Arsenic is a cause of mortality throughout the world; associated problems include heart, respiratory, gastrointestinal, liver, nervous and kidney diseases.
Arsenic interferes with cellular longevity by allosteric inhibition of an essential metabolic enzyme pyruvate dehydrogenase (PDH) complex, which catalyzes the oxidation of pyruvate to acetyl-CoA by NAD. With the enzyme inhibited, the energy system of the cell is disrupted resulting in a cellular apoptosis episode. Biochemically, arsenic prevents use of thiamine resulting in a clinical picture resembling thiamine deficiency. Poisoning with arsenic can raise lactate levels and lead to lactic acidosis.
Genotoxicity involves inhibition of DNA repair and DNA methylation.  The carcinogenic effect of arsenic arises from the oxidative stress induced by arsenic.  Arsenic's high toxicity naturally led to the development of a variety of arsenic compounds as chemical weapons, e.g. dimethylarsenic chloride. Some were employed as chemical warfare agents, especially in World War I.  This threat led to many studies on antidotes and an expanded knowledge of the interaction of arsenic compounds with living organisms.  One result was the development of antidotes such as British anti-Lewisite.  Many such antidotes exploit the affinity of As(III) for thiolate ligands, which convert highly toxic organoarsenicals to less toxic derivatives. It is generally assumed that arsenates bind to cysteine residues in proteins.
By contrast, arsenic oxide is an approved and effective chemotherapeutic drug for the treatment of acute promyelocytic leukemia (APL).