The Diagnostic Significance of Liver Cell Inhomogeneity: Serum Enzymes in Patients with Central Liver Necrosis and the Distribution of Glutamate Dehydrogenase in Normal Human Liver

Guder, W.G.; Habicht, Antje; Kleißl, J.; Schmidt, Udo; Wieland, O.

doi:10.1515/cclm.1975.13.7.311

Cited by 16 publications

(5 citation statements)

References 29 publications

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“…The increase in GLDH activity could be the result of a reduced oxygen saturation of hepatic venous blood during the race in some runners, causing liver cell damage and subsequent release of GLDH into the blood stream. Because the GLDH is unequally distributed within the liver lobule with a nearly twofold higher concentration in the centrolobular region as compared to the peripheral part (16), the greater sensitivity of the central area of the lobules to changes in oxygen supply (6) could even more contribute to the increased GLDH activity found in some runners (up to fifteenfold of the upper reference limit of 4 U/L). The relative hypoxia in liver is also consistent with measurements of Foigt Ct al.…”

Section: Discussionmentioning

confidence: 99%

Ultra-Long-Distance Running and the Liver*

Nagel

Seiler²,

Franz³

et al. 1990

Int J Sports Med

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During an ultra-long-distance race (1000 km in 20 days) the influence of running was examined on the enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), gamma-glutamyl-transferase (GGT), and glutamate dehydrogenase (GLDH) with regard to their release from the liver cells or their induction. Furthermore the liver synthetic capacity was assayed by measuring the enzyme activity of cholinesterase and the concentration of serum albumin during the race. Of the 110 participants, 55 finished the race and only the results of these runners were used in our study. AP increased continuously from day 0 (mean = 102 U/L) to day 19 (mean = 120 U/L). A fivefold increase of AST and a twentyfold increase of CK up to day 3 was followed by a significant decrease towards the end of the race. ALT rose as well up to day 6 from a mean value of 8 U/L to 24 U/L but remained at this level. Surprising was the individual increase of the enzymes GLDH (up to twentyfold) and GGT (up to sixfold) in more than half of the finishers on various days indicating liver cell injuries. The activity of CHE and the concentration of serum albumin decreased during the race, both were significantly correlated.

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Section: Discussionmentioning

confidence: 99%

Ultra-Long-Distance Running and the Liver*

Nagel

Seiler²,

Franz³

et al. 1990

Int J Sports Med

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“…Hence, enzyme release might depend on alterations in plasma membranes, mitochondrial dysfunction, and/or changes in cellular volume regulation [ 1 , 83 , 84 ]. In addition, the level of increased serum enzyme activities would also depend on the susceptibility of the liver cell type being damaged [ 85 , 86 ].…”

Section: Fluctuations Of Serum “Marker” Enzymes In the Model Of LImentioning

confidence: 99%

Is Liver Enzyme Release Really Associated with Cell Necrosis Induced by Oxidant Stress?

Contreras-Zentella

Hernández‐Muñoz

2015

Oxidative Medicine and Cellular Longevity

163

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Hepatic diseases are a major concern worldwide. Increased specific plasma enzyme activities are considered diagnostic features for liver diseases, since enzymes are released into the blood compartment following the deterioration of the organ. Release of liver mitochondrial enzymes is considered strong evidence for hepatic necrosis, which is associated with an increased production of ROS, often leading to greater hepatic lipid peroxidation. Lipotoxic mediators and intracellular signals activated Kupffer cells, which provides evidence strongly suggesting the participation of oxidant stress in acute liver damage, inducing the progression of liver injury to chronic liver damage. Elevated transaminase activities are considered as an index marker of hepatotoxicity, linked to oxidant stress. However, a drastic increase of serum activities of liver enzyme markers ought not necessarily to reflect liver cell death. In fact, increased serum levels of cytoplasmic enzymes have readily been observed after partial hepatectomy (PH) in the regenerating liver of rats. In this regard, we are now showing that in vitro modifications of the oxidant status affect differentially the release of liver enzymes, indicating that this release is a strictly controlled event and not directly related to the onset of oxidant stress of the liver.

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“…Different techniques (for recent reviews see [5,9,10]) have been employed to study metabolic zonation in hepatic nitrogen metabolism: histochemistry [12], immunohistochemistry [13][14][15][16][17], in situ hybridization [18,19], retrograde/antegrade liver perfusion [20,21], microdissection [22], autoradiography (B. Stoll, H. P. Buscher & D. Haiussinger, unpublished work), radiolabelincorporation studies [23,24], studies on zonal cell damage [25,26], use of micro-lightguides and mini-oxygen electrodes [27], attempts to separate periportal from perivenous hepatocytes [28][29][30] and the dual-digitonin-pulse perfusion [31]. These studies revealed a remarkable development of functional hepatocyte heterogeneity with respect to ammonia and glutamine metabolism.…”

Section: Acinar Organization Of Nitrogen-metabolizing Pathwaysmentioning

confidence: 99%

Nitrogen metabolism in liver: structural and functional organization and physiological relevance

Häussinger

1990

Biochemical Journal

316

166

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INTRODUCTIONThe liver was identified early in the fundamental work of Hans Krebs [1,2] as having a particular role in urea and glutamine metabolism. At the acinar level, these pathways are embedded into a sophisticated structural and functional organization with metabolic interactions between different hepatocyte populations. This provided a new insight into the role of the liver in maintaining ammoniat and bicarbonate homeostasis under physiological and pathological conditions.The functional units of the liver are the so-called acini [3,4], which extend from the terminal portal venule along the sinusoids to the terminal hepatic venule. Periportal hepatocytes (near the sinusoidal inflow) can be distinguished from more downstream located perivenous hepatocytes (near the sinusoidal outflow), whereas the borderline between the periportal and the perivenous compartment is not defined in general anatomical terms. The definition used here is a comparative-functional one, and thus will depend on the metabolic pathways under consideration. This is because periportal and perivenous hepatocytes differ in their complement of enzymes and their metabolic functions ('functional hepatocyte heterogeneity' or 'metabolic zonation'). The size of a periportal or perivenous 'metabolic zone' is pathway-specific. Thus, for example, a periportal compartment exhibiting a certain metabolic function can overlap with a perivenous compartment which is characterized by another pathway. Several reviews have appeared on this subject [5][6][7][8][9][10][11], and the subacinar localization of various metabolic pathways is summarized in Table 1. This article focuses on the functional significance of liver parenchymal cell heterogeneity in nitrogen metabolism.

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The Diagnostic Significance of Liver Cell Inhomogeneity: Serum Enzymes in Patients with Central Liver Necrosis and the Distribution of Glutamate Dehydrogenase in Normal Human Liver

Cited by 16 publications

References 29 publications

Ultra-Long-Distance Running and the Liver*

Ultra-Long-Distance Running and the Liver*

Is Liver Enzyme Release Really Associated with Cell Necrosis Induced by Oxidant Stress?

Nitrogen metabolism in liver: structural and functional organization and physiological relevance

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