Mayo Test Catalog, (Sorted By Test Name) - Mayo Medical ...

ASNA
89848
ASRU
89889
present in hair, as everybody is exposed to trace amounts of arsenic from the normal diet. The highest
hair arsenic observed at Mayo Clinic was 210 mcg/g dry weight in a case of chronic exposure that was
the cause of death.
Reference Values:
0-15 years: not established
> or =16 years: 0.0-0.9 mcg/g of hair
Clinical References: 1. Sthiannopkao S, Kim K-W, Cho KH, et al: Arsenic levels in human hair,
Kandal Province, Cambodia: The influences of groundwater arsenic, consumption period, age and gender.
Applied Geochemistry 2010;25:81–90 2. Pearse DC, Dowling K, Gerson, AR, et. al: Arsenic
microdistribution and speciation in toenail clippings of children living in a historic gold mining area.
Science of the Total Environment 2010;408:2590–2599
Arsenic, Nails
Clinical Information: Arsenic circulating in the blood will bind to protein by formation of a covalent
complex with sulfhydryl groups of the amino acid cysteine. Keratin, the major structural protein in hair
and nails, contains many cysteine residues and, therefore, is one of the major sites for accumulation of
arsenic. Since arsenic has a high affinity for keratin, the concentration of arsenic in nails is higher than in
other tissues. Several weeks after exposure, transverse white striae, called Mees' lines, may appear in the
fingernails.
Useful For: Detection of nonacute arsenic exposure
Interpretation: Nails grow at a rate of approximately 0.1 inch/month. Nail keratin synthesized today
will grow to the distal end in approximately 6 months. Thus, a nail specimen collected at the distal end
represents exposure of 6 months ago. Nail arsenic >1.00 mcg/g dry weight indicates excessive exposure.
It is normal for some arsenic to be present in nails, as everybody is exposed to trace amounts of arsenic
from the normal diet. The highest hair or nail arsenic observed at Mayo Clinic was 210 mcg/g dry weight
in a case of chronic exposure that was the cause of death.
Reference Values:
0-15 years: not established
> or =16 years: 0.0-0.9 mcg/g of nails
Clinical References: Hindmarsh JT, McCurdy RF: Clinical and environmental aspects of arsenic
toxicity. Crit Rev Clin Lab Sci 1986;23:315-347
Arsenic, Random, Urine
Clinical Information: Arsenic is perhaps the best known of the metal toxins, having gained notoriety
from its extensive use by Renaissance nobility as an antisyphilitic agent and, paradoxically, as an antidote
against acute arsenic poisoning. Even today, arsenic is still 1 of the more common toxicants found in
insecticides, and leaching from bedrock to contaminate groundwater. The toxicity of arsenic is due to 3
different mechanisms, 2 of them related to energy transfer. Arsenic covalently and avidly binds to
dihydrolipoic acid, a necessary cofactor for pyruvate dehydrogenase. Absence of the cofactor inhibits the
conversion of pyruvate to acetyl coenzyme A, the first step in gluconeogenesis. This results in loss of
energy supply to anaerobic cells, the predominant mechanism of action of arsenic on neural cells that rely
on anaerobic respiration for energy. Neuron cell destruction that occurs after long-term energy loss results
in bilateral peripheral neuropathy. Arsenic also competes with phosphate for binding to adenosine
triphosphate during its synthesis by mitochondria via oxidative phosphorylation, causing formation of the
lower energy adenosine diphosphate monoarsine. This results in loss of energy supply to aerobic cells.
Cardiac cells are particularly sensitive to this form of energy loss; fatigue due to poor cardiac output is a
common symptom of arsenic exposure. Arsenic furthermore binds avidly with any hydrated sulfhydryl
group on protein, distorting the 3-dimensional configuration of that protein, causing it to lose activity.
Interaction of arsenic with epithelial cell protein at the sites of highest physiologic concentration, the
Current as of January 3, 2013 2:22 pm CST 800-533-1710 or 507-266-5700 or MayoMedicalLaboratories.com Page 182