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Altered Urinary Porphyrin Excretion in a Human Po p ulation Chronically Exposed to Arsenic in Mexico

MRC Toxicology Unit, Hodkin Building, University of Leicester, Lancaster Road, Leicester LE1 9HN, UK

Luz M. Del Razo

Sección de Toxicologia Ambiental, Departamento de Farmacologia y Toxicologia, CINVESTAV-IPN, P.O. Box 14-740, Mexico, DF 07000, México

Mariano E. Cebrián

Sección de Toxicologia Ambiental, Departamento de Farmacologia y Toxicologia, CINVESTAV-IPN, P.O. Box 14-740, Mexico, DF 07000, México

Arnulfo Albores

Sección de Toxicologia Ambiental, Departamento de Farmacologia y Toxicologia, CINVESTAV-IPN, P.O. Box 14-740, Mexico, DF 07000, México

Patricia Ostrosky-Wegman

Instituto de Investigaciones Biomédicas, UNAM, México, DF, México

Regina Montero

Instituto de Investigaciones Biomédicas, UNAM, México, DF, México

Maria E. Gonsebatt

Instituto de Investigaciones Biomédicas, UNAM, México, DF, México

Chang K. Lim

MRC Toxicology Unit, Hodkin Building, University of Leicester, Lancaster Road, Leicester LE1 9HN, UK

Francesco De Matteis

MRC Toxicology Unit, Hodkin Building, University of Leicester, Lancaster Road, Leicester LE1 9HN, UK

1 A detailed study of the urinary excretion pattern of porphyrins in humans chronically exposed to As via drinking water was performed using high performance liquid chromatography (HPLC)

2 Thirty-six individuals (15 men and 21 women) were selected from a town which had 0.400 mg L ^-1 of As in drinking water. The control group consisted of thirty-one individuals (13 men and 18 women) whose As concentration in drinking water was 0.020 mg L^-1.

3 The major abnormalities in the urinary porphyrin excretion pattern observed in arsenic-exposed individuals were: (a) significant reductions in coproporphyrin III excretion resulting in decreases in the COPRO III/COPRO I ratio, and (b) significant increases in uroporphyrin excretion. Both alterations were responsible for the decrease in the COPRO/URO ratio.

4 No porphyrinogenic response was found in individuals with urinary As concentrations below 1,000 µg of As g^-1 of creatinine, However, as arsenic concentrations exceeded this value, the excretion of porphyrins (except coproporphyrin III) increased proportionally.

5 The prevalence of clinical signs of arsenicism showed a direct relationship to both As concentration in urine and time-weighted exposure to As. A direct relationship between time-weighted exposure and alterations in urinary porphyrin excretion ratios was also observed.

6 The alterations found are compatible with a lower uroporphyrinogen decarboxylase activity in arsenic-exposed individuals. However, the similarities in the urinary porphyrin excretion pattern between As-exposed individuals and Dubin-Johnson syndrome patients suggest that impairments in the excretion of coproporphyrin isomers may also contribute to the pattern observed.

Human & Experimental Toxicology, Vol. 13, No. 12, 839-847 (1994)
DOI: 10.1177/096032719401301204


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