models: A Call for Caution in Biomedical Research". Celll Reports. 10 (10): 1681–91. doi:10.1016/j.celrep.2015.02.034. PMID 25772356.
http://www.cell.com/cell-reports/pdf/S2211-1247(15)00180-1.pdf
Chatzispyrou IA, Held NM, Mouchiroud L, Auwerx J, Houtkooper RH (2015). "Tetracycline antibiotics impair mitochondrial function and its experimental use confounds research". Cancer Research. 75 (21): 4446–9. doi:10.1158/0008-5472.CAN-15-1626. PMID 26475870.
Wang X, Ryu D, Houtkooper RH, Auwerx J. Antibiotic use and abuse: A threat to mitochondria and chloroplasts with impact on research, health, and environment. Bioessays. 2015;37(10):1045-1053. doi:10.1002/bies.201500071.
Antibiotic use and abuse: A threat to mitochondria and chloroplasts with impact on research, health, and environment
Kohanski MA, Dwyer DJ, Hayete B, Lawrence CA, et al. 2007. A common mechanism of cellular death induced by bactericidal antibiotics. Cell 130: 797–810. [PubMed]
http://www.cell.com/cell/pdf/S0092-8674(07)00899-9.pdf
Ahler E, Sullivan WJ, Cass A, Braas D, York AG, et al. (2013) Doxycycline Alters Metabolism and Proliferation of Human Cell Lines. PLOS ONE 8(5): e64561. Doxycycline Alters Metabolism and Proliferation of Human Cell Lines
General info on bactericidal and bacteriostatic distinction in antibiotics: https://courses.lumenlearning.com/bo...obial-therapy/
Is there anything we can do to counter these harmful effects?
If the sole mechanism behind antibiotics’ disruption of mitochondrial function is through oxidative stress, then taking antioxidants like vitamin E, and doing things that support endogenous antioxidants during the antibiotic course could reduce the damage.
There is an “all positive” view of antibiotic usage in this community. My purpose in creating this thread is to open that view into discussion.
Regards
Logan
[1]: The comment below was added under the report by a reader. It appears the website has deleted the comments section from the web page. I had saved this comment when I first read this report a few months ago.
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