Porphyrins in Urine

Talman, Ellen L.; Schwartz, Samuel

doi:10.1016/b978-1-4831-9683-1.50021-6

Cited by 16 publications

(5 citation statements)

References 8 publications

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“…Blood protoporphyrin and haem contents were determined according to the method of Labbe et al (1979). Urinary coproporphyrin and uroporphyrin were estimated by the method of Talman (1958). whereas the concentration of urinary 5-aminolevulinic acid and porphobilinogen was determined by the method of Tomokuni and Ogata (1972) and Rimington (1971) respectively.…”

Section: Methodsmentioning

confidence: 99%

Porphyrin metabolism in some malignant diseases

El-Sharabasy

El-Waseef²,

Hafez³

et al. 1992

Br J Cancer

143

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Porphyrin metabolism was studied in 21 children of both sexes suffering from acute lymphoblastic leukaemia (ALL) and 34 adult patients of different ages and sexes suffering from ALL (n = 14), non-Hodgkin's lymphoma (NHL), n = 14, or Hodgkin's disease (HD), n = 6. In addition, two groups of healthy children (n = 14), and adults (n = 17) were studied for comparison. It was apparent from this study that the activity of uroporphyrinogen-1-synthetase (URO-1-S, E.C. 4.3.1.8) was highly significantly activated in the blood of children, while the activities of blood 5-aminolevulinic acid dehydrase (E.C. 4.2.1.24) and ferrochelatase (E.C. 4.99.1.1.), as expressed by protoporphyrin/haem ratio, were inhibited in those children. Also, free erythrocyte total porphyrins were increased, while the haem content was reduced. The concentrations of 5-aminolevulinic acid, coproporphyprin and uroporphyrin were increased in the urine of children with ALL. On the other hand, some dramatic changes were found in porphyrin metabolism in adult patients suffering from ALL, NHL and HD. The aforementioned disturbances were discussed in the light of some factors which may affect the enzymatic activities in the synthesis of porphyrins.

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Section: Methodsmentioning

confidence: 99%

Porphyrin metabolism in some malignant diseases

El-Sharabasy

El-Waseef²,

Hafez³

et al. 1992

Br J Cancer

143

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“…Urinary levels of uroporphyrin and coproporphyrin were determined fluorometrically, as described by Talman and Schwartz (14). Accompanying this decrease in heme biosynthetic pathway enzyme activities was a substantial elevation of urinary uroporphyrin and coproporphyrin levels in animals exposed to high doses of arsenic.…”

Section: Quantitation Of Urinary Heme Precursorsmentioning

confidence: 99%

Effects of Chronic Arsenic Exposure on Hematopoietic Function in Adult Mammalian Liver

Woods¹,

Fowler²

1977

Environmental Health Perspectives

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In these studies the effects of ingested arsenic (As+15) on hepatic heme biosynthetic capability and hemoprotein function in adult male rats were investigated. Animals exposed for 6 weeks to 0, 20, 40, or 85 ppm sodium arsenate in the drinking water suffered depression of hepatic 8-aminolevulinic acid (ALA) synthetase and heme synthetase (ferrochelatase) activities, with maximal decreases to 67 and 55% of control levels, respectively, at 85 ppm. Concomitantly, urinary uroporphyrin levels were elevated by as much as 12 times, and coproporphyrin by as much as 9 times, control values. The rate of incorporation of 3H-ALA into mitochondrial and microsomal hemes was depressed by 40-50%o at 20 ppm but was increased with regard to controls by as much as 150%o at the higher treatment levels. A similar biphasic pattern was observed in regard to "4C-leucine incorporation into cellular membranal proteins. In contrast, the levels of ALA dehydratase, uroporphyrinogen I synthetase, aminopyrine demethylase, and cytochrome P-450 were not significantly changed in As+5-treated rats. These results support the hypothesis that chronic, low level, arsenic exposure results in selective inhibition of mitochondrial-bound heme biosynthetic pathway enzymes (ALA synthetase and heme synthetase) resulting in a substantial increase in urinary porphyrins, uniquely characterized by a greater increase in uroporphyrin than coproporphyrin levels. These changes occur independent of, or prior to, alterations in hepatic hemoprotein-dependent functions and may thus serve in the clinical analysis of pretoxic exposure to arsenic compounds in human populations.

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“…Porphyrins and precursors: tn the original study (De Vilteneuve et al, 1964) uroporphyrin and uroporphyrinogen were determined spectrophotometrically according to Rimington and Sveinsson (11950) and Dresel and Falk (1956). For their isolation the method of Talman and Schwartz (1958) was followed.…”

Section: Methodsmentioning

confidence: 99%

A retrospective study of a patient with homozygous form of acute intermittent porphyria

Beukeveld

Wolthers

Nordmann

et al. 1989

J of Inher Metab Disea

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In 1964 a child with an exceptional form of porphyria was described; she excreted persistently excessive amounts of delta-aminolaevulinic acid, porphobilinogen and uroporphyrin in her urine from early childhood. The biochemical profile resembled that of acute intermittent porphyria (AIP). The child died at the age of 8 years. Reinvestigation of some urine samples by HPLC revealed differences in comparison with urines of other patients with AIP. The clinical picture characterized by porencephaly and severe retardation in development was completely different from that of AIP. Her mother suffered from AIP but the father never had attacks. Investigations on blood and urine samples of the father showed that he also was affected. Due to the early onset in the index patient, its persistent character, and the fact that both parents are affected we postulate retrospectively to have diagnosed a case of homozygous or a double heterozygous AIP, hitherto undescribed.

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Porphyrins in Urine

Cited by 16 publications

References 8 publications

Porphyrin metabolism in some malignant diseases

Porphyrin metabolism in some malignant diseases

Effects of Chronic Arsenic Exposure on Hematopoietic Function in Adult Mammalian Liver

A retrospective study of a patient with homozygous form of acute intermittent porphyria

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