Fat Accumulation in Acute Liver Injury

Rees, K. R.; Shotlander, Valerie L.

doi:10.1111/j.1749-6632.1963.tb57092.x

Cited by 26 publications

(3 citation statements)

References 32 publications

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“…Ceramides, cholesterol, free fatty acids, and phosphatidylinositol also appeared in significant quantities while lower levels of phosphatidylethanolamine and galactoceramide were found with this procedure. Therefore, these plates showed that lysoPCs were a significant proportion of the lipid component of blood plasma in rodents and humans, as reported by others [ 16 , 38 - 43 ]. However, published reports or calculations made from published reports provide a fairly wide range of estimates of the total lysoPC concentration in plasma (145 to 270 μM).…”

Section: Resultssupporting

confidence: 82%

Product inhibition of secreted phospholipase A2 may explain lysophosphatidylcholines' unexpected therapeutic properties

2008

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Background: Lysophosphatidylcholines (lysoPCs) are products of phospholipase A2 (PLA2) enzyme activity, and like the enzyme, have a direct role in toxic inflammatory responses in variety of organ systems. Paradoxically, reduced plasma lysoPC levels have been noted in sepsis patients and systemic treatment with lysoPCs is therapeutic in rodent models of sepsis and ischemia. These observations suggest that elevation of plasma levels of these lipids can actually help to relieve serious inflammatory conditions. We demonstrate that specific lysoPCs act as uncompetitive product inhibitors of plasma secreted PLA2 enzymes (sPLA2s), especially under conditions of elevated enzyme activity, thus providing a feedback mechanism for the observed anti-inflammatory effects of these compounds.

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Section: Resultssupporting

confidence: 82%

Product inhibition of secreted phospholipase A2 may explain lysophosphatidylcholines' unexpected therapeutic properties

2008

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“…Antioxidants. NN'-Diphenyl-p-phenylenediamine, atocopherol acetate and promethazine hydrochloride were injected intraperitoneally as described by Di Luzio & Costales (1965) and Rees & Shotlander (1963). Promethazine was also used for some experiments in vitro, at a final concentration of 0-1 mM (Judah, Ahmed & McLean, 1963).…”

Section: Methodsmentioning

confidence: 99%

Further studies on the stimulation of glycolysis by previous aerobiosis

Gaja

Ragnotti

Cajone

et al. 1967

Biochemical Journal

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1. A short period of incubation in oxygen increases the rate of anaerobic glycolysis in all the normal adult tissues that have been tested, with the exception of erythrocytes. 2. This stimulation does not occur in the six different tumours and in the two embryonic tissues that have been studied. 3. In rat liver and in chicken heart, stimulation is first seen at birth. 4. Stimulation in rat liver slices is decreased in the presence of some inhibitors of oxidative metabolism (cyanide, Amytal, dinitrophenol, malonate), but is not affected if the aerobic preincubation is carried out at 1 degrees . 5. The presence in the medium of some metabolites that are known to be important regulators of the glycolytic rate in living tissues has essentially no effect on stimulation. 6. The pretreatment of animals with inhibitors of oxidative metabolism and with antioxidants does not suppress stimulation; the observed effect of NN'-diphenyl-p-phenylenediamine is probably the consequence of the fall of the glycogen content in the liver. 7. The stimulation of anaerobic glycolysis by previous aerobiosis could not be demonstrated in liver homogenates.

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“…On the other hand, we have found a significant decrease of reduced glutathione in the liver and erythrocytes (ROSENBERG unpublished), suggesting an inhibition of enzymes with active thiol groups . This would thus lead to a defective utilization and transport of triglycerides in the liver and to an accumulation of fat, i. e. the hepatotoxic sign of injury (REES & SHOTLANDER 1963). Chloroform and carbon tetrachloride are believed to act by this mechanism in the production of fatty liver (%HOLLER 1966).…”

Section: Discussionmentioning

confidence: 99%

Hepatotoxicity of Halothane Metabolites in Vivo and Inhibition of Fibroblast Growth in Vitro

Rosenberg

Wahlström

1971

Acta Pharmacologica et Toxicologica

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Following single intraperitoneal doses the halothane metabolites, trifluoroethanol (TFE) and trifluoroacetaldehyde hydrate (TFAIH), produced a marked dose-dependent accumulation of fat in mouse liver, the maximal effect occuring at about 24 hours after administration. Slight fatty changes already occurred with non-lethal doses, but repeated administration did not, however, cause necrosis of the liver cells. Electron microscopy suggested that part of the fat was composed of phospholipids, which are known to accumulate during energy loss. The glycogen granules almost completely disappeared in the liver, this being also confirmed by chemical determination. Trifluoroacetic acid (TFAA) not only caused slight fat accumulation, but also an increase in liver glycogen. In human fibroblast cell cultures TFAIH, even in small concentrations, and TFAA in high concentrations, inhibited cell growth. TFE did not affect the growth of the fibroblasts, probably because no enzymatic system is available in these cells to metabolize TFE to the toxic aldehyde. Two mechanisms may be responsible for the hepatotoxicity of TFE and TFAIH: a) formation of phospholipids due to energy requirement and b) accumulation of liver triglycerides due to blocking of e. g. transport enzymes.

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Fat Accumulation in Acute Liver Injury

Cited by 26 publications

References 32 publications

Product inhibition of secreted phospholipase A2 may explain lysophosphatidylcholines' unexpected therapeutic properties

Product inhibition of secreted phospholipase A2 may explain lysophosphatidylcholines' unexpected therapeutic properties

Further studies on the stimulation of glycolysis by previous aerobiosis

Hepatotoxicity of Halothane Metabolites in Vivo and Inhibition of Fibroblast Growth in Vitro

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