Arsenic is termed as a heavy metal that exist in three forms such as yellow, black, grey and in ionic forms .The symbol of arsenic is As and it has atomic number 33. Sodium arsenite and arsenic trichloride are the most common trivalent compound and arsenic acid; arsenates are the most common pentavalent compounds. Inorganic arsenic is more toxic compared to organic arsenic. It is considering as carcinogenic as it has potential to cause cancer. Most cellular functions will inhibit as this heavy metal reacts with proteins, primarily thiol groups and affects the process of oxidative phosphorylation. (Charles Patrick Davis, 2018)
Sources and exposure pathway
Toxicity depends on the sources of exposure (air, food, water). The primary exposure pathway is ingestion of food and water. Vegetables and meat contain relatively low levels of arsenic. Moreover, alcohol consumption is another potential source of exposure to arsenic due to the use of pesticides on grapes. Gastrointestinal tract and lungs are the main organs through which arsenic is readily absorbed and widely distributed to the most of the tissues of the organisms. Inhalation is considering as a minor pathway and dermal exposure is minimal. People also exposed to arsenic in the workplaces as a result arsenic accumulation occurs in the liver, kidney, lungs and skin. (Ebele, 2009)
The metabolism of arsenic compounds play an important role in its toxic effect. Metabolism involves methyl transferase, which catalyzes the oxidative methylation of pentavalent results in reduction to a trivalent state. Toxicity of arsenic compounds depend on its valence such as trivalent are more poisonous than pentavalent. However, reactive oxygen species (ROS) generation, Ca2+ accumulation, caspase-3 up-regulation, Bcl-2 down-regulation, and p-53 deficiency such factors are responsible for arsenic toxicity includes carcinogenicity, cardiovascular, testicular, genotoxicity, diabetes, and nervous systems disorders. Arsenic-induced cancer may include oxidative stress, and tumor promotion, genotoxicity, altered DNA methylation, altered cell proliferation. Arsenic is capable of inhibiting the DNA replication or repair enzymes and arsenate’s action as a phosphate analogue. Mitochondrial enzymes may be inhibit through arsenic compounds, which results in impaired tissue respiration. It can also react with thiol groups (- SH) of the enzymes or cofactors, which possess two thiol groups such as dihydrolipoic acid results in the alteration of various enzyme. The pyruvate dehydrogenase complex (pyruvate decarboxylase, dihydrolipoyl transa-cetylase, dihydrolipoyl dehydrogenase, thiamine pyrophosphate, lipoic acid, coASH, FAD, NAD+) catalyzes the conversion of pyruvate to acetyl CoA during tissue respiration. Arsenic may attack Dihydrolipoic acid as a result dihydrolipoyl dehydrogenase and dihydrolipoyl transa-cetylase being altered thereby affecting the conversion of lipoic acid to acetyl lipoic acid and in turn acetyl CoA. (Ebele, 2009), (Ghosh and Sil, 2015)
The symptoms of arsenic poisoning can be acute or chronic depending on the method of exposure.
Acute exposure: Exposure to arsenic within a short period results in adverse effect.
1.Vomiting , Diarrhea
2.Abdominal pain and cramping muscles
Chronic exposure: Exposure to arsenic over a long period results in permanent adverse effect.
3.Bone marrow depression
6.Peripheral neuropathy, encephalopathy
7.Hepatomegaly, cirrhosis altered heme metabolism
8.Proximal tubule degeneration, papillary and cortical necrosis. (Alana Biggers, 2018) , (Ebele, 2009)
1. Thoroughly washing and rinsing affected skin.
2. Blood transfusions if needed.
3. Heart medication needed if the heart starts failing.
4. To minimize the risk of potentially fatal heart rhythm problems mineral supplements should be given.
5. Kidney function monitoring.
6. Chelating agent. Such as:•Dimercaprol (BAL),
•Dimercaptosuccinicacid acid (DMSA),
•Dimercaptopanesulfonic acid (DMPS).
7. Syrup of ipecac
8. Gastric lavage (Hall, 2002), (Alana Biggers, 2018)