Effect of alcohol on δ-aminolevulinic acid dehydratase and porphyrin metabolism in man

Sieg, I; Doss, M.; Kandels, Hubert; Schneider, Jürgen

doi:10.1016/0009-8981(91)90051-d

Cited by 24 publications

(8 citation statements)

References 25 publications

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“…Chronic alcohol intake and acute alcohol intake may have di!erent e!ects on heme metabolism, since the induction on hemoproteins occurs only in chronic alcoholism (Lieber, 1988). Unlike previous reports in alcoholic subjects (Sieg et al, 1991), the results reveal that measurement of erythrocyte ALA-D activity is not an adequate marker of chronic alcoholism in the rat.…”

Section: Discussioncontrasting

confidence: 99%

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Nonsynergic Effect of Ethanol and Lead on Heme Metabolism in Rats

Santos

Fontanellas

Morán

et al. 1999

Ecotoxicology and Environmental Safety

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Section: Discussioncontrasting

confidence: 99%

“…Hypoactivity of ALA-D has been reported in chronic alcoholism (Sieg et al, 1991), and this inhibition can be accompanied by increased urinary excretion of ALA and porphyrins (Schoenfeld et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Nonsynergic Effect of Ethanol and Lead on Heme Metabolism in Rats

Santos

Fontanellas

Morán

et al. 1999

Ecotoxicology and Environmental Safety

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“…By themselves, these factors are not able to cause PCT, but their role is important as they cause a partial disorder of heme biosynthesis and aggravate the hepatopathy, which is usually associated with PCT. [25][26][27] In our patient series, 65% of the patients had high alcohol intake at onset of PCT. The patients in the active phase of the disease had iron overload.…”

Section: Discussionmentioning

confidence: 62%

“…Alcohol inhibits certain enzymes in the heme biosynthetic pathway 25 and consumes heme, as it induces the synthesis of the cytochromes P450 like P450IIEI. 26 The fact that iron plays a role in PCT is certain 19 and confirmed by the study of experimental models.…”

Section: Discussionmentioning

confidence: 99%

Hepatic uroporphyrinogen decarboxylase activity in porphyria cutanea tarda patients: The influence of virus C infection

et al. 1998

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Porphyria cutanea tarda (PCT) is caused by a decreased activity of the hepatic enzyme uroporphyrinogen decarboxylase (URO-D). This deficiency causes overproduction, hepatic deposition, and increased excretion of uroporphyrin. Iron overload and hepatic viral infections are considered aggravating factors of the disease. Two forms of PCT have been described, as follows: a familial one with an inherited decrease of URO-D activity in all tissues and a sporadic one with a decreased activity of URO-D restricted to the liver. To assess whether the hepatic URO-D returns to normal during a remission of the disease, this activity was measured in liver biopsy samples in 24 sporadic PCT patients. The hepatic and urinary porphyrin concentrations were also measured. Viral status and histopathological findings were analyzed to assess their involvement in PCT. Six patients treated by phlebotomy to reduce hepatic iron and who were considered to be in clinical remission, characterized by a disappearance of cutaneous lesions, showed higher hepatic URO-D activities and lower hepatic porphyrin concentrations than did patients with overt PCT. The medians of these variables, however, did not achieve normal values. The hepatic URO-D activity showed a significant inverse relationship with both hepatic porphyrins and urinary uroporphyrin excretion. Hepatic URO-D activity was not reduced by hepatitis C virus (HCV) infection and liver damage. We conclude that the achievement of remission in PCT largely depends on the transient normalization of hepatic URO-D activity. A small increase in hepatic coproporphyrin in nonporphyric patients could reflect hepatic injury/iron/alcohol-induced oxidative stress oxidizing the accumulated heme precursors rather than a direct effect on hepatic URO-D enzyme. (HEPATOLOGY 1998; 27:584-589.)

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“…The disease entities that have been reported' to show elevated PBG-D activity in the blood include hemolytic anemia, iron deficiency anemia, sideroblastic anemia, lead poisoning, liver cirrhosis, and chronic alcohol consumption (Sieg et al, 1991;Kondo et al, 1990). The disease entities that have been reported' to show elevated PBG-D activity in the blood include hemolytic anemia, iron deficiency anemia, sideroblastic anemia, lead poisoning, liver cirrhosis, and chronic alcohol consumption (Sieg et al, 1991;Kondo et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Effect of Beryllium Chloride on Porphyrin Metabolism in Pregnant Mice Administered by Subcutaneous Injection

Sakaguchi¹

1997

Journal of Toxicology and Environmental Health Part A

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The effect of beryllium (Be) compounds on porphyrins was investigated in pregnant mice. The blood protoporphyrin (Proto) and zinc protoporphyrin (Zn Proto) concentrations were increased in pregnancy. Regardless of pregnancy or nonpregnancy, the Proto concentration was decreased after Be injection. Delta-aminolevulinic acid dehydratase (ALA-D) and porphobilinogen deaminase (PBG-D) activities in blood were significantly elevated in the pregnant untreated (Con-pregnant) group, compared to the nonpregnant mice untreated (Connonpregnant) and nonpregnant mice treated with Be (Be-nonpregnant) groups. The blood ALA-D activity of the pregnant mice treated with Be (Be-pregnant group) tended to decrease, compared to Con-pregnant group. The blood PBG-D activity in the Be-pregnant group was significantly lower compared with that of the Con-pregnant group. The ALA-D and PBC-D activities in the spleen were also significantly elevated in the Con-pregnant group, compared to nonpregnant groups. However, it was noted that these values in the Be-pregnant group were almost the same as that of the Con-nonpregnant group and were significantly lower than that in the Con-pregnant group. The elevation of A M -D and PBG-D activities in the blood and spleen, which play a role in the hematopoietic function of mice, was observed in the Con-pregnant mice compared to the nonpregnant mice. However, the phenomenon was not observed in the Be-pregnant mice, it suggesting that Be suppressed the pregnancy-induced increase in hematopoietic function.

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Effect of alcohol on δ-aminolevulinic acid dehydratase and porphyrin metabolism in man

Cited by 24 publications

References 25 publications

Nonsynergic Effect of Ethanol and Lead on Heme Metabolism in Rats

Nonsynergic Effect of Ethanol and Lead on Heme Metabolism in Rats

Hepatic uroporphyrinogen decarboxylase activity in porphyria cutanea tarda patients: The influence of virus C infection

Effect of Beryllium Chloride on Porphyrin Metabolism in Pregnant Mice Administered by Subcutaneous Injection

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