Editing Arsenic (section)

=== Biological mechanism ===

Arsenic's toxicity comes from the affinity of arsenic(III) oxides for [[thiol]]s. Thiols, in the form of [[cysteine]] residues and [[Cofactor (biochemistry)|cofactors]] such as [[lipoic acid]] and [[coenzyme A]], are situated at the active sites of many important [[enzyme]]s.<ref name="Ullmann" />

Arsenic disrupts [[Adenosine triphosphate|ATP]] production through several mechanisms. At the level of the [[citric acid cycle]], arsenic inhibits [[lipoic acid]], which is a cofactor for [[pyruvate dehydrogenase]]. By competing with phosphate, arsenate uncouples [[oxidative phosphorylation]], thus inhibiting energy-linked reduction of [[Nicotinamide adenine dinucleotide|NAD+]], mitochondrial respiration and ATP synthesis. Hydrogen peroxide production is also increased, which, it is speculated, has potential to form reactive oxygen species and oxidative stress. These metabolic interferences lead to death from multi-system [[organ failure]]. The organ failure is presumed to be from [[necrotic]] cell death, not [[apoptosis]], since energy reserves have been too depleted for apoptosis to occur.<ref name="Hughes">{{cite journal |doi = 10.1016/S0378-4274(02)00084-X |title = Arsenic toxicity and potential mechanisms of action |date = 2002 |last1 = Hughes |first1 = Michael F. |journal = Toxicology Letters |volume = 133 |pages = 1–16 |pmid = 12076506 |issue = 1| url = https://zenodo.org/record/1260065 }}</ref>
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