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Review Article Protective Action of Neurotrophic Factors and Estrogen Against Oxidative Stress-Mediated Neurodegeneration

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Review Article Protective Action of Neurotrophic Factors and Estrogen Against Oxidative Stress-Mediated Neurodegeneration Hindawi Publishing Corporation Journal of Toxicology Volume 2011, Article ID 405194, 12 pages doi:10.1155/2011/405194 Review Article Protective Action of Neurotrophic Factors and Estrogen against Oxidative Stress-Mediated Neurodegeneration Tadahiro Numakawa,1, 2 Tomoya Matsumoto,2, 3 Yumiko Numakawa,4 Misty Richards,1, 5 Shigeto Yamawaki,2, 3 and Hiroshi Kunugi1, 2 1 Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo 187-8502, Japan 2 Core Research for Evolutional Science and Technology Program (CREST), Japan Science and Technology Agency (JST), Saitama 332-0012, Japan 3 Department of Psychiatry and Neurosciences, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan 4 Peptide-prima Co., Ltd., 1-25-81, Nuyamazu, Kumamoto 861-2102, Japan 5 The Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, NY 12208, USA Correspondence should be addressed to Tadahiro Numakawa, [email protected] Received 11 January 2011; Revised 28 February 2011; Accepted 29 March 2011 Academic Editor: Laurence D. Fechter Copyright © 2011 Tadahiro Numakawa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Oxidative stress is involved in the pathogenesis of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. Low levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) are important for maintenance of neuronal function, though elevated levels lead to neuronal cell death. A complex series of events including excitotoxicity, Ca2+ overload, and mitochondrial dysfunction contributes to oxidative stress-mediated neurodegeneration. As expected, many antioxidants like phytochemicals and vitamins are known to reduce oxidative toxicity. Additionally, growing evidence indicates that neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and estrogens significantly prevent neuronal damage caused by oxidative stress. Here, we review and discuss recent studies addressing the protective mechanisms of neurotrophic factors and estrogen within this system. 1. Introduction it is important to clarify the detailed relationship between oxidative stress and cellular damage in neurodegenerative It is well established that the brain consumes a large quantity diseases and the aging process. In the cellular and molecular of oxygen and glucose [1–5]. Brain neurons utilize such mechanisms underlying oxidative stress-induced cell death, nutrients, requiring a consistent and steady supply in order it is well known that excitotoxicity, Ca2+ overload, mito- to function appropriately. Not surprisingly, brain neurons chondrial dysfunction, and the stimulation of intracellular arevulnerabletooxidativestress[6], which threatens the signaling cascades play a role [9]. As expected, antioxidants overall functionality of the brain. Though various systems including many phytochemicals and vitamins have been protecting against oxidative toxicity exist in the brain at found to support the survival of neurons under oxidative cellular and molecular levels, a disruption of the defensive stress. system may be involved in neurological deficits observed Brain-derived neurotrophic factor (BDNF), a member of in neurodegenerative diseases. Indeed, many studies suggest the neurotrophin family, is known to be a strong survival- that oxidative toxicity is related to Alzheimer’s disease (AD), promoting factor against various neuronal insults. As a Parkinson’s disease (PD), and Huntington’s disease (HD) result, the molecular mechanisms underlying neurotrophin- [7]. In addition, a correlation between an accumulation of dependent survival promotion when exposed to oxidative oxidative stress and aging has also been established [8]. Thus, stress have been extensively studied. BDNF plays a critical 2 Journal of Toxicology role in cell proliferation, cell differentiation, neuronal pro- oxidative stress-dependent damage occurs during normal tection, and the regulation of synaptic function in the central aging, which may cause a noticeable decline in cognitive nervous system (CNS) via stimulating key intracellular sig- function [8, 28]. Considering that cognitive deficits are naling cascades [10, 11]. In addition to BDNF, glial cell line- observed in neurodegenerative diseases such as AD as well, derived neurotrophic factor (GDNF) and hepatocyte growth a common mechanism underlying oxidative stress-mediated factor (HGF) are also effective for neuronal survival [12, 13]. neuronal cell death may exist. In the following section, Furthermore, estrogens, which regulate synaptic plasticity in we summarize the current knowledge concerning oxidative addition to sex differentiation of the brain [14–16], are found stress-mediated neuronal cell death. to exert protective actions against toxic conditions such as oxidative stress [17]. Here, we review the current issues concerning protective functions of neurotrophic factors and 3. Oxidative Stress-Mediated Neuronal estrogen on neurons under oxidative stress. Cell Death 3.1. Mitochondrial Dysfunction, Ca2+ Overload and Excito- 2. The Role of Oxidative Stress in toxicity. Apoptosis, a prototypic form of programmed cell Neurodegenerative Diseases death, is a major mode of cell death in neurodegenerative diseases. Various mechanisms including excitotoxicity, Ca2+ Low levels of ROS and RNS have a physiological effect overload, mitochondrial dysfunction, endoplasmic reticu- on cellular functions including neuronal plasticity [18]. lum stress, and oxidative stress have been found to contribute However, in excess, ROS/RNS cause oxidation/nitrosylation to apoptosis [9](Figure 1). Mitochondria produce low levels of lipids, proteins, and nucleic acids, resulting in neuronal of ROS in a process known as cellular respiration through cell death (Figure 1). Such damage occurs as a result of the electron transport chain (ETC). The ETC consists of either overproduction of ROS/RNS or reduced activity five protein complexes (I–V), and a disruption of this of enzymatic and nonenzymatic antioxidants. Thus, the electron transport system leads to excess generation of ROS delicate balance between pro- and antioxidant reactions is [29]. Importantly, a number of studies reported possible critical for maintaining normal neuronal function. involvement of mitochondrial dysfunction, including altered Oxidative stress-mediated toxicity may be closely related activity of the ETC, in patients and animal models for AD to the pathogenesis of neurodegenerative diseases such as [30], PD [31], HD [32], and stroke [33]. Some reports AD, PD, and HD [7]. For example, in AD brains, mark- suggest that patients with psychiatric disorders, such as ers for protein oxidation (protein carbonyls and 3-nitro- schizophrenia [34], depression [35], and bipolar disorder tyrosine (3-NT)), lipid oxidation (4-hydroxy-2-nonenal (4- [36], also display mitochondrial dysfunction. HNE)), and DNA oxidation (8-hydroxy-2-deoxyoguanine In addition, mitochondria regulate/impact/affect Ca2+ (8-OHdG)) are elevated [19]. Indeed, the accumulation homeostasis by sequestering excess cytosolic Ca2+ into their of amyloid beta (Aβ), a hallmark of AD, produces ROS matrix (named Ca2+ loading). However, an uncontrolled 2+ including hydrogen peroxide (H2O2) in the presence of Ca loading may be involved in neurodegeneration. In a Fe3+ or Cu2+ [20–22], but see [23]. In PD brains, in study investigating striatal mitochondria of Hdh150 knock- which a selective and progressive loss of dopamine (DA) in HD mice, a disrupted Ca2+ homeostasis was found neurons in the substantia nigra pars compacta occurs, 4- [37]. Another study discovered that a deficiency of phos- HNE, protein carbonyls, 3-NT, and 8-OHdG are all increased phatase and tensin homolog deleted on chromosome 10 while glutathione (GSH, a major intracellular antioxidant) (PTEN)-induced putative kinase 1 (PINK1, a mitochondrial is decreased [24]. Interestingly, 4-HNE covalently binds to kinase linked to familial PD) results in mitochondrial alpha-synuclein (α-Syn), a central protein in PD patho- Ca2+ accumulation in cultured neurons [38]. Endoplasmic genesis, resulting in neurotoxic effects on DAergic and reticulum also regulates intracellular Ca2+ concentration GABAergic neuronal cultures [25]. Similarly, HD brains through inositol-1,4,5-triphosphate receptors (InsP3Rs) and (where significant neuronal loss in the striatum and cor- ryanodine receptors (RyRs). Interestingly, presenilin (PS) 1 tex is observed) demonstrate elevated 3-NT, lipofuscin (a and 2, genes involved in the pathogenesis of AD, acted as product of unsaturated fatty acid peroxidation), malondi- a passive endoplasmic reticulum Ca2+ channel to maintain aldehyde (a marker for lipid oxidation), and 8-OHdG [26]. steady-state Ca2+ levels, which was disrupted by mutant PS1- Reduced levels of GSH were also confirmed in cultured M146V and PS2-N141I [39, 40]. These PS mutants enhanced neurons from mice expressing mutant Huntingtin protein the gating activity of InsP3Rs, leading to Aβ generation [41]. (Htt140Q/140Q) [27]. Furthermore, it was shown that Aβ-containing senile plaques Oxidative toxicity is also involved in cerebral ischemia/ cause Ca2+ overload [42]. Taken together, it seems likely that reperfusion
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