Essential role of polyamine metabolism in hepatic regeneration

Luk, Gordon D.

doi:10.1016/0016-5085(86)90394-x

Cited by 109 publications

(18 citation statements)

References 32 publications

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“…It has been reported that the induction of ODC is essential in hepatic regeneration (Luk, 1986) and that putrescine may be involved in the healing or protection from hepatitis induced in rats by GaIN alone (Daikuhara et al, 1979;Nishiguchi et al, 1990). Our results indicate that putrescine is also effective in delaying the GaiN-induced sensitization to LPS, IL-1 and TNF.…”

Section: Effects Of Lipopolysaccharide-pretreatment On the Action Of supporting

confidence: 62%

Ornithine and histidine decarboxylase activities in mice sensitized to endotoxin, interleukin‐1 or tumour necrosis factor by d‐galactosamine

Endo

Kikuchi

Nakamura

1992

British J Pharmacology

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An injection of d‐galactosamine (GalN) into mice together with a lipopolysaccharide (LPS or endotoxin), interleukin‐1 (IL‐1) or tumour necrosis factor (TNF), sensitized the mice and induced fulminant hepatitis with severe congestion resulting in rapid death. Since LPS and these cytokines induce ornithine decarboxylase (ODC) and histidine decarboxylase (HDC) in the liver and spleen of mice, the effects of GalN on the induction of ODC and HDC in these organs were examined. The induction of ODC by LPS, IL‐1 or TNF was suppressed by GalN in the liver, and this suppression preceded the hepatic congestion. There was good agreement between the degree of hepatic congestion and the suppression of ODC induction by various amounts of GalN. The induction of ODC in the spleen was suppressed only at the highest dose of GalN examined. GalN is known to deplete uridine 5′‐triphosphate (UTP), resulting in the suppression of RNA and protein synthesis. An injection of uridine, the precursor of UTP, diminished the GalN‐induced suppression of ODC induction by LPS and prevented the hepatic congestion and death. LPS‐pretreatment before injection of LPS plus GalN prevented the suppression of ODC activity and prevented the hepatic congestion and death. An injection of putrescine, the product of ODC, prolonged survival time and delayed the development of hepatic congestion. However, injection of an ODC inhibitor into the mice given LPS did not produce hepatic congestion. The induction of HDC in the liver by LPS, IL‐1 or TNF was not suppressed by GalN and, at high doses, the response to LPS was enhanced. An inhibitor of HDC neither prevented the hepatic congestion nor enhanced the protective effect of putrescine. Although GalN in combination with IL‐1α induced a markedly higher HDC activity than was observed when it was combined with TNFα, and suppressed the induction of ODC, the former combination at the doses used did not produce hepatic congestion or death. However, the sensitization to TNFα by GalN was markedly potentiated by IL‐1α. These results suggest that suppression of the induction of ODC by GalN may be one cause of the sensitization to LPS, IL‐1 or TNF, and that the induction of HDC, i.e. histamine formation, may not be involved in this sensitization. These results are consistent with the hypothesis that both IL‐1 and TNF are involved in the sensitization to LPS.

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Section: Effects Of Lipopolysaccharide-pretreatment On the Action Of supporting

confidence: 62%

Ornithine and histidine decarboxylase activities in mice sensitized to endotoxin, interleukin‐1 or tumour necrosis factor by d‐galactosamine

Endo

Kikuchi

Nakamura

1992

British J Pharmacology

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“…6) Its toxicity was low, 5) and we could not find any toxic effect when a higher dose was administered (100 mmol/rat per day for a week), as assessed microscopically, hematologically and from the blood chemistry. 6) Rat liver regeneration was chosen as a model of cell growth as a result of established methodology that had been widely applied in polyamine research and due to the still unresolved role of polyamines, 13,14) although Alhonen et al 15) reported the importance of spd and spm at the initiation stage.…”

Section: Discussionmentioning

confidence: 99%

“…The supernatants were separated by centrifugation and stored at 4°C. The supernatants (0.1 ml) were mixed with internal standards containing 2 nmol of 13 C, 15 N-double-labelled putrescine, 15 nmol of double-labelled spermidine, 15 nmol of double-labelled spermine, with the addition of a standard mixture of 1 nmol of putrescine, 7 nmol of spermidine and 7 nmol of spermine to one tube in duplicate. The mixtures were fractionated by CM-cellulose to collect the polyamine fraction, followed by derivatization to HFB-polyamines, which were determined using an API 300 mass spectrometer (PE-SCIEX, Thornhill, Canada) with an attached IS-ionization interface, as described previously.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Putrescine Aminopropyltransferase Influences Rat Liver Regeneration

Kobayashi

Takao

Shiota

et al. 2006

Biological & Pharmaceutical Bulletin

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A close relationship between rat liver regeneration and the concentration ratio of spermidine to spermine (spd : spm) was demonstrated by the oral administration of trans-4-methylcyclohexylamine (MCHA), a specific inhibitor of putrescine aminopropyltransferase. A decrease in recovery rate of remnant liver with MCHA, as a percentage index of remnant liver weight to body weight, correlated well with a decrease of the spd : spm value, with a correlation coefficient of 0.952 for the remnant livers on day 3 after partial hepatectomy. The decrease in recovery rate could be explained by a prolonged cell cycle based on the data of the proliferating cell nuclear antigen labelling index and mitotic cell index in both livers of day 2 and day 3 after partial hepatectomy. The results presented here will give a new aspect in the field of polyamine regulation to control cell growth in vivo.

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“…Putrescine and the other polyamines appear to be essential for liver regeneration to take place [71]. Furthermore, the addition of exogenous putrescine was shown to enhance regeneration in models of acute liver disease [72].…”

Section: Portal Venous Embolizationmentioning

confidence: 99%

Review: Research Toward Safer Resectionof the Cirrhotic Liver

Moser

Kneteman

2000

HPB Surgery

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Despite recent advances in hepatic surgery, resection of the cirrhotic liver continues to be fraught with high morbidity and mortality rates. As a result, for many patients requiring resection of HCC the postoperative course is complicated and the probability of cure is diminished by coexisting cirrhosis. In this review, we discuss the characteristics of the cirrhotic liver which make it poorly tolerant of resection and the most common complications that follow such surgery. The main purpose of this paper is to review recent attempts to identify interventions that might be beneficial to cirrhotic patients undergoing resection. These interventions include assessment of liver reserve, advances in surgical technique, and improvement in liver function and regeneration.

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Essential role of polyamine metabolism in hepatic regeneration

Cited by 109 publications

References 32 publications

Ornithine and histidine decarboxylase activities in mice sensitized to endotoxin, interleukin‐1 or tumour necrosis factor by d‐galactosamine

Ornithine and histidine decarboxylase activities in mice sensitized to endotoxin, interleukin‐1 or tumour necrosis factor by d‐galactosamine

Inhibition of Putrescine Aminopropyltransferase Influences Rat Liver Regeneration

Review: Research Toward Safer Resectionof the Cirrhotic Liver

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