Environmental Pollution, Oxidative Stress and Thioretinaco Ozonide: Effects of Glyphosate, Fluoride and Electromagnetic Fields on Mitochondrial Dysfunction in Carcinogenesis, Atherogenesis and Aging

Ann Clin Lab Sci. 2020 May;50(3):408-411.


Environmental pollutants, such as pesticides, herbicides, additives to food and water, and electromagnetic fields threaten public health by promotion of cancer, heart disease and chronic diseases of aging. Many of these pollutants cause adverse health outcomes by effects on mitochondrial function to produce oxidative stress through loss of the active site complex for oxidative phosphorylation, thioretinaco ozonide oxygen nicotinamide adenine dinucleotide phosphate, from opening of the mitochondrial permeability transition pore. Glyphosate, fluoride, and electromagnetic fields are examples of carcinogenic pollutants that promote loss and decomposition of the active site for oxidative phosphorylation, producing mitochondrial dysfunction and oxidative stress. Ionizing radiation has long been known to be carcinogenic, and non-ionizing electromagnetic fields from microwaves, radar, cell phones and cathode ray screens are carcinogenic and produce deleterious effects on capillaries, nerve cells, blood brain barrier, embryonic and germ cells, lenses and cardiac function. Adverse health effects of electromagnetic fields include cataracts, infertility, congenital malformations, cancer, lymphocytosis, leukemia, hearing loss, blindness, retinal hemorrhages, cardiac arrhythmias, dermatitis, hair loss, depression, memory loss, premature aging, heart attacks, and weaponized mind control. The hyperhomocysteinemia, suppressed immunity, and altered oxidative metabolism observed in atherosclerosis and dementia are attributed to deficiency of adenosyl methionine which results from increased polyamine biosynthesis by pathogenic microbes that are demonstrated in atherosclerotic plaques and cerebral plaques. Thus, environmental pollutants potentially promote diseases of aging, atherosclerosis, cancer, and premature aging by production of mitochondrial dysfunction.

Keywords: adenosine triphosphate; adenosyl methionine; atrial fibrillation; autonomic nervous system; carcinogenesis; cardiac arrhythmia; cellular senescence; cycloastragenol; electromagnetic field; environmental pollution; fluoride; glyphosate; homocysteine; inflammation; melatonin; mitochondrial dysfunction; mitochondrial membrane potential; mitochondrial permeability transition pore; mycotoxin; oxidative phosphorylation; oxidative stress; ozone; telomere; thioretinaco ozonide.

Publication types

  • Review

MeSH terms

  • Aging / pathology
  • Animals
  • Atherosclerosis / metabolism
  • Carcinogenesis / metabolism
  • Carcinogenesis / pathology
  • Electromagnetic Fields / adverse effects
  • Environmental Pollution / adverse effects*
  • Fluorides / adverse effects
  • Glycine / adverse effects
  • Glycine / analogs & derivatives
  • Homocysteine / analogs & derivatives
  • Homocysteine / metabolism
  • Humans
  • Hyperhomocysteinemia / metabolism
  • Mitochondria / drug effects*
  • Mitochondria / metabolism
  • Neoplasms / metabolism
  • Oxidative Phosphorylation / drug effects
  • Oxidative Stress / drug effects*
  • Vitamin B 12 / analogs & derivatives
  • Vitamin B 12 / metabolism


  • thioretinaco
  • Homocysteine
  • glyphosate
  • Vitamin B 12
  • Fluorides
  • Glycine