Antibiotic Induced Changes to Mitochondria, a Potential Mechanism for Antibiotic Induced Carcinogenesis
Sameer Calghatgi (2013) demonstrated that 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. The antibiotics tested were from 3 categories; quinolonesorganofluorine compounds such as ofloxacin, norfloxacin (noroxin), ciprofloxacin (Cipro), moxifloxacin (Avelox); aminoglycosides-Gentamicin, amikacin which create holes in the outer cell wall of bacteria suggesting mitochondria might be at risk of similar damage[1] β-lactams or penicillin derivatives such as cephalosporins, monobactams, carbapenems, carbapenems that inhibit cell wall synthesis in bacteria and by inference mitochondrial reproduction. Read more about a