Navegando por Palavras-chave "liver injury"

Agora exibindo 1 - 3 de 3
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Enhancement of lindane-induced liver oxidative stress and hepatotoxicity by thyroid hormone is reduced by gadolinium chloride
    (Taylor & Francis Ltd, 2002-10-01) Simon-Giavarotti, K. A.; Giavarotti, L.; Gomes, L. F.; Lima, A. F.; Veridiano, A. M.; Garcia, E. A.; Mora, O. A.; Fernandez, V; Videla, L. A.; Junqueira, VBC; Univ Chile; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
    The role of Kupffer cells in the hepatocellular injury and oxidative stress induced by lindane (20mg/kg; 24h) in hyperthyroid rats (daily doses of 0.1mg L-3,3',5-triioclothyronine (T-3)/kg for three consecutive days) was assessed by the simultaneous administration of gadolinium chloride (GdCl3; 2 doses of 10mg/kg on alternate days). Hyperthyroid animals treated with lindane exhibit enhanced liver microsomal superoxide radical (O-2(.-)) production and NADPH cytochrome c reductase activity, with lower levels of cytochrome P450, superoxide dismutase (SOD) and catalase activity and glutathione (GSH) content over control values. These changes are paralleled by a substantial increase in the lipid peroxidation potential of the liver and in the O-2(.-) generation/SOD activity ratio, thus evidencing a higher oxidative stress status that correlates with the development of liver injury characterized by neutrophil infiltration and necrosis. Kupffer cell inactivation by GdCl3 suppresses liver injury in lindane/T-3-treated rats with normalization of altered oxidative stress-related parameters, excepting the reduction in the content of GSH and in catalase activity. It is concluded that lindane hepatotoxicity in hyperthyroid state, that comprises an enhancement in the oxidative stress status of the liver, is largely dependent on Kupffer cell function, which may involve generation of mediators leading to pro-oxidant and inflammatory processes.
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Liver necrosis induced by acute intraperitoneal ethanol administration in aged rats
    (Taylor & Francis Ltd, 2002-03-01) Giavarotti, L.; D'Almeida, V; Giavarotti, KAS; Azzalis, L. A.; Rodrigues, L.; Cravero, AAM; Videla, L. A.; Koch, O. R.; Junqueira, VBC; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Univ Buenos Aires; Univ Chile
    It is generally agreed that the deleterious pathophysiological effects of ethanol are caused, at least partially by an increase in free radical production. However, little attention has been directed to the effects of ethanol upon elderly organisms. Male Wistar rats at ages 3, 6,12,18 and 24 months were treated either with a single i.p. dose of 35% ethanol (v/v) at 3 g ethanol/kg body weight or an isovolumetric amount of 0.9% saline solution. We then assessed the plasma levels of transaminases and hepatic levels of oxidative stress-related parameters, followed by liver histological evaluation. the younger rats (3 months old) were not affected by the treatment with ethanol with respect to any of the studied parameters except for a lowering of total hepatic GSH and an increase in hepatic thiobarbituric acid reactants (TBARS) formation, while animals older than 3 months were increasingly more affected by the treatment. Acute ethanol treatment elicited the similar responses to those in the 3 months-old group, plus a decrease in the hepatic and plasma levels of beta-carotene and the plasma level of alpha-tocopherol, as well as an increase in the activity of plasma transaminases. in the 12,18 and 24 months old groups, there was increasing liver necrosis. These findings suggest that liver damage induced by acute ethanol administration in elderly rats may involve a lack of antioxidants.
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Prolonged phenobarbital pretreatment abolishes the early oxidative stress component induced in the liver by acute lindane intoxication
    (Elsevier B.V., 2000-04-10) Videla, L. A.; Arisi, ACM; Fuzaro, A. P.; Koch, O. R.; Junqueira, VBC; Universidade Federal de São Paulo (UNIFESP); Univ Chile; Universidade de São Paulo (USP); Univ Buenos Aires
    Lindane administration to rats (60 mg/kg b.w.) led to an enhancement in the oxidative stress status of the liver at 4 h after treatment, characterized by increases in hepatic thiobarbituric acid reactants (TBARS) formation and chemiluminescence, reduced glutathione (GSH) depletion, and diminution in the biliary content and release of GSH. These changes were observed in the absence of changes in either microsomal functions (cytochrome P450 content, NADPH-dependent superoxide radical production, and NADPH-cytochrome P450 reductase or NADPH oxidase activities) or in oxidative stress-related enzymatic activities (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, and glutathione-S-transferases), over control values. Phenobarbital (PB) administration (0.1% in drinking water; 15 days) elicited an enhancement in liver microsomal functions, lipid peroxidation, and GSH content, without changes in oxidative stress-related enzymatic activities, except for the elevation in those of glutathione reductase and glutathione-S-transferase, compared to control rats. Lindane given to PB-pretreated rats did not alter liver microsomal functions, lipid peroxidation, glutathione status, or oxidative stress-related enzymatic activities, as compared to PB-pretreated animals. in addition, lindane induced periportal necrosis with hemorrhagic foci in untreated rats, but not in PB-pretreated animals. It is concluded that the early oxidative stress response of the liver to lindane and hepatic injury are suppressed by PB pretreatment via induction of microsomal enzymes in all zones of the hepatic acinus. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.