Ion exchange analysis of porphyrins in urine

Pedersen, Jane Serup

doi:10.1080/00365517809108424

Cited by 15 publications

(2 citation statements)

References 11 publications

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“…The analytical method used was recently described in detail (With and Pedersen, 1978). The readings were performed in a Beckman Model 25 double beam recording spectrophotometer, and in all cases tracings in the region of 380-430 nm were performed to control the Soret maximum.…”

Section: Methodsmentioning

confidence: 99%

“…As we have recently (With and Pedersen, 1978) described an easy, rapid, and cheap ion exchange technique for the determination of total porphyrin in urine, we collected reference material of blood donors, laboratory personnel, and medical inpatients with this technique and included tracings of the absorption curve in the range 380-430 nm to get the best possible check on analytical accuracy.…”

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confidence: 99%

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Urinary total porphyrins by ion exchange analysis: reference values for the normal range and remarks on preformed prophyrins in acute porphyria urine.

Fogstrup¹,

With²

1979

J Clin Pathol

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SUMMARY Determination of total porphyrin with a rapid and easy method (ion exchange; spectrophotometry) was performed on 57 morning urine samples from laboratory personnel, 59 arbitrary day urine samples from blood donors, and 90 24-hour urines from medical inpatients. The upper reference limit for morning urine was 0'32 ,tmol/1 but even a value as high as 0 7 ,umol/l was found.In the donor urines the upper limit was 0-155 tkmol/l. The 24-hour urines showed an upper reference limit of 271 ug/24 h. These values are in good agreement with values from the literature, mostly based on extraction analyses. Tracings of the absorption curves in the region of 380-430 nm were performed in all analyses and showed that the non-porphyrin absorption was close to linear in most cases. Studies of porphyric urines gave no support to the claim that preformed porphyrins not formed from porphobilinogen are excreted in this disease.The reference values for urinary porphyrins in the normal range found in the literature are based on various techniques, but primarily on rather timeconsuming solvent extraction methods, while satisfactory reference materials based on the more rapid and simple ion exchange analysis have not been presented. As we have recently (With and Pedersen, 1978) described an easy, rapid, and cheap ion exchange technique for the determination of total porphyrin in urine, we collected reference material of blood donors, laboratory personnel, and medical inpatients with this technique and included tracings of the absorption curve in the range 380-430 nm to get the best possible check on analytical accuracy.We also included 10 patients with latent porphyria (acute intermittent type) from our material (With, 1969)

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Urinary total porphyrins by ion exchange analysis: reference values for the normal range and remarks on preformed prophyrins in acute porphyria urine.

Fogstrup¹,

With²

1979

J Clin Pathol

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Differential Expression of Hepatocyte Growth Factor, Transforming Growth Factor–α and Transforming Growth Factor–β1 Messenger Rnas in Two Experimental Models of Liver Cell Proliferation

et al. 1992

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Hepatocyte growth factor, a potent hepatocyte mitogen in vitro, appears to trigger hepatocyte regeneration after partial hepatectomy and after acute liver cell necrosis. Transforming growth factor-alpha and transforming growth factor-beta 1 may also be involved in the control of liver regeneration. In this study we assessed possible roles of hepatocyte growth factor, transforming growth factor-alpha and transforming growth factor-beta 1 on liver cell proliferation in vivo, using a model of choline deficiency that is associated with liver cell necrosis and a model of a hypolipidemic agent (4-chloro-6-(2,3 xylidino)-2-pyrimidinylthio (N-beta-hydroxyethyl) acetamide) without liver necrosis. Male F344 rats were fed a choline-deficient diet or 0.16% 4-chloro-6-(2,3 xylidino)-2-pyrimidinylthio (N-beta-hydroxyethyl) acetamide diet for 6 and 4 wk, respectively. Rats were killed periodically, and the expression of hepatocyte growth factor messenger RNA in the liver, lung and kidney was determined by Northern-blot analysis. The levels of transforming growth factor-alpha and transforming growth factor-beta 1 messenger RNAs in the liver were also determined. Feeding a choline-deficient diet for 1 to 6 wk led to gradual increases in the levels of hepatocyte growth factor, transforming growth factor-alpha and transforming growth factor-beta 1 messenger RNAs in the liver. Feeding a 4-chloro-6-(2,3 xylidino)-2-pyrimidinylthio (N-beta-hydroxyethyl) acetamide diet for 3 days and 2 wk induced marked enhancement of liver cell proliferation as judged by hepatocyte 5-bromo-2-deoxyuridine incorporation.(ABSTRACT TRUNCATED AT 250 WORDS)

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Immunoelectron microscopy identification of early proliferating cells in rat liver tissue during hyperplasia induced by lead nitrate

et al. 1993

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Recent studies have suggested that hepatic stem cells may be involved in at least some forms of liver epithelial growth. To obtain further information on this controversial hypothesis, we treated rats with lead nitrate to induce liver growth and identified the cells undergoing early DNA synthesis by bromodeoxyuridine immunohistochemistry, using both light and electron microscopic detection methods. Eight hours after an intravenous injection of lead nitrate 100 mumol/kg, DNA synthesis was detected in a few scattered hepatocytes and in nonparenchymal cells in portal connective tissue. At the light microscopic level, identification of nonparenchymal cells was limited to bile duct epithelial cells. Other cell types were also labeled, but their identity could not be established. At the ultrastructural level, however, four types of nonparenchymal cells were identified as containing bromodeoxyuridine immunogold particles. These four types included bile duct epithelial cells, fibroblasts, macrophages and nondescript periductular cells. These periductular cells displayed certain ultrastructural features of bile duct cells but did not line a lumen or display microvilli on their apical membrane, nor did they reside within the bile duct basement membrane. Because proliferation of nonparenchymal cells in portal areas preceded that of hepatocytes, it is suggested that the former reaction reflects a direct mitogenic effect of lead nitrate and not an adaptive growth response secondary to parenchymal enlargement. However, whether DNA synthesis in periductular cells or bile duct cells reflects activation of hepatic stem cells cannot be established from the present morphological observations. If so, such a progenitor compartment must be dormant because it does not seem to play a functional role in this and other forms of adult liver epithelial growth.

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Ion exchange analysis of porphyrins in urine

Cited by 15 publications

References 11 publications

Urinary total porphyrins by ion exchange analysis: reference values for the normal range and remarks on preformed prophyrins in acute porphyria urine.

Urinary total porphyrins by ion exchange analysis: reference values for the normal range and remarks on preformed prophyrins in acute porphyria urine.

Differential Expression of Hepatocyte Growth Factor, Transforming Growth Factor–α and Transforming Growth Factor–β1 Messenger Rnas in Two Experimental Models of Liver Cell Proliferation

Immunoelectron microscopy identification of early proliferating cells in rat liver tissue during hyperplasia induced by lead nitrate

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