Received: January 16, 2020 Published: February 03, 2020
Corresponding author: Jorma Jyrkkanen, UBC Zoology Grad and SFU Education, Kelowna, Canada
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.
Researchers reporting in Frontiers in Microbiology found that short chain fatty acids (SCFA) from resident bacteria were important in protecting the immune system, and inflammation control. Both of these side effects have important ramifications for prevention of cancer initiation. Antibiotics diminished resident bacteria carrying out this role and supplemental SCFA were not effective in ameliorating the effect. Dysbiosis of resident microbes is unequivocally associated with immune-related disorders and opportunistic and pathogenic infections which can themselves set the stage for cancer . If Helicobacter pylori, Streptococcus bovis, Salmonella typhae, Fusobacterium, Chlamydophyla, Bartonella or caries bacteria proliferate as a consequence this can lead to increased risk of cancers particularly in epithelial tissue. Seeing that these changes were consistent with steps found in carcinogenesis  I asked the question, what is the clinical and epidemiological evidence that antibiotics increase the risk of cancer? It appears others have also addressed this question [6-8]. In addition, one of the antibiotics classes tested was linked to a decline in pyruvate, the feed stock for the citric acid cycle and ATP and NAD production or OP, thus relegating the cell to a low oxygen environment. This is called the Warburg Effect which cancer cells have been shown to prefer in which they employ glycolysis instead of oxidative phosphorylation for their energy. It can be expected that this ideal environment for glycolysis favoring cancer cells will be the norm whenever and wherever mitochondria are damaged as they are with these antibiotics tested and with common pesticides. Clearly regulatory agencies need to pay more attention to these findings. Since 50% of cancers have a mutated P53 gene from prior studies and lipid peroxide is linked to mutagenesis and carcinogenesis in at least two cancers. I propose the hypothesis that these findings point to a DNA+P53 damaging ROS increasing-Lipid Peroxide increasing-mutagenic-(possible decreased pyruvate)+glutathione deficiency immune compromise syndrome underlying the mechanism for antibiotic carcinogenesis.
Further research suggested by these studies includes testing all antibiotics for their mitochondrial impacts. These findings also raise the question are there pesticides with similar consequences and there are intriguing findings in China. 9/12 common pesticides tested fragmented mitochondria at normal application doses . These results in turn raise the obvious question, are the consequences similar in terms of potential long-term carcinogenicity? Another interesting question . The heart muscle is full of mitochondria . Do antibiotics and pesticides affect the hearts mitochondria and if so in what way and for how long? I would expect this heart loss of OP combined with ROS and increased peroxides to lead to a condition  like chronic fatigue and possibly compromised coronary function. These findings in normal mitochondria of their stress response to antibiotic biocides is consistent with their evolutionary origin from bacteria and are linked to biochemical pathways already shown linked to carcinogenesis and confirmed in the literature .
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