30/05/2025
Have you been affected by antibiotics?
BREAKING: New Study Unveils How Fluoroquinolone Antibiotics Damage Human Mitochondria – A Step Toward Hope for FQAD Patients?
In a groundbreaking study published in Angewandte Chemie International Edition in February 2025, researchers revealed alarming new insights into the hidden dangers of fluoroquinolone (FQ) antibiotics - a widely prescribed drug class that includes ciprofloxacin and levofloxacin. Using cutting-edge chemical proteomics, the study titled “Chemical Proteomics Reveals Human Off‐Targets of Fluoroquinolone Induced Mitochondrial Toxicity” has mapped for the first time how these drugs directly disrupt human mitochondrial function, shedding light on a mystery that has plagued countless patients suffering from Fluoroquinolone-Associated Disability (FQAD).
The Mechanism: How Fluoroquinolones Attack Our Cells
Researchers found that fluoroquinolones:
1. Disrupt the Electron Transport Chain (ETC): FQs inhibit key mitochondrial complexes —>> Complex I and Complex IV. This causes cellular energy production to collapse and triggers overwhelming oxidative stress inside cells.
2. Directly Bind Critical Mitochondrial Proteins: Using photo-affinity profiling, they discovered FQs binding to
>AIFM1 (Apoptosis-Inducing Factor 1), crucial for mitochondrial protein import and electron transport chain assembly.
>IDH2 (Isocitrate Dehydrogenase 2), responsible for maintaining antioxidant balance inside mitochondria. Their disruption leads to mitochondrial destabilization, oxidative injury, and impaired survival of affected cells.
3. Inhibit NUDT1 Enzyme: FQs also block NUDT1, an enzyme responsible for cleaning up oxidatively damaged nucleotides. Inhibiting NUDT1 allows damaged DNA to accumulate, promoting mutagenesis and chronic cellular stress.
Additional Discovery: Fluoroquinolone Accumulation Over Time
The study highlights that mitochondrial toxicity does not occur immediately after fluoroquinolone exposure. Instead, mitochondrial dysfunction develops over a longer time with prolonged drug treatment and potential accumulation within cells. Specifically, the researchers wrote: “FQs do not exhibit acute cell toxicity and primarily a different mode of action must be responsible for the observed mitochondrial toxicity, which rather develops over a longer time of drug treatment and potentially accumulation."
This delayed toxicity model may explain why many FQAD patients:
• Feel relatively normal initially but progressively worsen,
• Experience persistent symptoms long after stopping the antibiotic,
• Show signs of long-term mitochondrial dysfunction, despite no ongoing antibiotic exposure.
Global Impact: Why This Matters
These discoveries could finally explain why so many patients develop severe fatigue, neuropathies, musculoskeletal damage, and cognitive impairments after taking fluoroquinolones - symptoms that have often been ignored or misdiagnosed.
The study provides a molecular fingerprint of the destruction:
• Cellular energy collapse • Oxidative stress buildup • DNA instability, and opens new pathways to finally diagnose and treat FQAD sufferers, a medical community long waiting for answers.
Can this finding lead to a treatment for FQAD?
Absolutely, and it offers real hope. Now that specific molecular targets (like AIFM1, IDH2, and NUDT1) have been identified, researchers can begin:
• Designing therapies to protect or repair damaged mitochondria,
• Developing specialized antioxidants or redox-restoring treatments,
• Exploring gene therapies or small molecules that can reactivate damaged pathways.
Moreover, targeted therapies might stop or slow disease progression in patients suffering from FQAD today.
Fluoroquinolone Resistance in Bacteria: A Growing Public Health Concern
Beyond human mitochondrial toxicity, fluoroquinolones are increasingly linked to the rise of antibiotic-resistant bacteria. Bacteria can develop resistance to fluoroquinolones through several mechanisms:
• Mutations in Target Enzymes: Changes in DNA gyrase and topoisomerase IV reduce drug binding, diminishing efficacy.
• Efflux Pumps: Overexpression of efflux pumps expels the antibiotic from bacterial cells, lowering intracellular concentrations.
• Plasmid-Mediated Resistance: Genes such as qnr can be transferred between bacteria via plasmids, spreading resistance traits rapidly.
Notably, resistance can develop swiftly, sometimes even during a single course of treatment. The widespread use of fluoroquinolones in both human medicine and agriculture has exacerbated this issue, leading to the proliferation of multidrug-resistant bacterial strains. This growing resistance not only compromises the effectiveness of fluoroquinolones but also poses a significant challenge to public health, as infections become harder to treat and control.
Could fluoroquinolone damage cause mutations passed to future generations?
This is a potential major concern. By damaging mitochondrial DNA and interfering with DNA repair pathways, fluoroquinolone exposure might:
• Cause mutations not just in somatic (body) cells but also in germ cells (s***m and eggs),
• Lead to transmission of mitochondrial dysfunction or genetic defects to offspring,
• Increase risks of inherited diseases in future generations.
Additionally, fluoroquinolones are well known to induce bacterial hypermutation, speeding up antibiotic resistance.This dual threat - genetic damage in humans and rising superbugs in the environment - poses a serious long-term public health risk.
Conclusion: A Wake-Up Call to the World
This study is not just an academic breakthrough, it’s a global health warning. It exposes the hidden costs of widespread fluoroquinolone use and demands immediate action:
>Tighter antibiotic prescribing guidelines,
> Long-term patient monitoring,
> New therapies to protect and regenerate mitochondrial health.
And for the millions already suffering from FQAD, this breakthrough offers the first real hope that help may finally be on the horizon.
_____________________________________________
Reference:
T. Reinhardt, Y. El Harraoui, A. Rothemann, A. T. Jauch, S. Müller-Deubert, M. F. Köllen, T. Risch, L. J. Jacobs, R. Müller, F. R. Traube, D. Docheva, S. Zahler, J. Riemer, N. C. Bach, S. A. Sieber.
Chemical Proteomics Reveals Human Off-Targets of Fluoroquinolone Induced Mitochondrial Toxicity.
Angew. Chem. Int. Ed. 2025, 64, e202421424.
https://doi.org/10.1002/anie.202421424
and for downloadable version here: https://onlinelibrary.wiley.com/doi/epdf/10.1002/anie.202421424?fbclid=IwY2xjawKTlr1leHRuA2FlbQIxMABicmlkETFSU0ZFZmV3aEV5T2NnNVFoAR7WeFWXtx_q3qiD1FfirPps7zMAEMGEa0H5UfuHpkRPFCFvJfzJSutYiNa6oA_aem_aOCtxb0iCTipP3I30Sb6yg
Drugs in the fluoroquinolone class (incl: Cipro/ciprofloxacin, Levaquin (off market)/levofloxacin, Avelox/moxifloxacin etc) in all forms for humans and pets: https://fq100.org/drug-list
Fluoroquinolone support groups in multiple countries:
https://fq100.org/find-help
Support groups and resources:
https://fq100.org/find-help
https://fq100.org/find-medical
Toxicity warnings: https://fq100.org/
YouTube channel: https://www.youtube.com/
X/Twitter: https://twitter.com/FQ_100
Disclaimer: Fluoroquinolone Toxicity Study does not provide medical advice, and all articles and written content are intended for informational purposes only. We do our best to provide accurate information. Such information is not a substitute for professional medical advice, diagnosis or treatment. For multiple reasons, supplements, treatments, and pharmaceutical effects and outcomes can possibly vary significantly among those affected by fluoroquinolone drugs.
BREAKING: New Study Unveils How Fluoroquinolone Antibiotics Damage Human Mitochondria – A Step Toward Hope for FQAD Patients?
In a groundbreaking study published in Angewandte Chemie International Edition in February 2025, researchers revealed alarming new insights into the hidden dangers of fluoroquinolone (FQ) antibiotics - a widely prescribed drug class that includes ciprofloxacin and levofloxacin. Using cutting-edge chemical proteomics, the study titled “Chemical Proteomics Reveals Human Off‐Targets of Fluoroquinolone Induced Mitochondrial Toxicity” has mapped for the first time how these drugs directly disrupt human mitochondrial function, shedding light on a mystery that has plagued countless patients suffering from Fluoroquinolone-Associated Disability (FQAD).
The Mechanism: How Fluoroquinolones Attack Our Cells
Researchers found that fluoroquinolones:
1. Disrupt the Electron Transport Chain (ETC): FQs inhibit key mitochondrial complexes —>> Complex I and Complex IV. This causes cellular energy production to collapse and triggers overwhelming oxidative stress inside cells.
2. Directly Bind Critical Mitochondrial Proteins: Using photo-affinity profiling, they discovered FQs binding to
>AIFM1 (Apoptosis-Inducing Factor 1), crucial for mitochondrial protein import and electron transport chain assembly.
>IDH2 (Isocitrate Dehydrogenase 2), responsible for maintaining antioxidant balance inside mitochondria. Their disruption leads to mitochondrial destabilization, oxidative injury, and impaired survival of affected cells.
3. Inhibit NUDT1 Enzyme: FQs also block NUDT1, an enzyme responsible for cleaning up oxidatively damaged nucleotides. Inhibiting NUDT1 allows damaged DNA to accumulate, promoting mutagenesis and chronic cellular stress.
Additional Discovery: Fluoroquinolone Accumulation Over Time
The study highlights that mitochondrial toxicity does not occur immediately after fluoroquinolone exposure. Instead, mitochondrial dysfunction develops over a longer time with prolonged drug treatment and potential accumulation within cells. Specifically, the researchers wrote: “FQs do not exhibit acute cell toxicity and primarily a different mode of action must be responsible for the observed mitochondrial toxicity, which rather develops over a longer time of drug treatment and potentially accumulation."
This delayed toxicity model may explain why many FQAD patients:
• Feel relatively normal initially but progressively worsen,
• Experience persistent symptoms long after stopping the antibiotic,
• Show signs of long-term mitochondrial dysfunction, despite no ongoing antibiotic exposure.
Global Impact: Why This Matters
These discoveries could finally explain why so many patients develop severe fatigue, neuropathies, musculoskeletal damage, and cognitive impairments after taking fluoroquinolones - symptoms that have often been ignored or misdiagnosed.
The study provides a molecular fingerprint of the destruction:
• Cellular energy collapse • Oxidative stress buildup • DNA instability, and opens new pathways to finally diagnose and treat FQAD sufferers, a medical community long waiting for answers.
Can this finding lead to a treatment for FQAD?
Absolutely, and it offers real hope. Now that specific molecular targets (like AIFM1, IDH2, and NUDT1) have been identified, researchers can begin:
• Designing therapies to protect or repair damaged mitochondria,
• Developing specialized antioxidants or redox-restoring treatments,
• Exploring gene therapies or small molecules that can reactivate damaged pathways.
Moreover, targeted therapies might stop or slow disease progression in patients suffering from FQAD today.
Fluoroquinolone Resistance in Bacteria: A Growing Public Health Concern
Beyond human mitochondrial toxicity, fluoroquinolones are increasingly linked to the rise of antibiotic-resistant bacteria. Bacteria can develop resistance to fluoroquinolones through several mechanisms:
• Mutations in Target Enzymes: Changes in DNA gyrase and topoisomerase IV reduce drug binding, diminishing efficacy.
• Efflux Pumps: Overexpression of efflux pumps expels the antibiotic from bacterial cells, lowering intracellular concentrations.
• Plasmid-Mediated Resistance: Genes such as qnr can be transferred between bacteria via plasmids, spreading resistance traits rapidly.
Notably, resistance can develop swiftly, sometimes even during a single course of treatment. The widespread use of fluoroquinolones in both human medicine and agriculture has exacerbated this issue, leading to the proliferation of multidrug-resistant bacterial strains. This growing resistance not only compromises the effectiveness of fluoroquinolones but also poses a significant challenge to public health, as infections become harder to treat and control.
Could fluoroquinolone damage cause mutations passed to future generations?
This is a potential major concern. By damaging mitochondrial DNA and interfering with DNA repair pathways, fluoroquinolone exposure might:
• Cause mutations not just in somatic (body) cells but also in germ cells (s***m and eggs),
• Lead to transmission of mitochondrial dysfunction or genetic defects to offspring,
• Increase risks of inherited diseases in future generations.
Additionally, fluoroquinolones are well known to induce bacterial hypermutation, speeding up antibiotic resistance.This dual threat - genetic damage in humans and rising superbugs in the environment - poses a serious long-term public health risk.
Conclusion: A Wake-Up Call to the World
This study is not just an academic breakthrough, it’s a global health warning. It exposes the hidden costs of widespread fluoroquinolone use and demands immediate action:
>Tighter antibiotic prescribing guidelines,
> Long-term patient monitoring,
> New therapies to protect and regenerate mitochondrial health.
And for the millions already suffering from FQAD, this breakthrough offers the first real hope that help may finally be on the horizon.
_____________________________________________
Reference:
T. Reinhardt, Y. El Harraoui, A. Rothemann, A. T. Jauch, S. Müller-Deubert, M. F. Köllen, T. Risch, L. J. Jacobs, R. Müller, F. R. Traube, D. Docheva, S. Zahler, J. Riemer, N. C. Bach, S. A. Sieber.
Chemical Proteomics Reveals Human Off-Targets of Fluoroquinolone Induced Mitochondrial Toxicity.
Angew. Chem. Int. Ed. 2025, 64, e202421424.
https://doi.org/10.1002/anie.202421424
and for downloadable version here: https://onlinelibrary.wiley.com/doi/epdf/10.1002/anie.202421424?fbclid=IwY2xjawKTlr1leHRuA2FlbQIxMABicmlkETFSU0ZFZmV3aEV5T2NnNVFoAR7WeFWXtx_q3qiD1FfirPps7zMAEMGEa0H5UfuHpkRPFCFvJfzJSutYiNa6oA_aem_aOCtxb0iCTipP3I30Sb6yg
Drugs in the fluoroquinolone class (incl: Cipro/ciprofloxacin, Levaquin (off market)/levofloxacin, Avelox/moxifloxacin etc) in all forms for humans and pets: https://fq100.org/drug-list
Fluoroquinolone support groups in multiple countries:
https://fq100.org/find-help
Support groups and resources:
https://fq100.org/find-help
https://fq100.org/find-medical
Toxicity warnings: https://fq100.org/
YouTube channel: https://www.youtube.com/
X/Twitter: https://twitter.com/FQ_100
Disclaimer: Fluoroquinolone Toxicity Study does not provide medical advice, and all articles and written content are intended for informational purposes only. We do our best to provide accurate information. Such information is not a substitute for professional medical advice, diagnosis or treatment. For multiple reasons, supplements, treatments, and pharmaceutical effects and outcomes can possibly vary significantly among those affected by fluoroquinolone drugs.
