Fluoroquinolone Antibiotics Damage Mitochondria – FDA Does Little

[libertyjam]

#‎FDAFRAUD‬ Alert on antibiotics under class called fluoroquinolone

Names listed here: Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin – are damaging human mitochondria and inducing large amounts of oxidative stress that wreaks havoc on many areas of health. The FDA knows about this, and they are doing nothing about it. Actually, worse than doing nothing, they are increasing the length of the warning label, so that when victims go to sue the companies (Bayer makes Cipro and Avelox and Johnson & Johnson makes Levaquin) that damaged their cells and gave them a multi-symptom, chronic disease, they are told that their symptoms are on the warning label and thus they gave informed consent to be crippled by an antibiotic.

http://www.hormonesmatter.com/fluoro...-adds-warning/
Focusing on Fluoroquinolones

Though several kinds of bactericidal antibiotics have been shown to damage mitochondria, I’m going to focus this article on fluoroquinolone antibiotics because, a) there are multiple journal articles that note that fluoroquinolone antibiotics damage mitochondria, b) fluoroquinolone antibiotics have been shown to not just damage mitochondria, but to deplete mitochondrial DNA as well, and c) adverse reactions to fluoroquinolones involve multi-symptom, chronic illness that typifies mitochondrial injury.
Fluoroquinolone antibiotics – cipro/ciprofloxacin, levaquin/levofloxacin, avelox/moxifloxacin and floxin/ofloxacin – are damaging human mitochondria. This has been shown repeatedly, and even the FDA (never first to the party) acknowledges that the mechanism for damage done by fluoroquinolones is mitochondrial damage and the ensuing oxidative stress that occurs when mitochondria are damaged.
FDA Report Notes that Fluoroquinolones Damage Mitochondria

In their April 27, 2013 Pharmacovigilance Review, “Disabling Peripheral Neuropathy Associated with Systemic Fluoroquinolone Exposure,” the FDA notes that the mechanism for action through which fluoroquinolones induce peripheral neuropathy is mitochondrial toxicity. The report says:

Ciprofloxacin has been found to affect mammalian topoisomerase II, especially in mitochondria. In vitro studies in drug-treated mammalian cells found that nalidixic acid and ciprofloxacin cause a loss of motichondrial DNA (mtDNA), resulting in a decrease of mitochondrial respiration and an arrest in cell growth. Further analysis found protein-linked double-stranded DNA breaks in the mtDNA from ciprofloxacin-treated cells, suggesting that ciprofloxacin was targeting topoisomerase II activity in the mitochondria.

The FDA Pharmacovigilance Report also notes that mitochondrial damage (and the ensuing oxidative stress that occurs when mitochondria are damaged) is related to multi-symptom, chronic diseases like optic neuropathy, neuropathic pain, hearing loss, muscle weakness, cardiomyopathy, lactic acidosis, Parkinson’s, Alzheimer’s and amyotrophic lateral sclerosis (ALS).
Bactericidal Antibiotics Damage Mitochondria

A study entitled “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells” that was published in Science Translational Medicine in 2013 notes that:

Clinically relevant doses of bactericidal antibiotics – quinolones (fluoroquinolones), aminoglycosides, and Beta-lactams – cause mitochondrial dysfunction and ROS overproduction in mammalian cells. We demonstrated that these bactericidal antibiotic-induced effects lead to oxidative damage to DNA, proteins and membrane lipids. Mice treated with bactericidal antibiotics exhibited elevated oxidative stress markers in the blood, oxidative tissue damage, and up-regulated expression of key genes involved in antioxidant defense mechanisms, which points to the potential physiological relevance of these antibiotic effects.

Fluoroquinolones Deplete Antioxidants

Fluoroquinolone antibiotics damage the cellular mechanisms that are needed to repair mitochondrial damage – namely intracellular antioxidant production. The FDA report notes that, “Under normal circumstances, there is a mechanism to remove or prevent the generation of ROS to avoid cellular damage such as lipid peroxidation, mtDNA mutations, and DNA strand breaks; if this does not happen, it can then lead to even more oxidative damage.”

[Kotin]

yeah these are quite nasty.. when I was taking microbiology, these were some of the most destructive antibiotics I studied.

[donnay]

~Bump~

[Acala]

In my opinion, a person should only be taking antibiotics when the alternative is likely death. Got syph? Take the pill. Got bronchitis? Change you lifestyle.

edit: and if you have syph you should probably ALSO change your lifestyle.