: High
arsenic (As) levels in food and
drinking water, or under some occupational conditions, can precipitate chronic toxicity and in some cases
cancer. Millions of people are exposed to unacceptable amounts of As through
drinking water and food. Highly exposed individuals may develop acute, subacute, or chronic signs of
poisoning, characterized by skin lesions, cardiovascular symptoms, and in some cases, multi-organ failure. Inorganic
arsenite(III) and organic
arsenicals with the general formula R-As2+ are bound tightly to
thiol groups, particularly to vicinal dithiols such as
dihydrolipoic acid (DHLA), which together with some seleno-
enzymes constitute vulnerable targets for the
toxic action of As. In addition, R-As2+-compounds have even higher affinity to
selenol groups, e.g., in
thioredoxin reductase that also possesses a
thiol group vicinal to the
selenol. Inhibition of this and other ROS scavenging seleno-
enzymes explain the oxidative stress associated with
arsenic poisoning. The development of
chelating agents, such as the dithiols BAL (dimercaptopropanol),
DMPS (dimercapto-
propanesulfonate) and
DMSA (
dimercaptosuccinic acid), took advantage of the fact that As had high affinity towards vicinal dithiols. Primary prevention by reducing exposure of the millions of people exposed to unacceptable As levels should be the prioritized strategy. However, in acute and subacute and even some cases with chronic As
poisonings chelation treatment with therapeutic dithiols, in particular
DMPS appears promising as regards alleviation of symptoms. In acute cases, initial treatment with BAL combined with
DMPS should be considered.