trolox/hemorrhage

OBJECTIVE To investigate the role of redox-sensitive transcription factors nuclear factor kappa-B (NF-kappaB) or activator protein-1 (AP-1) for hepatic gene expression of heme oxygenase (HO)-1 and inducible nitric oxide synthase (iNOS) in models of hemorrhagic or endotoxic shock. METHODS Prospective

BACKGROUND Reactive oxygen species (ROS) are produced in many metabolic and physiologic processes. Antioxidative mechanisms remove these harmful species. Our aim was to assess whether serum total antioxidant capacity and total oxidant status altered during first trimester pregnancies with vaginal

Ischemia and reperfusion result in a hepatocellular stress gene response, characterized by a zonal heterogeneity with pericentral hepatocytes being the primary target. In the present study, we assessed cell type-specific and zonal pattern of activation of redox-sensitive transcription factors

Trans-sodium crocetinate (TSC) has been found to alleviate the symptoms of hemorrhagic shock in that, after the drug is given to hemorrhaged rats, blood pressure rises, elevated lactate levels are reduced, cellular damage in the liver and kidney is less, and survival is increased. The mechanism of

Red blood cell (RBC) transfusions for controlling hemorrhaging induce systemic ischemia reperfusion, resulting in a decrease in hepatic cytochrome P450 (CYP) levels. Carbon monoxide (CO), when bound to red blood cells (CO-RBC) has the potential to protect the hepatic CYP protein to produce a

OBJECTIVE To investigate the role of the vasodilator systems heme oxygenase-1/heat shock protein 32 (HO-1/HSP32) and nitric oxide synthase-II (NOS-II), generating carbon monoxide and nitric oxide respectively, as modulators of liver injury in an experimental model of reversible hemorrhagic

Reactive oxygen species (ROS) generated during hemorrhage and subsequent resuscitation (H/R) may contribute to cellular injury but may also regulate an adaptive cellular response to stress. Heme oxygenase (HO)-1 has been recognized as an important stress-inducible gene conferring protection after

Hemoglobin (Hb) has been demonstrated to be neurotoxic when injected into the cerebral cortex in vivo. However, associated systemic factors such as ischemia and epileptogenesis have limited investigations of Hb toxicity in the intact central nervous system (CNS). In this study, the neurotoxicity of

Anti-oxidant therapy has been effective for treatment of experimental shock. In this study, the efficacy of Trolox (Aldrich Chemical Co., Milwaukee, WI), a water-soluble vitamin E analogue, and ascorbic acid (vitamin C) was evaluated in a rat model of hemorrhagic shock and resuscitation. In two

The present paper studies a marker of oxidative stress such as heme oxygenase-1 (HO-1), the main heat shock protein. HO-1 expression was induced in the focal region of the cerebellum following experimental subarachnoid hemorrhage (SAH). Lysed blood was injected into the subarachnoid space or

Thiamine deficiency (TD) produces severe neurodegenerative lesions. Studies have suggested that primary neurodegenerative events are associated with both oxidative stress and inflammation. Very little is known about the downstream effects on intracellular signaling pathways involved in neuronal

Nonheme iron accumulates in CNS tissue after ischemic and hemorrhagic insults and may contribute to cell loss. The source of this iron has not been precisely defined. After blood-brain barrier disruption, CNS cells may be exposed to plasma concentrations of transferrin-bound iron (TBI), which exceed

OBJECTIVE Preterm premature rupture of fetal membranes has been associated with infection, cigarette smoking, and bleeding. Hypochlorous acid (a reactive oxygen species) is central to the body's response to infection, yet it may damage surrounding tissue while destroying pathogens. We examined in

Amyloid-beta protein (A beta) deposition in the cerebral vascular walls is one of the key features of Alzheimer's disease and hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D). A beta(1-40) carrying the 'Dutch' mutation (HCHWA-D A beta(1-40)) induces pronounced degeneration of

Hemin is cytotoxic, and contributes to the brain damage that accompanies hemorrhagic stroke. In order to better understand the basis of hemin toxicity in astrocytes, the present study quantified hemin metabolism and compared it to the pattern of cell death. Heme oxygenase-1 (HO-1) expression was