Accumulation of Acrolein–Protein Adducts after Traumatic Spinal Cord Injury

Luo, Jian; Uchida, Koji; Shi, Riyi

doi:10.1007/s11064-005-2602-7

Cited by 99 publications

(150 citation statements)

References 22 publications

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“…3,46 The presence of protein-bound acrolein could be detected by an antibody (mAb5F6) raised against the acrolein-modified proteins using immunoblot assay. 47,48 To visualized the accumulation of acroleinmodified proteins, immunohistochemical staining can be used with the same antibody against the acrolein-modified proteins. 47,48 8-Iso-prostaglandin F 2a .…”

Section: Nucleusmentioning

confidence: 99%

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Oxidative stress in spinal cord injury and antioxidant-based intervention

Jia

Zhu

Li³

et al. 2011

Spinal Cord

267

176

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Study design: Literature review. Objectives: Spinal cord injury (SCI) remains a major public health issue in developed countries as well as worldwide. The pathophysiology of SCI is characterized by an initial primary injury followed by secondary deterioration. Although the etiology and pathogenesis of SCI remain to be fully understood, it has been suggested that reactive oxygen species (ROS) and oxidative stress have a significant role in the pathophysiology of SCI. Thus, alleviating oxidative stress may be an effective strategy for therapeutic intervention of SCI. The aim of this review was to describe (i) the sources of ROS as well as the major antioxidant defenses with particular attention being paid to lipid peroxidation; (ii) the biomarkers of oxidative stress in SCI and (iii) the neuroprotective effects of various compounds with antioxidative properties in animal models of SCI. Methods: PubMed, one of the most comprehensive biomedical databases, was searched from 1976-2011. All relevant papers were read by title, abstract and full-length article. Results: Oxidative stress is considered a hallmark of injury of SCI. Thus, alleviating oxidative stress may be an effective way of therapeutic intervention of SCI. Two of these agents, the glucocorticoid steroid methylprednisolone and the non-glucocorticoid 21-aminosteroid tirilazad, have been shown to possess significant antioxidant activities and improve recovery of SCI patients in clinical trials. Other promising botanical compounds and their molecular targets and mechanisms of action with regard to potential protection against SCI were also described. These include carotenoids and phenolic compounds. Conclusion: ROS and oxidative stress have a significant role in the pathophysiology of SCI. Alleviating oxidative stress is be an effective strategy for therapeutic intervention of SCI. Extensive research over the past several decades has identified numerous bioactive compounds that have antioxidative stress benefits in animal models of SCI. Thus, continued studies on bioactive compounds with ROS-scavenging capacity may lead to the development of effective antioxidant-based modalities for treating SCI in human subjects.

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Section: Nucleusmentioning

confidence: 99%

“…47,48 To visualized the accumulation of acroleinmodified proteins, immunohistochemical staining can be used with the same antibody against the acrolein-modified proteins. 47,48 8-Iso-prostaglandin F 2a . 8-Iso-prostaglandin F 2a is an isoprostane that has been shown to be useful for assessing oxidative stress in spinal cord ischemia.…”

Section: Nucleusmentioning

confidence: 99%

Oxidative stress in spinal cord injury and antioxidant-based intervention

Jia

Zhu

Li³

et al. 2011

Spinal Cord

267

176

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“…1,2 This is based on its high direct toxicity to various cells by attacking DNA, proteins, lipids, and mitochondria, [3][4][5][6] perpetuating oxidative stress by further stimulating the production of free radicals, 1,5 and having an extended presence within biological systems to exert its prolonged toxicity. 7,8 In light of the pathological importance of acrolein, the detection and quantification of acrolein is of significant importance in delineating the pathogenesis of various diseases. In this regard, we aim to utilize acrolein as a biomarker for making diagnosis, assessing diseases progression, and validating treatments that specifically target acrolein.…”

Section: Introductionmentioning

confidence: 99%

Determination of Urine 3-HPMA, a Stable Acrolein Metabolite in a Rat Model of Spinal Cord Injury

Zheng

Park

Walls

et al. 2013

Journal of Neurotrauma

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Acrolein has been suggested to be involved in a variety of pathological conditions. The monitoring of acrolein is of significant importance in delineating the pathogenesis of various diseases. Aimed at overcoming the reactivity and volatility of acrolein, we describe a specific and stable metabolite of acrolein in urine, N-acetyl-S-3-hydroxypropylcysteine (3-HPMA), as a potential surrogate marker for acrolein quantification. Using the LC/MS/MS method, we demonstrated that 3-HPMA was significantly elevated in a dose-dependent manner when acrolein was injected into rats IP or directly into the spinal cord, but not when acrolein scavengers were co-incubated with acrolein solution. A nonlinear mathematic relationship is established between acrolein injected directly into the spinal cord and a correlated dosedependent increase of 3-HPMA, suggesting the increase of 3-HPMA becomes less apparent as the level of injected acrolein increases. The elevation of 3-HPMA was further detected in the rat spinal cord injury, a pathological condition known to be associated with elevated endogenous acrolein. This finding was further validated by concomitant confirmation of increased acrolein-lysine adducts using established dot immunoblotting techniques. The noninvasive nature of measuring 3-HPMA concentrations in urine allows for long-term monitoring of acrolein in the same animal and ultimately in human clinical studies. Due to wide spread involvement of acrolein in human health, the benefits of this study have the potential to enhance human health significantly.

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“…As a consequence, the identification of acrolein adducts has been proposed as a biologic marker for oxidative stress (Kehrer and Biswal, 2000). Accordingly, acrolein levels have been found increased in pathological conditions associated with oxidative stress, such as spinal cord injury (Luo et al, 2005), diabetic nephropathy (Suzuki and Miyata, 1999) and Alzheimer's Disease (AD) (Markesbery and Lovell, 1998,Calingasan et al, 1999,Lovell et al, 2001). …”

mentioning

confidence: 99%

Acrolein induces selective protein carbonylation in synaptosomes

et al. 2007

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Acrolein, the most reactive of the α,β-unsaturated aldehydes, is endogenously produced by lipid peroxidation, and has been found increased in the brain of patients with Alzheimer's disease. Although it is known that acrolein increases total protein carbonylation and impairs the function of selected proteins, no study has addressed which proteins are selectively carbonylated by this aldehyde. In this study we investigated the effect of increasing concentrations of acrolein (0, 0.005, 0.05, 0.5, 5, 50 μM) on protein carbonylation in gerbil synaptosomes. In addition, we applied proteomics to identify synaptosomal proteins that were selectively carbonylated by 0.5 μM acrolein. Acrolein increased total protein carbonylation in a dose-dependent manner. Proteomic analysis (2-D electrophoresis followed by mass spectrometry) revealed that tropomyosin-3-gamma isoform 2, tropomyosin-5, β-actin, mitochondrial Tu translation elongation factor (EFTu mt ) and voltagedependent anion channel (VDAC) were significantly carbonylated by acrolein. Consistent with the proteomics studies that have identified specifically oxidized proteins in Alzheimer's Disease (AD) brain, the proteins identified in this study are involved in a wide variety of cellular functions including energy metabolism, neurotransmission, protein synthesis, and cytoskeletal integrity. Our results suggest that acrolein may significantly contribute for oxidative damage in AD brain.Acrolein (2-propen-1-al), the most reactive of the α,β-unsaturated aldehydes (Esterbauer et al., 1991), is a toxic compound found in automobile exhaust gases, overheated cooking oils and a metabolite of cyclophosphamide and allyl alcohol (Halliwell and Gutteridge, 1999). Acrolein can also be endogenously produced as a product of lipid peroxidation (Adams and Klaidman, 1993,Uchida, 1999) and from polyamine metabolism (Takano et al., 2005 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2008 July 13. Published in final edited form as:Neuroscience. 2007 July 13; 147(3): 674-679. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript . As a consequence, the identification of acrolein adducts has been proposed as a biologic marker for oxidative stress (Kehrer and Biswal, 2000). Accordingly, acrolein levels have been found increased in pathological conditions associated with oxidative stress, such as spinal cord injury (Luo et al., 2005), diabetic nephropathy (Suzuki and Miyata, 1999) and Alzheimer's Disease (AD) (Markesbery and Lovell, 1998,Cal...

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Accumulation of Acrolein–Protein Adducts after Traumatic Spinal Cord Injury

Cited by 99 publications

References 22 publications

Oxidative stress in spinal cord injury and antioxidant-based intervention

Oxidative stress in spinal cord injury and antioxidant-based intervention

Determination of Urine 3-HPMA, a Stable Acrolein Metabolite in a Rat Model of Spinal Cord Injury

Acrolein induces selective protein carbonylation in synaptosomes

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