Substances that MAY damage your mitchondria and mitochondrial safety analysis. 2022-01-08. Jorma Jyrkkanen.

Eating A LOT OF plants HIGH IN oxalic acid MAY damage your mitochondria and affect your heart and other effects. Mitochondria energize your heart. Other substances can as well including antibiotics, pesticides, spike proteins and these following substances. DRUGS-INDUCED MITOCHONDRIAL AND MTDNA TOXICITY Redox Biology, Volume 15, May 2018, Pages 207-215 Oxalate induces mitochondrial dysfunction and disrupts redox homeostasis in a human monocyte derived cell line (These plants contain oxalic acid: Image result for Plant foods with oxalic acid: Vegetables; spinach, chard, potatoes, beets, turnips, yams, okra, carrots. Legumes: navy beans, fava beans, kidney beans, refried beans. Nuts: almonds, walnuts, pistachios, macadamia nuts, cashews. Seeds: sunflower seeds, pumpkin seeds. AMOUNT MATTERS.THIS MUST BE DETERMINED EXPERIMENTALLY IN LIGHT OF CONSIDERATIONS OF ALL RELATED RISK FACTORS EXPOSURE. Authors Mikita Patela, Vidhush Yarlagaddaa, Oreoluwa Adedoyinb Vikram Sainic Dean G.Assimosa Ross P.Holmes a Tanecia Mitchella {See also Drugs besides the pesticides I have already published on and the antibiotics and covid infection effects}. Meyer JN, Leung MC, Rooney JP, et al. Mitochondria as a target of environmental toxicants. Toxicol Sci. 2013;134(1):1-17. doi:10.1093/toxsci/kft102 Drugs Can Cause Many Off-Target Mitochondrial Effects Recognition that mitochondrial toxicity is a key “off-target” effect of many drugs is also a relatively recent development. Drugs have now been identified that inhibit and uncouple the ETC; inhibit mitochondrial transport pathways, fatty acid oxidation or uptake, the citric acid cycle, mtDNA replication, and mitochondrial protein synthesis (a common mode of toxicity of antibiotics that target bacterial ribosomes, to which mitochondrial ribosomes are similar due to mitochondria’s evolutionary origins); generate (or exacerbate generation of) ROS; and more (Begriche et al., 2011; Cohen, 2010; Dykens and Will, 2007; Kovacic et al., 2005; Mehta et al., 2008; Neustadt and Pieczenik, 2008; Pacheu-Grau et al., 2010; Rowe et al., 2001). One well-studied example is adriamycin (doxorubicin), a chemotherapeutic whose clinical use is limited by the fact that it also causes irreversible and cumulative cardiomyopathy (Wallace, 2007). It appears to act largely by poisoning mitochondria, both via redox cycling to generate ROS and by inhibiting ATP production via uncoupling of oxidative phosphorylation. Although its antineoplastic function is largely a result of DNA intercalation and topoisomerase II inhibition in the nucleus, a substantial amount reaches mitochondria, where it has a high binding affinity for cardiolipin, a lipid found only in the mitochondrial inner membrane (Mustonen and Kinnunen, 1993). Another example is the nucleoside reverse transcriptase inhibitors (NRTIs) that are used to combat human immunodeficiency virus (HIV) infection. NRTIs act by inhibiting the reverse transcriptase activity required for viral replication. They have been highly successful in treating adults and in preventing transmission of HIV from pregnant mothers to their children, but unfortunately many NRTIs also inhibit the mtDNA polymerase γ. This has resulted mtDNA depletion- and mutation-mediated mitochondrial toxicity, and even death, in patients and in animal models (Benhammou et al., 2007; Blanche et al., 1999; Chan, 2007; Claessens et al., 2003; Divi et al., 2010; Kohler and Lewis, 2007). Similar effects have been observed with nucleoside analogs intended for other viruses as well (McKenzie et al., 1995). Thus, chemicals that damage mtDNA or alter its copy number can have very serious health consequences. Such toxicities have led to failed clinical trials, “Black Box” warnings and withdrawal of drugs from the market, and have driven the pharmaceutical industry to develop better methods for detection of drug-induced mitochondrial dysfunction (Begriche et al., 2011; Dykens et al., 2007; Marroquin et al., 2007; Nadanaciva et al., 2009; Pereira et al., 2009). Mitochondrial safety analysis for drug development https://www.nadcro.com/mitochondrial-toxicity-analysis-service.html?gclid=EAIaIQobChMIuJrvqPmn9QIVUR6tBh2cnQBkEAMYAiAAEgLqPPD_BwE