Mitochondria are Our Cellular Energy Producers
Mitochondria are small cell structures that are outside of the nucleus of a cell that are the essential energy producing cellular component and considered the power plants of cells. Mitochondrial DNA (mtDNA) are derived from maternal cells only as the paternal DNA from sperm are abolished after the egg is fertilized . Mitochondria are found in every organism with cells that contain a nucleus. Mitochondria are found in mammals, fish, trees, plants, insects but not in viruses or bacteria. The origin of mtDNA is thought to be from ancient bacterial ancestors and is now incorporated as a separate unit in all living cells.
Mitochondria are Complex and Vulnerable to Harm from Toxins
The structure of these round or oval shaped mitochondria is complex with a double cell membrane with multiple infoldings of the inner membrane that have many critical cellular functions. Not only do they convert energy from nutrients (sugars, proteins, fats) to ATP, the universal cellular energy unit, they also function in an important regulatory manner, signaling programmed cell death, steroid hormone biosynthesis, calcium, copper, and iron homeostasis, and they indirectly affect cell replication. About 1000 to 1500 proteins are imported into the mitochondria to carry out these functions thus mitochondria in different organ cells have different levels of these proteins. Mitochondria have their own DNA and replicate within the cell. The DNA in mitochondria, however, are not protected by the nucleus and do not have their own DNA repair mechanisms thus are more vulnerable to DNA damage through a variety of toxicants.
Oxidation is a Primary Mechanism of Harm to Mitochondria
Numerous studies have shown that excess creation of reactive oxygen species causes oxidation and destruction of cell structures. Oxidation is a primary cause of injury due to toxic chemicals and scientific research is also demonstrating that non-ionizing electromagnetic radiation such as from wireless devices and cell towers causes cellular damage mediated through oxidation.
UCSD Professer of Medicine, Dr. Beatrice Golomb, has written a seminal and comprehensive paper called “Oxidative Stress and mitochondrial injury in chronic Multisystem Conditions :From Gulf War Illness to Autism Spectrum Disorder.” She notes,
“Chronic multisymptom illnesses (CMI), including chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, multiple chemical sensitivity and Gulf War illness (GWI), show strong overlap1-4. Autism spectrum disorder (ASD), despite little cooccurrence with GWI (due to military self-selection and selection), encompasses multisymptom subsets bearing muscle, gastrointestinal, sleep and other symptoms germane to CMI. These are suggested to reflect a condition arising from similar mechanisms in a different developmental milieu….
Chronic multisymptom illnesses (CMI), including chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, multiple chemical sensitivity and Gulf War illness (GWI), show strong overlap1-4. Autism spectrum disorder (ASD), despite little cooccurrence with GWI (due to military self-selection and selection), encompasses multisymptom subsets bearing muscle, gastrointestinal, sleep and other symptoms germane to CMI. These are suggested to reflect a condition arising from similar mechanisms in a different developmental milieu.”
See research below.
Mutations in Mitochondrial DNA are Inherited
Mutations can occur that can be inherited by the next generation. Mitochondrial mutations are thought to be related to aging, cancer and neurodegenerative disease.
Mitochondrial Effects Research
- Monash University Research on Mitochondria. Medicine, Nursing and Health Sciences. http://www.med.monash.edu.au/biochem/research/projects/mitochondria.html
- Role of Mitochondria in the Oxidative Stress Induced by Electromagnetic Fields: Focus on Reproductive Systems. (2018) Santini SJ et al. . Oxid Med Cell Longev. 2018 Nov 8;2018. https://www.ncbi.nlm.nih.gov/pubmed/30533171
Published Scientific Literature
- 2450 MHz EMR exposure causes cognition deficit with mitochondrial dysfunction & activation of intrinsic pathway of apoptosis in rats. (2018) Gupta SK et al. J Biosciences. June 2018, Vol 43, pg 263. https://link.springer.com/article/10.1007/s12038-018-9744-7
- Exposure to 1.8 GHz electromagnetic fields affects morphology, DNA-related Raman spectra and mitochondrial functions in human lymphs-monocytes. (2018) Lasalvia M et al. PLoS One. 2018 Feb 20;13(2):e0192894. https://www.ncbi.nlm.nih.gov/pubmed/29462174.
- Mitochondrial DNA damage and oxidative damage in HL-60 cells exposed to 900MHz radiofrequency fields. (2017) Sun Y et al. Mutat Res. 2017 Mar 7;797-799:7-14. doi: 10.1016/j.mrfmmm.2017.03.001. https://www.ncbi.nlm.nih.gov/pubmed/28340409
- Mobile phones electromagnetic radiation and NAD+-dependent Isocitrate Dehydrogenase as a mitochondrial marker in Asthenozoospermia. Abeer M. Biochimie Open. Available online July 25, 2016. http://bit.ly/2b69gh9
- Respiratory function decline and DNA mutation in mitochondria, oxidative stress and altered gene expression during aging. Wei YH. Chang Gung Med J. 2009 Mar-Apr;32(2):113-32.
- Possible plant mitochondria involvement in cell adaptation to drought stress. A case study: durum wheat mitochondria. Pastore D. J Exp Bot. 2007;58(2):195-210. https://www.ncbi.nlm.nih.gov/pubmed/17261694
- [Role of mitochondria in reactive oxygen species generation and removal; relevance to signaling and programmed cell death]. Czarna M Postepy Biochem. 2006;52(2):145-56. Czarna M. https://www.ncbi.nlm.nih.gov/pubmed/17078504
- Protein-mediated energy-dissipating pathways in mitochondria. Starkov AA. Chem Biol Interact. 2006 May 15;161(1):57-68. Epub 2006 Apr 11. https://www.ncbi.nlm.nih.gov/pubmed/16584718
- Mitochondrial metabolism of reactive oxygen species. Andreyev AY. Biochemistry (Mosc). 2005 Feb;70(2):200-14. https://www.ncbi.nlm.nih.gov/pubmed/15807660
- Mobile phone radiation induces reactive oxygen species production and DNA damage in human spermatozoa in vitro. (2009) De Luliis. PLoS One. 2009 Jul 31;4(7):e6446. https://www.ncbi.nlm.nih.gov/pubmed/19649291
- Ultrastructural changes and diffusion of acetylcholine in rat brain after microwave irradiation. (1982) Kása P, Bánsághy K, Gulya K. J Neurosci Methods. 1982 Mar;5(3):215-20. https://www.ncbi.nlm.nih.gov/pubmed/7078254/
Related Articles Mitochondria
- Metabolic features of the cell danger response. Naviaux RK. Mitochondrion. 2014 May;16:7-17. . https://www.ncbi.nlm.nih.gov/pubmed/23981537
- Reactive oxygen species and nitric oxide in plant mitochondria: origin and redundant regulatory systems. Blokhina O. Physiol Plant. 2010 Apr;138(4):447-62. https://www.ncbi.nlm.nih.gov/pubmed/20059731
- Mitochondria as a Target of Environmental Toxicants. J Meyer. Toxicol Sci (2013) 134 (1): 1-17 https://academic.oup.com/toxsci/article/134/1/1/1666668/Mitochondria-as-a-Target-of-Environmental “Mitochondria are essential organelles best known for ATP generation and their involvement in apoptosis. They also play critical roles in other key processes including calcium, copper, and iron homeostasis; heme and iron-sulfur cluster assembly; synthesis of pyrimidines and steroids; thermogenesis and fever response; and calcium signaling. The great majority of the ~1000–1500 (Calvo and Mootha, 2010) proteins that carry out these functions are imported from the cytoplasm via mitochondria targeting sequences or other mechanisms (Bolender et al., 2008), and the proteins present vary significantly with tissue (Johnson et al., 2007). This variability probably reflects extensive variability in function, ranging from energy production in muscle mitochondria to steroid synthesis in adrenal mitochondria (Vafai and Mootha, 2012)…
- Mitochondrial DNA and disease. (2012) Greaves LC et al. J Pathol. 2012 Jan;226(2):274-86. https://www.ncbi.nlm.nih.gov/pubmed/21989606
- Mitochondria, metabolic disturbances, oxidative stress and the kynurenine system, with focus on neurodegenerative disorders. (2007) Sas K et al. J Neurol Sci. 2007 Jun 15;257(1-2):221-39. https://www.ncbi.nlm.nih.gov/pubmed/17462670
- MITOCHONDRIAL DNA MUTATIONS IN HUMAN DISEASE. (2005) Taylor RW and Tumbull DM. Nat Rev Genet. 2005 May;6(5):389-402. Review. https://www.ncbi.nlm.nih.gov/pubmed/15861210
- Metabolism and function of coenzyme Q. (2004) Turunen M et al. Biochimica et Biophysica Acta (BBA) – Biomembranes . Volume 1660, issues 1,2. January 2004, Pages 171-199
- Accumulation of mitochondrial DNA mutations in ageing, cancer, and mitochondrial disease: is there a common mechanism? (2002) Chinnery PF et al. Lancet. 2002 Oct 26;360(9342):1323-5. https://www.ncbi.nlm.nih.gov/pubmed/12414225