Distribution and Time-Course of 4-Hydroxynonenal, Heat Shock Protein 110/105 Family Members and Cyclooxygenase-2 Expression in the Hippocampus of Rat During Trimethyltin-Induced Neurodegeneration

被引:0
作者
V. Corvino
E. Marchese
N. Zarkovic
K. Zarkovic
M. Cindric
G. Waeg
F. Michetti
M. C. Geloso
机构
[1] Università Cattolica del Sacro Cuore,Institute of Anatomy and Cell Biology
[2] Laboratory for Oxidative Stress,Division of Molecular Medicine
[3] Rudjer Boskovic Institute,Department of Pathology, Neuropathology Unit
[4] University of Zagreb School of Medicine,Institute of Molecular Biosciences
[5] University Hospital Center,undefined
[6] Karl Franzens University of Graz,undefined
来源
Neurochemical Research | 2011年 / 36卷
关键词
Neurodegeneration; 4-hydroxynonenal; Heat shock proteins; COX-2; Trimethyltin; Lipid peroxidation;
D O I
暂无
中图分类号
学科分类号
摘要
Trimethyltin (TMT), an organotin compound considered a useful tool to obtain an experimental model of neurodegeneration, exhibits neurotoxicant effects selectively localised in the limbic system and especially in the hippocampus, which are different in the rat and in mice. In the rat hippocampus, we investigated the expression of aldehyde 4-hydroxynonenal, a major bioactive marker of membrane lipid peroxidation, heat shock protein (HSP) 110/105 family members, markers of oxidative stress, and the neuroinflammatory marker cyclooxygenase-2 after TMT-intoxication at various time points after treatment. Our data show that TMT-induced neurodegeneration in the rat hippocampus is associated specifically with oxidative stress and lipid peroxidation, but not with HSP expression, indicating species-specific differences in the neurotoxicity of TMT between rats and mice.
引用
收藏
页码:1490 / 1500
页数:10
相关论文
共 155 条
  • [31] Billingsley ML(1996)How does trimethyltin affect the brain: facts and hypotheses Acta Neurobiol Exp 56 587-596
  • [32] Chang LW(2008)Dysregulation of intracellular calcium homeostasis is responsible for neuronal death in an experimental model of selective hippocampal degeneration induced by trimethyltin J Neurochem 105 2109-2121
  • [33] Tiemeyer TM(2004)The neurotoxicant trimethyltin induces apoptosis via caspase activation, p38 protein kinase, and oxidative stress in PC12 cells Toxicol Lett 147 63-72
  • [34] Wenger GR(2008)Altered expression of heat shock protein 110 family members in mouse hippocampal neurons following trimethyltin treatment in vivo and in vitro Neuropharmacology 55 693-703
  • [35] Chang LW(2008)In vivo depletion of endogenous glutathione facilitates trimethyltin-induced neuronal damage in the dentate gyrus of mice by enhancing oxidative stress Neurochem Int 52 761-769
  • [36] Dyer RS(2009)Endogenous and esogenous glucocorticoids prevent trimethyltin from causing neuronal degeneration in the mouse brain in vivo: involvement of oxidative stress pathway J. Pharmacol. Sci. 110 424-436
  • [37] Harry GJ(1946)Estimation of nuclear population from microtome sections Anat Rec 94 239-247
  • [38] Lefebvre d’Hellencourt C(2007)Transplantation of foetal neural stem cells into the rat hippocampus during trimethyltin-induced neurodegeneration Neurochem Res 32 2054-2061
  • [39] O’Callagan JP(1996)Monoclonal antibodies for detection of 4-hydroxynonenal modified proteins Free Radic Res 25 149-159
  • [40] Niedwiecke DM(2010)Advances in methods for the determination of biologically relevant lipid peroxidation products Free Radic Res 44 1172-1202