Open AccessIn vivo study on lead and alcohol interaction and the inhibition of erythrocyte delta-aminolevulinic acid dehydratase in man.
Author(s) -
Spomenka Telišman,
D Prpic-Majic,
S Kezic
Publication year - 1984
Publication title -
scandinavian journal of work, environment and health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.621
H-Index - 103
eISSN - 1795-990X
pISSN - 0355-3140
DOI - 10.5271/sjweh.2335
Subject(s) - ingestion , porphobilinogen , urine , chemistry , dehydratase , alcohol , levulinic acid , excretion , medicine , endocrinology , ethanol , biochemistry , enzyme , catalysis
The effect on alcohol (EtOH) consumption on the inhibition of erythrocyte delta-amino-levulinic acid dehydratase (ALAD) was investigated in 13 male lead workers and 7 "normal" male subjects. Lead and zinc protoporphyrin in blood and lead, delta-aminolevulinic acid, porphobilinogen and coproporphyrin in 24-h urine specimens were also determined. During 1 h the subjects drank 122.8 (SD 18.65) ml of an almost lead-free brandy, ie, a dose of 11.07 mmol/kg of body weight. This dose resulted in a trend toward a parallel decrease in ALAD activity and an increase in lead in blood (PbB), both of which approached the prealcohol value 24 h after the initial alcohol ingestion. A trend toward increased lead excretion in urine (PbU) was observed on the day of alcohol ingestion, as compared to the preceding and succeeding 24-h urine specimens. However, the observed increase in PbB and PbU cannot be attributed to the small amount of lead ingested through the brandy, ie, 7.09 (SD 1.06) nmol. The characteristic dose-effect relationship between PbB and ALAD (examined prior to and 1, 3, 5, and 24 h after the initial alcohol ingestion) reached the highest correlation coefficient 3 h after the initial alcohol ingestion (p less than 0.001). The data obtained appear to support the hypothesis of a possible role for the body lead pool and the lead-mediated influence of alcohol consumption on ALAD activity in man.