The peroxisome proliferator nafenopin does not suppress hepatocyte apoptosis in guinea-pig liver in vivo nor in human hepatocytes in vitro

1998 ◽  
Vol 72 (12) ◽  
pp. 777-783 ◽  
Author(s):  
Susan C. Hasmall ◽  
Neil H. James ◽  
Anthony R. Soames ◽  
Ruth A. Roberts
Keyword(s):  
Guinea Pig ◽  
Human Hepatocytes ◽  
Peroxisome Proliferator ◽  
Hepatocyte Apoptosis ◽  
Pig Liver ◽  
Guinea Pig Liver

In vitro and in vivo studies on the metabolism of estrogens and their sulfates in guinea pigs

1977 ◽  
Vol 55 (4) ◽  
pp. 390-397 ◽  
Author(s):  
R. Hobkirk ◽  
D. J. Freeman ◽  
P. R. C. Harvey ◽  
Mona Nilsen ◽  
Barbara Jennings
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Mature Male ◽  
In Vivo Studies ◽  
Pig Liver ◽  
Male And Female ◽  
Estradiol 17Β ◽  
Guinea Pig Liver

Labelled estradiol-17β(E2) or estrone (E1), when incubated with guinea pig liver slices, is metabolized by two main pathways. Part of each substrate is converted to estrone-3-glucuronide and estradiol-3-glucuronide. A further part of each is metabolized to estradiol-3-sulfate (E23S) and estrone-3-sulfate (E13S), which are interconverted. The latter conjugate appears to be the substrate for a 16α-hydroxylase forming 16α-hydroxyestrone-3-sulfate (16αOHE13S). This, in turn, is further sulfurylated to yield 16α-hydroxyestrone-3,16-disulfate, accompanied by estriol-3,16-disulfate. A relatively small amount of tentatively identified '6-hydroxyestrone disulfate' accompanies these other two diconjugates. The guinea pig liver system suggests itself as a useful and relatively simple model for further study of 16α-hydroxylation of E13S. The use of the latter as a natural substrate in the system in vitro is supported by our observation that E13S and E23S are present in liver, kidney, blood, gallbladder bile, intestine, uterus, and placenta after injection of labelled E2 into mature male and female guinea pigs. Some evidence has been obtained for the disulfate fraction (above) in liver and bile after injection of labelled E1.

Precision-cut Guinea-pig Liver Slices as a Tool for Studying the Toxicity of Volatile Anaesthetics

1990 ◽  
Vol 18 (1_part_1) ◽  
pp. 191-199
Author(s):  
Hanan N. Ghantous ◽  
Jeanne Fernando ◽  
Scott E. Morgan ◽  
A. Jay Gandolfi ◽  
Klaus Brandel
Keyword(s):  
Guinea Pig ◽  
Rank Order ◽  
Normal Liver ◽  
Liver Slice ◽  
Volatile Anaesthetics ◽  
Pig Liver ◽  
Liver Slices ◽  
Guinea Pig Liver ◽  
Krebs Henseleit Buffer

Cultured precision-cut liver slices retain normal liver architecture and physiological biochemical functions. Hartley male guinea-pig liver slices have proven to be a good model for studying the biotransformation and toxicity of halothane. This system was used to evaluate the biotransformation and toxicity of different volatile anaesthetics (halothane, enflurane, isoflurane and sevoflurane), and compare their effects to those of new anaesthetics (desflurane). Liver slices (250–300μm thick) were incubated in sealed roller vials, containing Krebs Henseleit buffer at 37°C under 95% O2:5% CO2 atmosphere. Volatile anaesthetics were delivered by volatilisation after pre-incubation for 1 hour to produce a constant concentration in the medium. Production of the metabolites, trifluroacetic acid and fluoride ion, was measured. Intracellular potassium ion content, protein synthesis and secretion were determined as indicators of viability of the slices. The rank order of biotransformation of anaesthetics by the liver slices was halothane >sevoflurane>isoflurane and enflurane>desflurane. The rank order of hepatotoxicity of these anaesthetics was halothane>isoflurane and enflurane>sevoflurane and desflurane. Halothane is the anaesthetic which is metabolised furthest and has the most toxic effect, while desflurane is the least metabolised anaesthetic and has the least toxicity. This in vitro cultured precision-cut liver slice system appears to be suitable for studying the biotransformation of volatile anaesthetics and correlating its role in the resulting toxicity.

scholarly journals Guinea-pig liver tryptophan pyrrolase. Absence of detectable apoenzyme activity and of hormonal induction by cortisol and possible regulation by tryptophan

1974 ◽  
Vol 138 (3) ◽  
pp. 445-451 ◽  
Author(s):  
Abdulla A.-B. Badawy ◽  
Myrddin Evans
Keyword(s):  
Guinea Pig ◽  
Liver Enzyme ◽  
Guinea Pigs ◽  
Actinomycin D ◽  
The Other ◽  
Pig Liver ◽  
Latent Form ◽  
Tryptophan Pyrrolase ◽  
Guinea Pig Liver

1. When assayed in fresh homogenates, guinea-pig liver tryptophan pyrrolase exists only as holoenzyme. It does not respond to agents that activate or inhibit the rat liver enzyme in vitro. Only by aging (for 30min at 5°C) does the guinea-pig enzyme develop a requirement for ascorbate. 2. The guinea-pig liver enzyme is activated by the administration of tryptophan but not cortisol, salicylate, ethanol or 5-aminolaevulinate. 3. The tryptophan enhancement of the guinea-pig liver pyrrolase activity is prevented by 0, 34 and 86% by pretreatment with actinomycin D, cycloheximide or allopurinol respectively. 4. The guinea-pig liver tryptophan pyrrolase is more sensitive to tryptophan administration than is the rat enzyme. On the other hand, the concentrations of tryptophan in sera and livers of guinea pigs are 45–52% less than those in rats. 5. It is suggested that tryptophan may regulate the activity of guinea-pig liver tryptophan pyrrolase by mobilizing a latent form of the enzyme whose primary function is the detoxication of its substrate.

scholarly journals Changes in Lipopolysaccharide O Antigen Distinguish Acute versus Chronic Leptospira interrogans Infections

2005 ◽  
Vol 73 (6) ◽  
pp. 3251-3260 ◽  
Author(s):  
Jarlath E. Nally ◽  
Emilie Chow ◽  
Michael C. Fishbein ◽  
David R. Blanco ◽  
Michael A. Lovett
Keyword(s):  
Monoclonal Antibody ◽  
Guinea Pig ◽  
Pulmonary Hemorrhage ◽  
Asymptomatic Infection ◽  
Renal Tubules ◽  
Pig Liver ◽  
O Antigen ◽  
Lethal Infection ◽  
Guinea Pig Liver

ABSTRACT Leptospirosis is the most geographically widespread zoonotic disease in the world. A severe pulmonary form of leptospirosis (SPFL) is being recognized with increased frequency. We have reported that human SPFL isolates of Leptospira cause acute lethal infection with prominent pulmonary hemorrhage in guinea pigs. We have found that the same SPFL strains cause asymptomatic infection and chronic renal shedding in rats, where infection is restricted to the renal tubules. To address the antigenic composition of host tissue-derived Leptospira (HTL), motile leptospires were purified from guinea pig liver by centrifugation on Percoll density gradients and compared to Percoll-purified in vitro-cultivated Leptospira (IVCL). The lipopolysaccharide O antigen (Oag) content of guinea pig liver-derived HTL was markedly reduced compared to that of IVCL, as demonstrated both by immunoblotting with a monoclonal antibody that was serovar specific for Oag and by periodate-silver staining. Confocal microscopy of HTL in guinea pig liver and kidney with the Oag-specific monoclonal antibody provided further evidence that diminution of the Oag content occurred in situ during lethal infection. In contrast, the Oag content of HTL in chronically infected rat renal tubules was indistinguishable from that of IVCL. These findings suggest that there may be regulation of Oag synthesis by Leptospira specific to the animal host infected. The hypothesis that the Oag content is related to whether lethal infection or chronic renal tubular colonization occurs remains to be tested.

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