What is the Biologic Fate of Arsenic in the Body?

Metabolism

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Arsenic is absorbed into the blood stream at the cellular level and is taken up by

• red blood cells,
• white blood cells, and
• other cells that reduce arsenate to arsenite [Winski and Carter ; Wang et al. ].

Reduction of arsenate (As V) to arsenite (As III) is needed before methylation can occur. This reaction requires glutathione (GSH) [Miller et al. ; Vahter et al. ].

A portion of arsenite (As III) is methylated in the liver by enzymatic transfer of the methyl group from S-adenosylmethionine (SAM) to methyl arsonate (MMA V) and dimethyl arsenate (DMA V) [Aposhian et al. ; Styblo et al. ].

The resulting metabolites are more readily excreted.

Methylation has long been considered the main route of arsenic detoxification, but more recently there has been a growing body of literature supporting other detoxification mechanisms. For example, a number of animal species lack arsenic methylation and excrete inorganic arsenic [Vahter ]. The implication is that there may be other more important arsenic detoxification mechanisms in mammals. Other studies have suggested additional detoxification mechanisms such as

• antioxidant defenses,
• resistance to apoptosis, or
• transport [Yoshida et al. ].

There have also been studies of arsenic metabolism suggesting that methylation of inorganic arsenic may be a toxification, rather than a detoxification pathway and that trivalent methylated arsenic metabolites, particularly monomethylarsonous acid (MMA III) and dimethylarsinous acid (DMA III), are 'unusually capable of interacting with cellular targets such as proteins and DNA' [Kitchin ].

Methylation efficiency in humans appears to decrease at high arsenic doses. Patterns of methylated arsenic species in urine are similar between siblings and between siblings and parents, which suggests that arsenic methylation is genetically linked [Chung et al. ].

When the methylating capacity of the liver is exceeded, exposure to excess levels of inorganic arsenic results in increased retention of arsenic in soft tissues.

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Treatment and Management'Acute Over Exposure

Gut decontamination and hemodynamic stabilization are key factors in the initial management of acute arsenic intoxication.

Patients with suspected acute arsenic poisoning generally require rapid stabilization with fluid and electrolyte replacement in an intensive care setting.

• Aggressive intravenous fluid replacement therapy may be life'saving in severe poisoning.
• Gastric lavage may be useful soon after an acute ingestion to prevent further absorption.
• The efficacy of activated charcoal is controversial, but its administration together with a cathartic (such as sorbitol) is frequently recommended.
• If profuse diarrhea is present, cathartics should be withheld.
• Hemodialysis may be beneficial in a patient with concomitant renal failure.

Chelating agents administered within hours of arsenic absorption may successfully prevent the full effects of arsenic toxicity.

Dimercaprol (2, 3 dimercaptopropanol, also known as British anti Lewisite or BAL), was previously the most frequently recommended chelating agent for arsenic. The currently recommended treatment is 2-3-dimercapto-1-propanesulfonate (DMPS) or meso 2, 3-dimer-captosuccinic acid (DMSA). These are more water soluble than BAL, and can be administered orally with lower toxicity [Mazumder et. al. ].

All known chelating agents have adverse side effects and should be used with caution.

• In animal models, the efficacy of chelation therapy generally declines as the time elapsed since exposure increases.
• If patients are treated within several hours after arsenic ingestion, chelation is likely to be beneficial. Therefore, even if arsenic ingestion is only suspected, but not confirmed, consultation with a clinical specialist with expertise in the treatment and management of arsenic poisoning is key.

Data supporting duration of treatment are limited, and regimens may warrant adjustment. If acute renal insufficiency develops, hemodialysis may be of value.

If the source of arsenic exposure has not been determined, the patient may be at risk for further arsenic intoxication.

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