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 β-lactams or penicillin derivatives such as cephalosporins, monobactams, carbapenems, carbapenems that inhibit cell wall synthesis in bacteria and by inference mitochondrial reproduction. 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  has been linked to carcinogenesis in the molecular basis of alcoholism and red meat and treated meat carcinogenesis . Lipid peroxide is a mutagen. Calghatgi also found damage to DNA. This is another finding often associated with carcinogenesis. It has also been found that antibiotics can render the immune system less effective in infection and inflammation control.