Dichloroacetic acid (DCA), sometimes known as bichloroacetic acid, is a chemical compound with the formula CHCl2 (BCA).
2COOH has a chemical structure with acetic acid, but with two of the three hydrogens in the methyl group substituted by chlorine atoms. Similar to other chloroacetic acids, this one has a wide range of potential applications. Salts and esters of dichloroacetic acid are known as dichloroacetates. DCA salts have been studied as potential medications due to their ability to inhibit pyruvate dehydrogenase kinase.
Studies on animals and in test tubes suggest that DCA may slow the progression of certain malignancies, but there is not yet enough evidence to recommend using it in DCA for cancer treatment.
A language based on hemispheres and randomness
Dichloroacetic acid, like other halogenated organic acids, has a unique chemical composition. Associating with the family of chloroacetic acids. It is the dichloroacetate ion that is produced when the acid is diluted with water. Pure dichloroacetic acid, with a pKa of 1.35, is a potent organic acid that, if breathed, may severely damage the upper respiratory tract’s mucous membranes and airway passageways.
Seaweed, at least Asparagopsis taxiformis, has been discovered to naturally contain DCA. It is a trace result of the chlorination of drinking water and is produced during the metabolism of several drugs and substances containing chlorine. DCA is typically made by reducing trichloroacetic acid (TCA). Chloral hydrate may be converted into DCA by mixing it with calcium carbonate, sodium cyanide, and water, then adding hydrochloric acid. It’s also possible to use hypochlorous acid to react with acetylene.
In the laboratory, DCA and TCA are often used as precipitants to convert macromolecules like proteins from a solution to a solid.
Therapy Efficiency
Local chemical vaporization
DCA and TCA are used for both topical genital wart chemoablation and cosmetic operations (such as chemical peels and tattoo removal). It may also be used to kill off good cells.
Lactic acidosis
Though DCA was well tolerated in a randomized controlled trial, it did not enhance clinical outcomes for newborns with congenital lactic acidosis. A second trial of DCA for MELAS (a disorder of low mitochondrial activity leading to lactic acidosis) found that all 15 children who participated in the research had significant nerve damage without any sign of benefit from the drug, necessitating the early cancellation of the investigation. DCA decreased blood lactate levels in adults with lactic acidosis, however the drug had no therapeutic impact and did not improve patients’ hemodynamics or survival in the research.
Therefore, controlled trials have shown no therapeutic efficacy of DCA in this circumstance, despite earlier case reports and preclinical research suggesting DCA may be beneficial for lactic acidosis. In addition, rising toxicities prevented patients from continuing to use DCA as a study drug in clinical trials.
Cancer
Media and internet sources stated in 2007 that University of Alberta researchers Evangelos Michelakis and colleagues had shown that sodium dichloroacetate (the sodium salt of dichloroacetic acid) shrank tumors in rats and eliminated cancer cells in vitro. Unprecedented interest among readers” was shown in a recent story in New Scientist on a “cheap and straightforward therapy” that is “known to be fairly safe” and can cure most malignancies. According to an editorial accompanying the study, the inability to patent the chemical means that no drug company will work to have it approved as a cancer medication. There was a follow-up paper in the journal that outlined the potential side effects, such as nerve damage. Selling chemicals under the false pretense that they are cancer cures without first receiving FDA approval is now unlawful in the United States.
In 2012, when asked if DCA should be used in cancer treatment, the American Cancer Society said, “available evidence does not support the use of DCA at this time.” Several medical professionals have stressed the need of taking precautions before using DCA and have warned against its use outside of a controlled clinical trial. If you’re interested in doing this, you could run into trouble obtaining the chemical. A 33-month sentence was handed down to a scam artist who targeted cancer patients by claiming the white powder he sold them contained the drug DCA when it was really simply starch.
Nonetheless, only five persons with glioblastoma were included in the sole controlled in-person administration of DCA to humans, and the purpose of the study was not to assess the drug’s efficacy against their condition. Instead, this study aimed to determine whether a certain dose could be given without triggering any negative reactions (e.g. neuropathy). All 5 people who took part in the study were also receiving other therapies. It seems that DCA may kill glioblastoma cancer cells by inducing their abnormal mitochondria to depolarize, which in turn triggers the cells’ own apoptosis, based on results from in vitro and ex vivo studies (programmed cell death). In vitro research on neuroblastomas, which have poorly understood mitochondrial abnormalities, has demonstrated that DCA is effective against malignant, undifferentiated cells. In a case report published in 2016, DCA’s potential application in treating central nervous system malignancies is examined and evaluated. Published in 2018, study showed that DCA promoted a metabolic switch in tumor cells from glycolysis to mitochondrial OXPHOS (the Warburg effect) and an increase in reactive oxygen stress. This behavior was not seen in normal cells.
Neuropathy
Some DCA clinical studies were discontinued because to neuropathy, although a 2008 research in the British Journal of Clinical Pharmacology found that this problem did not develop in other DCA trials. It is unclear how DCA produces neuropathy. Neurons cultured in vitro have shed light on how DCA produces its neuropathic side effect. DCA was shown to induce dose- and time-dependent demyelination of neurons (stripping of the nerve’sheath), which was partially reversible over time after the medication was withdrawn. Although, in 2008, researchers analyzed the same data and determined that “this neurotoxicity matched the pattern of length-dependent, axonal, sensory polyneuropathy without demyelination.” A study by Kaufman et al. from 2006 was cited.
Long-term heart failure
DCA has been investigated as a possible therapeutic for recovery after ischemia.
An additional benefit of DCA is that it speeds up metabolism by boosting NADH production, albeit this may lead to NADH depletion in the presence of enough oxygen.
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