Commentary - Clinical Investigation (2020) Volume 10, Issue 1

Antibiotic induced changes to mitochondria result in potential contributions to carcinogenesis

Glutathione is an antioxidant that soaks up ROS and is essential for many neurological and other body functions. Glutathione is capable of preventing damage to important cellular components caused by reactive oxygen species such as free radicals, peroxides, lipid peroxides, and heavy metals. ROS has been linked to mutation of the cell’s DNA protector, the P53 gene and lipid peroxide [5] has been linked to oesophageal carcinogenesis and in the molecular basis of alcoholism and red meat and treated meat carcinogenesis [6]. Lipid peroxide is a mutagen. Kalghatgi also found damage to DNA. This is another finding often associated with carcinogenesis.


Mitochondrial job and creation of toxic mix by antibiotic Mitochondria, a primitive endosymbiotic bacteria, related to extant SARII marine bacteria and Rickettsias, in eukaryotes is responsible for Oxidative Phosphorylation (OP) and ATP and NAD production, when exposed to clinically equivalent doses of antibiotics that target bacteria (cipromycin, ampicillin, kanamycin), exhibited a decline in glutathione titre, an increase in Reactive Oxygen (ROS) and an increase in lipid peroxide [1,2]. Modes of action of antibiotics on mitochondria and microbiome 1. Quinolones: Commonly prescribed antibacterial organofluorine compounds that act by inhibition of bacterial DNA synthesis and result in rapid cell death [3]. They could be expected to do collateral damage to mitochondria and the human microbiome. This group contains Ofloxacin, Norfloxacin (Noroxin), Ciprofloxacin (Cipro), Moxifloxacin (Avelox)

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