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from the α-cell may serve to disrupt normal secretion patterns. In addition to its impact on hormone secretion, UCP2 has been functionally linked to the limitation of reactive oxygen species (ROS) formation ( Negre-Salvayre et al . 1997 , Arsenijevic
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Department of Physiology and Pathophysiology, Institutes of Biomedical Sciences, Department of Endocrinology, Shanghai Medical College
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investigate the change of EPC proliferation under the effect of high glucose (HG) and its relationship with cell cycle, apoptosis, and reactive oxygen species (ROS) production. This may help to further understand the mechanism of diabetic vascular
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J Shirotani T Ichinose K Brownlee M 2003 Mitochondrial reactive oxygen species reduce insulin secretion by pancreatic beta-cells . Biochemical and Biophysical Research Communications 300 216 – 222 . doi:10.1016/S0006-291X(02
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of reactive oxygen species (ROS) and activation of both the hexosamine biosynthesis pathway (HBP) and protein kinase C (PKC) signalling ( Hsieh et al. 2002 , 2003 ). These investigations established that the intrarenal expression of ANG gene and
Department of Physiology, Aging-associated Vascular Disease Research Center, Department of Obstetrics and Gynecology, Department of Biochemistry and Molecular Biology, Department of Internal Medicine, College of Medicine, Yeungnam University, Daegu 705-717, South Korea
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Department of Physiology, Aging-associated Vascular Disease Research Center, Department of Obstetrics and Gynecology, Department of Biochemistry and Molecular Biology, Department of Internal Medicine, College of Medicine, Yeungnam University, Daegu 705-717, South Korea
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Department of Physiology, Aging-associated Vascular Disease Research Center, Department of Obstetrics and Gynecology, Department of Biochemistry and Molecular Biology, Department of Internal Medicine, College of Medicine, Yeungnam University, Daegu 705-717, South Korea
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Department of Physiology, Aging-associated Vascular Disease Research Center, Department of Obstetrics and Gynecology, Department of Biochemistry and Molecular Biology, Department of Internal Medicine, College of Medicine, Yeungnam University, Daegu 705-717, South Korea
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binding buffer, the level of annexin V-FITC conjugation was detected using the FL1 setting of the FACSCalibur (BD Bioscience). Reactive oxygen species generation The generation of reactive oxygen species (ROS) was measured using flow cytometry and live
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al . 1998 ). Since microglia are a principal source of a variety of cytotoxic compounds, including reactive oxygen species, reactive nitrogen species, pro-inflammatory cytokines, and prostaglandins ( Banati et al . 1993 ); microglial activation is
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activation of microglia and astrocytes in the hippocampus and consequent enhanced release of reactive oxygen species and proinflammatory cytokine may play an important role in KA-induced neurodegenerative processes ( Wang et al . 2005 ). Ghrelin, a novel 28
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College of Health and Biomedicine, School of Biomedical Sciences, Biosciences Research Precinct, School of Pharmacy, Victoria University, St Albans, Victoria 3021, Australia
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College of Health and Biomedicine, School of Biomedical Sciences, Biosciences Research Precinct, School of Pharmacy, Victoria University, St Albans, Victoria 3021, Australia
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College of Health and Biomedicine, School of Biomedical Sciences, Biosciences Research Precinct, School of Pharmacy, Victoria University, St Albans, Victoria 3021, Australia
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tissues to optimally respond to insulin, hyperglycemic events are common and these, per se , promote the aberrant production of reactive oxygen species (ROS) and an overwhelmed detoxification system in insulin-responsive cells, which leads to oxidative
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Reactive oxygen species (ROS) play a fundamental role in both apoptotic and necrotic cell death. Their importance is highlighted by studies showing that they mediate cell death in response to radiotherapy and to some forms of chemotherapy. Here we provide the first evidence for a role of ROS in response to an antiendocrine agent currently undergoing clinical trials. Using the oestrogen receptor (ER) containing rat pituitary GH3 cell line, we show that cell death is induced by the pure steroidal antioestrogen, ZM 182780, and that this is blocked by the antioxidant, N-acetyl cysteine (NAC). By flow cytometry, we show that, prior to the onset of DNA breakdown measured by ELISA, ZM 182780 exposure has no significant effect on intracellular oxidant concentrations. In contrast, ZM 182780 exposure greatly increases sensitivity to oxidants generated by blocking cellular antioxidant pathways and from exogenous administration of hydrogen peroxide (H2O2). As both necrosis and apoptosis are controlled by mitochondrial function, further experiments conducted to determine mitochondrial membrane potential (Delta|gWm) have indicated that the ZM 182780-induced loss of ER function increases the ease with which oxidants collapse mitochondrial activity and, as a consequence, cell death.
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Introduction Reactive oxygen species (ROS) are derived from O 2 and comprise molecules with varying oxidant properties. At low concentrations, ROS modulate many cellular processes through redox-dependent signalling, including proliferation