This website was developed by undergraduate biology researchers working with Dr. Karen Bernd at Davidson College.

Dichloroacetic Acid (DCA)

What is DCA?  
Dichloroacetic acid (DCA) is a byproduct of the chlorine disinfection process (Uden & Miller, 1983) and produced in vivo during breakdown of trichloroethylene (TCE), a widely used industrial solvent (Stacpoole, 2011; Bull, 2000).
On one side DCA has shown potential in treating cancer metabolic disorders; on the other side, it can also be toxic and carcinogenic and can cause peripheral neuropathy.
  A B
DCA in the environment
  • DCA is so ubiquitous that some degree of chronic exposure is inevitable” (Stacpoole, 2011; Ammini & Stacpoole, 2003; IARC, 2004)
  • Drinking water:
    • 9th most prevalent contaminant in U.S. water systems (EWG, 2009)
    • Almost 130 million Americans are serviced by 12,002 water systems across 37 states that have levels of DCA above health guidelines (EWG, 2009)
  • Chlorinated Pools:
    • Dermal absorption of DCA – bathing or swimming in chlorinated pools (Stacpoole, 2011)
  • Showering inhalation (Xu & Weisel, 2003)
  • Produced in vivo during breakdown of trichloroethylene (TCE), a widely used industrial solvent (Bull, 2000)



Toxicology of DCA
  • Can cause reversible peripheral neuropathy in vivo (Stacpoole, 2011; Stacpoole, 1989; Moser et al., 1999; Calcutt et al., 2009)
  • Carcinogenic (IARC, 2004; Stacpoole et al., 1998)
    • The IARC (International Agency for Research on Cancer) classified DCA as possibly carcinogenic in humans, but has been proven carcinogen in experimental animals (IARC, 2004).
  • DCA inhibits its own breakdown, depending on an individual’s genetics and age. This delays the plasma clearance of DCA so in those people 'safe' levels of exposure could potentially accumulate to harmful levels with multiple exposures and(Stacpoole, 2011).
  • Studies have shown decreased viability and signs of oxidative stress in various types of cells exposed to DCA:
    • Macrophage cells (Hassoun & Ray, 2002)
    • Liver cells (Hassoun & Dey, 2008; Herren-Freund et al., 1987; Bull et al., 2002)
    • Different tissues exhibit varying sensitivities to DCA (Plewa et al., 2010)
    • lung cells (Bernd lab, unpublished results)
DCA and medicine
  • DCA inhibits pyruvate dehydrogenase kinase (PDK), which normally inactivates pyruvate dehydrogenase (PDH). PDH otherwise “primes: the citric acid cycle (Stacpoole, 2011). Thus, when DCA inhibits PDK, PDH remains active and favors the citric acid cycle. Consequences have been studied for:
  • This has been applied to metabolic and other diseases such as:
    • Congenital lactic acidosis, generally caused by a mutation leading to a disfunction in PDH (Stacpoole, 2006; Stacpoole, 1997; Stacpoole, 2003) – but treatment never passed trial phase because of incidences of reversible peripheral neuropathy (Stacpoole, 2006)
    • Diabetis (Stacpoole & Greene, 1992; Stacpoole, 1978)
    • Hyperlipoproteinemia (Stacpoole, 1978; Stacpoole, 1979), hypercholesteremia (Moore & Stacpoole, 1979)
    • Acute treatment of coronary heart disease (Wargovich et al., 1989), congestive heart failure (Bersin, 1994, Michelakis, 2002) 
    • DCA as metabolic therapy for myocardial ischemia and failure (Stacpoole, 1997)
  • Due to its metabolic effects, DCA has also been studied in relation to exercise both in health people and in people suffering from diseases such as COPD:
    • Initially, DCA showed promise in enhancing performance (Ludvik, 1993); however, in a later study adverse effects on the respiratory system following DCA administration outweighed those results (Ciufo, 2001)
    • Dichloroacetate Enhances Performance and Reduces Blood Lactate during Maximal Cycle Exercise in Chronic Obstructive Pulmonary Disease (Calvert, 2008)
  • DCA’s property of keeping PDH active, contributes to reversing the Warburg effect shifting them away from glycolysis inhibiting growth, but DCA also helps induce apoptosis (Bonnet et al., 2008; Wong et al., 2008; Madhok et al., 2010; Michelakis et al., 2010; Heshe, 2011). DCA has shown promise in treating cancer in the following types of cells:
    • non-small cell lung cells
    • glioblastoma cells (Michelakis et al., 2010)
    • breast cells
    • endometrial cells
    • colorectal cells (Madhok et al., 2010)
    • neuroblastoma (Vella, 2012)
    • epithelial ovarian cancer cells (Saed et al., 2011)
DCA in the Bernd lab
  • In our lab, we are conducting studies similar to those by Hassoun and Ray (2000), except that we are testing the effects of DCA on lung cells, specifically, rat alveolar type II cells.
  • The effects of DCA have not been studied on lung cells before, but adverse effects on the respiratory system from exercising after administration of DCA have been observed clinically (Ciufo, 2001).
  • Studies in our lab have shown decreased cell viability and signs of oxidative stress as suggested by increases in antioxidant enzymes superoxide dismutase (SOD) and catalase.
  • Our studies have shown exposure time and concentration dependent reactions to DCA.







Send comments, concerns or questions to Dr. Karen Bernd