1. Arsenic species excretion after dimercaptopropanesulfonic acid (DMPS) treatment of an acute arsenic trioxide poisoning
R. Heinrich-Ramm, K.H. Schaller, J. Horn J. Angerer. Arch Toxicol (2003) 77: 63–68
Arsenic trioxide has a century-long history as a human poison and cases of acute intoxication due to its oral ingestion, e.g. in order to commit suicide, may still be observed nowadays (Foa et al. 1984; Lovell and Farmer 1985; Moore et al. 1994; Kruszewska et al. 1996; Wax and Thornton 2000; Blythe and Joyce 2001). The clinical therapy of choice is the administration of sulfhydryl-containing chelators as DMPS (2,3-dimercaptopropane-1-sulfonic acid, sodium salt), DMSA (meso-2,3-dimercaptosuccinic acid) or, formerly, BAL (British anti-Lewisite, 2,3-dimercaptopropanol). These dimercapto chelators compete with sulfhydrylic groups in tissues or enzymes for binding arsenic trioxide. This results in a more eﬀective elimination of arsenic. Among them, DMPS (Dimaval) is considered to be favoured because it has a high therapeutic index (in protecting experimental animals from a lethal dose of arsenic trioxide) (Aposhian et al. 1984) and a low acute toxicity. In contrast to BAL, DMPS is water-soluble and may be administered orally (bioavailability 39%) or intravenously, and not only by (painful) intramuscular injection (Hurlbut et al. 1994; Muckter et al. 1997). DMPS is rapidly eliminated via the kidneys, mainly as disulphide metabolites and, to a smaller percentage, as the parent compound (half-life of total DMPS 20 h) (Hurlbut et al. 1994).
2. DMPS reverts morphologic and mitochondrial damage in OK cells exposed to toxic concentrations of HgCl2
Pilar Carranza-Rosales, Nancy E. Guzman-Delgado, Delia E. Cruz-Vega. Cell Biol Toxicol 2007; 23: 163–176.
DMPS antioxidant activity
The antioxidant activity ofDMPSwas determined in vitro by comparing the chemical reduction of
DPPH by DMPS, versus DMSA, and DPA according to Zhang et al. (2005), with minor modiﬁcations. Brieﬂy, on a 96-well microplate, 150 μl of 150 μM DPPH solution in methanol were added to 50 μl of the chelating agents tested at 100 μM in methanol. The microplate was incubated for 30min at roomtemperature, protected by the light. Absorbance at 545 nm was determined after the incubation period, and the scavenging activity (DPPH reduction), which directly correlates with antioxidant activity, was calculated as a percent-age of the radical reduction. Ascorbic acid was used as positive control, and the vehicle as negative control.