hepatic veno-occlusive disease/glutathione

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Support of sinusoidal endothelial cell glutathione prevents hepatic veno-occlusive disease in the rat.

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Depletion of sinusoidal endothelial cell glutathione (GSH) has been proposed as a common mechanism leading to hepatic veno-occlusive disease (HVOD). This study examines whether intraportal infusion of GSH can prevent HVOD in the monocrotaline rat model. HVOD was induced in rats with monocrotaline

Induction of hepatic veno-occlusive disease in dogs.

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The authors attempted to induce hepatic veno-occlusive disease (VOD) in 64 dogs. Preparative treatments included combinations of total-body irradiation (TBI) or localized hepatic irradiation (LI) or both and chemotherapy consisting of dimethylbusulfan (DMB), L-phenylalanine mustard (L-PAM),

Dacarbazine toxicity in murine liver cells: a model of hepatic endothelial injury and glutathione defense.

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The pathophysiology of hepatic veno-occlusive disease is poorly understood. These studies were undertaken to determine the initial cellular target and the role of glutathione detoxification of dacarbazine, a toxin implicated in hepatic veno-occlusive disease. Sinusoidal endothelial cells (SECs) and

Glutathione S-transferase A1 polymorphisms and acute graft-vs.-host disease in HLA-matched sibling allogeneic hematopoietic stem cell transplantation.

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Busulfan and the metabolites of cyclophosphamide are conjugated with glutathione and catabolized by enzymes of the cytosolic glutathione S-transferases family. There are clearly linked single nucleotide polymorphisms in the promoter region of the glutathione S-transferase A1 gene (i.e., GSTA1*A,

Induction of glutathione synthesis explains pharmacodynamics of high-dose busulfan in mice and highlights putative mechanisms of drug interaction.

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Busulfan is an example of a drug eliminated through glutathione S-transferase (GST)-catalyzed conjugation with reduced glutathione (GSH). We studied the pharmacokinetics and toxicity of busulfan in C57BL6 mice in correlation with liver GST activity and GSH synthesis by accurate determination of

Use of vitamin E and glutamine in the successful treatment of severe veno-occlusive disease following bone marrow transplantation.

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Veno-occlusive disease of the liver is a common complication following the administration of conditioning regimens to patients undergoing bone marrow transplantation. Free-radical damage to the liver is believed to be the cause of the hepatic outflow occlusion, and maintenance of adequate

Glutamine and vitamin E in the treatment of hepatic veno-occlusive disease following high-dose chemotherapy.

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Hepatic veno-occlusive disease (VOD) of the liver is a common complication following high-dose cytotoxic therapy for bone marrow transplantation (BMT). Liver injury is believed to occur following free radical damage to endothelial cells of the sinusoids and small hepatic veins. Glutathione the main

[Efficiency of prevention and treatment of veno-occlusive disease of the liver after allogeneic stem cell transplantation].

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OBJECTIVE Veno-occlusive disease of the liver (VOD) is one of the most common complications in patients after hematopoietic stem cell transplantation (HSCT). So far, the mortality of severe VOD is almost 100%. How to deal with the disease remains to be an unresolved problem. This study was to

Overexpression of glutathione S-transferase A1-1 in ECV 304 cells protects against busulfan mediated G2-arrest and induces tissue factor expression.

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1. The antineoplastic drug busulfan is frequently used in preconditioning regimens for bone marrow transplantation. Pharmacokinetics vary tremendously between patients due to extensive metabolism in the liver via conjugation to glutathione catalysed by glutathione S-transferase (GST) A1-1. Since

Glutathione monoethyl ester can selectively protect liver from high dose BCNU or cyclophosphamide.

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Normal Swiss Webster mice were treated with monocrotaline or high doses of three antitumor alkylating agents (BCNU, cyclophosphamide, or mitomycin C), all of which have been connected with hepatic veno-occlusive disease at our clinic. Prior administration of WR-2721 did not improve the survival of

Influence of glutathione S-transferase A1, P1, M1, T1 polymorphisms on oral busulfan pharmacokinetics in children with congenital hemoglobinopathies undergoing hematopoietic stem cell transplantation.

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BACKGROUND Busulfan (BU), often used in high dose for myeloablation before hematopoietic stem cell transplantation (HSCT), has been implicated in certain HSCT toxicities, including the occurrence of hepatic veno-occlusive disease (HVOD). In addition to weight and age, gene polymorphisms in specific

Veno-occlusive disease: cytokines, genetics, and haemostasis.

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Identifikohuni Regjistrohu

Hepatic veno-occlusive disease (VOD) is a major cause of morbidity and mortality following high dose cytotoxic therapy for stem cell transplantation (SCT). Pre-existing liver damage, SCT-related therapy, and genetic polymorphisms all appear to increase the risk of developing VOD. Studies of

Effects of monocrotaline, a pyrrolizidine alkaloid, on glutathione metabolism in the rat.

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Monocrotaline (MONO), a pyrrolizidine alkaloid, causes veno-occlusive disease of the liver, pulmonary arterial hypertension, and right ventricular hypertrophy. Toxicity is due to the hepatic formation of a pyrolic metabolite that can be detoxified by conjugation with glutathione (GSH). We have shown

Sinusoidal obstruction syndrome (hepatic veno-occlusive disease).

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Identifikohuni Regjistrohu

Hepatic sinusoidal obstruction syndrome (SOS) is an obliterative venulitis of the terminal hepatic venules, which in its more severe forms imparts a high risk of mortality. SOS, also known as veno-occlusive disease (VOD), occurs as a result of cytoreductive therapy prior to hematopoietic stem cell

Busulfan and metronidazole: an often forgotten but significant drug interaction.

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OBJECTIVE To report the case of a clinically significant drug interaction between intravenous busulfan and oral metronidazole observed through busulfan therapeutic drug monitoring (TDM). METHODS A 7-year-old boy with a history of myelodysplasia that progressed to acute myeloid leukemia received

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