Sodium arsenate is an exogenous inorganic compound with the formula AsH2NaO4 and an average molecular weight of 163.92 g/mol. It exists as a solid at room temperature. Sodium arsenate belongs to the alkali metal arsenates, a subclass of alkali metal oxoanionic compounds within the inorganic compounds. It is classified as a mixed metal/non-metal compound and functions biologically as a carcinogenic agent.
The compound interacts with 32 recorded protein targets. Arsenic binds to hemoglobin (HBA1, HBB), haptoglobin, and various forms of actin, including cytoplasmic 1 (ACTB), cytoplasmic 2 (ACTG1), alpha skeletal muscle (ACTA1), and aortic smooth muscle (ACTA2). It also binds to the glucocorticoid receptor (NR3C1) and the estrogen receptor (ESR1). Binding to XPA is believed to induce carcinogenesis by affecting DNA repair. Additionally, arsenic binds glutathione reductase, mitochondrial (GSR), which results in the inhibition of essential biochemical reactions, alteration of cellular redox status, and eventual cytotoxicity.
Sodium arsenate disrupts ATP production through several mechanisms. Within the citric acid cycle, it inhibits pyruvate dehydrogenase (PDHA1, PDHA2, PDHB, and DLAT). By competing with phosphate, it uncouples oxidative phosphorylation, thereby inhibiting mitochondrial respiration, energy-linked reduction of NAD+, and ATP synthesis. This process is accompanied by increased production of hydrogen peroxide, which may lead to oxidative stress and the formation of reactive oxygen species.
belongs to the class of inorganic compounds known as alkali metal arsenates. These are inorganic compounds in which the largest oxoanion is arsenate, and in which the heaviest atom not in an oxoanion is an alkali metal.
Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (9, 1)
Metabolism
Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (3)
Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (9, 3)
Symptoms
Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (9).
Treatment
Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (3)
