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Obesity decreases hepatic glutathione concentrations and markedly potentiates allyl alcohol-induced periportal necrosis in the overfed rat.
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Liver biopsies from 9 out of every 10 obese individuals exhibit pathological changes of unknown aetiology and 3 out of every 10 reflect severe injury in the form of periportal fibrosis. To examine the hypothesis that excessive fibrosis in obesity arises in part from a predisposition to injury of the
Cell kinetics of repair after allyl alcohol-induced liver necrosis in mice.
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The cellular kinetics of repair and scarring which occurs after induction of periportal necrosis in mice by allyl alcohol were examined by histology and immunohistochemistry. Thirty-six six-week-old female C57BI/6J mice were injected intraperitoneally with two doses of allyl alcohol on day 0 and
Peritoneoscopic study on rat liver cell necrosis induced by carbon tetrachloride and allyl formate.
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The surface changes of acute centrolobular and perilobular necrosis were studied in rat liver using peritoneoscopy. Centrolobular necrosis as induced by carbon tetrachloride and perilobular necrosis by allyl formate. Vessels observed on the control rat liver surface were identified as terminal
Necrotropic protective effect of Ca-Mg gluconolactate on allyl alcohol-induced liver necrosis in rats.
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The prevention of liver damage in rats intoxicated with allyl alcohol was attempted with 5 per cent Ca--Mg gluconolactate in reiterated doses. This preparation prevented or reduced liver necrosis only in the presence of spleen: splenectomy annihilated the effect of Ca--Mg gluconolactate.
Participation of small intraportal stem cells in the restitutive response of the liver to periportal necrosis induced by allyl alcohol.
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To determine the involvement of different hepatocyte populations in response to periportal injury, the restitutive response to allyl alcohol (AA) injury was examined. Adult female Sprague-Dawley rats were injected intraperitoneally (IP) with 0.62 mmol/kg AA, killed at 6, 9, 12, 33, 57, 81, and 153
S-allyl-L-cysteine sulfoxide inhibits tumor necrosis factor-alpha induced monocyte adhesion and intercellular cell adhesion molecule-1 expression in human umbilical vein endothelial cells.
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Garlic and its water-soluble allyl sulfur-containing compound, S-Allyl-L-cysteine Sulfoxide (ACSO), have shown antioxidant and anti-inflammatory activities, inhibiting the development of atherosclerosis. However, little is known about the mechanism(s) underlying the therapeutic effect of ACSO in
Electron microscopic identification of putative liver stem cells and intermediate hepatocytes following periportal necrosis induced in rats by allyl alcohol.
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The ultrastructural characteristics of the putative liver stem cells that repopulate the necrotic periportal zones after allyl alcohol induced liver injury are described. Periportal liver cell necrosis was induced in adult female Sprague-Dawley rats by i.p. injection with 0.62 mmol/kg of allyl
Allyl isothiocyanate (AITC) and phenyl isothiocyanate (PITC) inhibit tumour-specific angiogenesis by downregulating nitric oxide (NO) and tumour necrosis factor-alpha (TNF-alpha) production.
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Angiogenesis, a crucial step in the growth and metastasis of cancers, is initiated with vasodilation mediated by nitric oxide (NO). The pro-inflammatory cytokine, tumour necrosis factor-alpha (TNF-alpha), is a mediator of nitric oxide synthesis. We analyzed the effect of allyl isothiocyanate (AITC)
[Behavior of serum transaminase activity (glutamic acid-ox-alacetic acid transaminase) in allyl alcohol necrosis of rat liver].
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Retraction. S-Allyl-L-cysteine sulfoxide inhibits tumor necrosis factor-alpha induced monocyte adhesion and intercellular cell adhesion molecule-1 expression in human umbilical vein endothelial cells.
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[Biochemical aspects of liver necrosis caused by allyl formate; behavior of aspartic- and alanine-ketoglutaric transaminases and phosphoglucomutases in blood and liver tissue].
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Dynamics of functional and ultrastructural changes in the liver cells during the development of allyl alcohol necrosis.
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The productoin of periportal necrosis by allyl alcohol in the rat [proceedings].
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[The influence of antibiotics and sulfonamides on liver necrosis in allyl alcohol test].
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Mechanism of allyl alcohol-induced hepatic necrosis.
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