Fluoroquinolone Antibiotics Linked to Mitochondrial Damage

Aside from the growing threat of antibiotic resistant superbugs, there is now mounting evidence pointing to mitochondrial damage caused by antibiotics belonging to the class known as fluoroquinolones, which includes Levaquin and Cipro. The fluoroquinolones are a family of broad spectrum, systemic antibacterial agents that have been used widely as treatment for respiratory and urinary tract infections.

The common side effects of fluoroquinolones are gastrointestinal disturbances, headaches, skin rash and allergic reactions. More severe side effects reported include seizures, hallucinations, tendon rupture, swelling of tissue under the skin, and photosensitivity. A series of studies have linked side effects of Levaquin and Cipro to nerve damage and kidney injury. In July 2008, the FDA required that a “black box” warning be added to fluoroquinolone drug warnings indicating increased risk of tendon rupture with intake of Levaquin and other fluorquinolone antibiotics.  

The Southern Network on Adverse Reactions (SONAR), a multidisciplinary pharmacovigilance group that conducts studies of adverse events reported to the FDA and other databases, estimates that mitochondrial toxicity could be the cause of as many as 31% of the nearly 80,000 Levaquin adverse events reported between November 1, 1997 and February 3, 2011. The group also notes that only between 1% and 10% of adverse events are estimated to actually be reported, suggesting the true extent of the problems may be substantially greater.

As of August 2013, the U.S. Food and Drug Administration (FDA) has required the drug labels and Medication Guides for all fluoroquinolone antibacterial drugs be updated to better describe the serious side effect of peripheral neuropathy. “This serious nerve damage potentially caused by fluoroquinolones may occur soon after these drugs are taken and may be permanent,” reports the FDA.

Bacterial antibiotics have been shown to increase toxic free radicals (ROS) in bacteria, leading to mitochondrial dysfunction. Researchers have found that cells given the bactericidal antibiotics have structural damage caused by oxidative stress—harm caused by the binding and oxidation of free radicals (ROS).

An interesting theory postulates as to why the mitochondria may be a target of this class of drugs. According to the endosymbiotic theory, mitochondria originated from free-living, aerobic bacteria. It is possible that antibiotics target mitochondria and mitochondrial components, similar to their action in bacteria that are being treated with the antibiotics.

In a paper titled, Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells, scientists suggest that patients with compromised antioxidant defense systems or those genetically disposed to developing a mitochondrial dysfunction disease might be at greater risk from bactericidal antibiotic treatments.

Clinical studies have shown that the detrimental effects of bactericidal antibiotics were alleviated when the antioxidant, N-acetyl-L-cysteine (NAC), was given in addition to the antibiotics. A research team at Boston University studying this effect found that the NAC reduced the antibiotic-induced increase of free radicals, but importantly it didn’t affect the antibiotics’ bactericidal activities. Mice given a urinary tract infection, then treated with an antibiotic, cleared the bacteria just as effectively whether or not they were given NAC along with an antibiotic treatment.

The growing concern over fluorquinolone-induced mitochondrial damage has some doctors reviewing their choice of antibiotic treatment. Overall, the message is that antibiotics should be used judiciously and only when absolutely necessary.

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