Hydroxyoctadecadienoic acid and oxidatively modified peroxiredoxins in the blood of Alzheimer's disease patients and their potential as biomarkers

Yoshida, Yasukazu; Yoshikawa, Akiko; Kinumi, Tomoya; Ogawa, Yoko; Saito, Yoshiro; Ohara, Kunitoshi; Yamamoto, Hisako; Imai, Yumiko; Niki, Etsuo

doi:10.1016/j.neurobiolaging.2007.06.012

Cited by 93 publications

(62 citation statements)

References 42 publications

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“…Linoleic acid is one of the most abundant fatty acids in the body and is a major component of the plasma membrane of nearly all cells. Under conditions such as inflammation, cytotoxicity, or hypotension, linoleic acid is rapidly oxidized to form biologically active metabolites such as 9-HODE and 13-HODE (14)(15)(16). Both 9-HODE and 13-HODE were released in increasing amounts from mouse skin biopsies exposed to a noxious temperature range (Figure 2, C and D).…”

Section: Resultsmentioning

confidence: 99%

Heat generates oxidized linoleic acid metabolites that activate TRPV1 and produce pain in rodents

Patwardhan¹,

Akopian²,

Ruparel³

et al. 2010

J. Clin. Invest.

220

216

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The transient receptor potential vanilloid 1 (TRPV1) channel is the principal detector of noxious heat in the peripheral nervous system. TRPV1 is expressed in many nociceptors and is involved in heat-induced hyperalgesia and thermoregulation. The precise mechanism or mechanisms mediating the thermal sensitivity of TRPV1 are unknown. Here, we have shown that the oxidized linoleic acid metabolites 9-and 13-hydroxyoctadecadienoic acid (9-and 13-HODE) are formed in mouse and rat skin biopsies by exposure to noxious heat. 9-and 13-HODE and their metabolites, 9-and 13-oxoODE, activated TRPV1 and therefore constitute a family of endogenous TRPV1 agonists. Moreover, blocking these substances substantially decreased the heat sensitivity of TRPV1 in rats and mice and reduced nociception. Collectively, our results indicate that HODEs contribute to the heat sensitivity of TRPV1 in rodents. Because oxidized linoleic acid metabolites are released during cell injury, these findings suggest a mechanism for integrating the hyperalgesic and proinflammatory roles of TRPV1 and linoleic acid metabolites and may provide the foundation for investigating new classes of analgesic drugs. IntroductionThe TRP family of ligand-gated ion channels consists of several subgroups, including the vanilloid subfamily (transient receptor potential vanilloid [TRPV]). The first member of the subfamily to be discovered, TRPV1, is an extensively studied channel (1-5) that is expressed in a substantial proportion of pain-sensing sensory neurons, termed nociceptors. TRPV1 can be activated by a variety of endogenous lipids (including lipoxygenase and phospholipase D metabolites of arachidonic acid) and by exogenous substances such as capsaicin (the pungent compound in hot chili peppers) (6). We recently discovered that linoleic acid metabolites are synthesized in the spinal dorsal horn following the afferent barrage due to stimuli such as peripheral inflammation and constitute what we believe to be a novel, physiologically active family of endogenous TRPV1 ligands that mediates central sensitization to mechanical stimuli (7).In the periphery, TRPV1 also serves as a detector for noxious heat (> 43°C) (6), and pharmacological and gene deletion studies have shown that TRPV1 is important in inflammatory heat hyperalgesia and thermoregulation (8-9). However, the precise mechanism of heat activation of TRPV1 remains unknown. We found that endogenous TRPV1 agonists are formed on exposure of cell membranes to noxious heat. The released compounds activate TRPV1 and contribute to the thermal responsiveness of this channel.

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Section: Resultsmentioning

confidence: 99%

Heat generates oxidized linoleic acid metabolites that activate TRPV1 and produce pain in rodents

Patwardhan¹,

Akopian²,

Ruparel³

et al. 2010

J. Clin. Invest.

220

216

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“…In contrast, the linoleic acid metabolites are well recognized to be involved in numerous neurological and non-neurological disorders (9,(24)(25)(26)(27)(28). The known receptors for these metabolites cannot explain all of their observed effects (29)(30).…”

Section: Discussionmentioning

confidence: 99%

Activation of TRPV1 in the spinal cord by oxidized linoleic acid metabolites contributes to inflammatory hyperalgesia

Patwardhan¹,

Scotland

Akopian³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

196

191

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Transient receptor potential vanilloid 1 (TRPV1) plays a major role in hyperalgesia and allodynia and is expressed both in the peripheral and central nervous systems (CNS). However, few studies have evaluated mechanisms by which CNS TRPV1 mediates hyperalgesia and allodynia after injury. We hypothesized that activation of spinal cord systems releases endogenous TRPV1 agonists that evoke the development of mechanical allodynia by this receptor. Using in vitro superfusion, the depolarization of spinal cord triggered the release of oxidized linoleic acid metabolites, such as 9-hydroxyoctadecadienoic acid (9-HODE) that potently activated spinal TRPV1, leading to the development of mechanical allodynia. Subsequent calcium imaging and electrophysiology studies demonstrated that synthetic oxidized linoleic acid metabolites, including 9-HODE, 13-HODE, and 9 and 13-oxoODE, comprise a family of endogenous TRPV1 agonists. In vivo studies demonstrated that intrathecal application of these oxidized linoleic acid metabolites rapidly evokes mechanical allodynia. Finally, intrathecal neutralization of 9-and 13-HODE by antibodies blocks CFA-evoked mechanical allodynia. These data collectively reveal a mechanism by which an endogenous family of lipids activates TRPV1 in the spinal cord, leading to the development of inflammatory hyperalgesia. These findings may integrate many pain disorders and provide an approach for developing analgesic drugs.inflammation ͉ pain T ransient receptor potential vanilloid 1 (TRPV1) plays a pivotal role in many pain models, leading to the development of hyperalgesia and/or allodynia (1-2). TRPV1 is expressed in the peripheral as well as central nervous systems (CNS) including several areas involved in nociceptive transmission (3). Numerous studies have demonstrated that peripheral TRPV1 is activated by noxious heat and protons and is regulated by endogenous ligands (2), contributing to peripheral mechanisms of heat hyperalgesia (4). However, TRPV1 is also expressed in the CNS, where comparatively little is known about the role of this receptor in mediating central pain mechanisms.Recent studies have used TRPV1 antagonists to evaluate the role of CNS TRPV1 in inflammatory hyperalgesia. Interestingly, the systemic/spinal administration of TRPV1 antagonists blocks inflammation-induced heat hyperalgesia, as well as mechanical allodynia (5-6). These findings were unexpected since TRPV1 is not activated by mechanical stimuli, suggesting that spinal TRPV1 activation leads to central sensitization to both thermal and mechanical stimuli (7-8). Based upon these observations, we hypothesized that the afferent barrage resulting from peripheral tissue injury leads to generation of endogenous TRPV1 ligands in the spinal cord that activate TRPV1 in the CNS resulting in central sensitization. Results Depolarization of Spinal Cord Results in the Release of EndogenousTRPV1 Ligands. To evaluate the hypothesis that endogenous TRPV1 agonists are released from spinal cord neurons, freshly isolated male rat spinal cords w...

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“…Hydroperoxides and ketones as well as hydroxides of both free and ester forms of linoleic acid are measured as tHODE. The level of tHODE is related to various diseases [25][26][27][28] . Carbon tetrachloride, which is a strong inducer of free radicals, induced a drastic increase in the level tHODE in rodent livers 29) .…”

mentioning

confidence: 99%

Evaluation of Acute Oxidative Stress Induced by NiO Nanoparticles In Vivo and In Vitro

Horie

Fukui

Nishio

et al. 2011

Journal of Occupational Health

Self Cite

101

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Evaluation of Acute Oxidative Stress Induced by NiO Nanoparticles In Vivo and In Vitro:Masanori Horie, et al. Health Research Institute -Objectives: Nickel oxide (NiO) is an important industrial material, and it is also a harmful agent. The toxicity of NiO is size-related: nanoparticles are more toxic than fine-particles. The toxic mechanism induced by NiO nanoparticles remains unexplained, and the relationship between in vitro and in vivo NiO toxicity results is unclear. In the present study, we focused on the oxidative stress caused by NiO nanoparticles by examining and comparing in vitro and in vivo acute responses induced by NiO nanoparticles. Methods: Cellular responses induced by black NiO nanoparticles with a primary particle size of 20 nm, were examined in human lung carcinoma A549 cells. In vivo responses were examined by instillation of NiO nanoparticles into rat trachea. Bronchoalveolar lavage fluid (BALF) was collected after intratracheal instillation at different time points, and concentrations of lipid peroxide heme oxygenase-1 (HO-1), surfactant protein-D (SP-D) and lactate dehydrogenase (LDH) in BALF were measured. Results: The levels of intracellular reactive oxygen species and lipid peroxidation in A549 cells increased with increasing exposure to NiO nanoparticles, and increases in gene expressions of HO-1 and SP-D were observed in A549 cells. The lipid peroxide level in BALF significantly increased after 24 h instillation but decreased three days later. LDH leakage was also observed three days later. Conclusions: NiO nanoparticles induce oxidative stress-related lung injury. In vivo and in vitro oxidative stress was induced resulting in activation of antioxidant systems. Based on these responses, we conclude that the results of the in vivo and in vitro studies tend to correspond. (J Occup Health 2011; 53: 64-74)

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Hydroxyoctadecadienoic acid and oxidatively modified peroxiredoxins in the blood of Alzheimer's disease patients and their potential as biomarkers

Cited by 93 publications

References 42 publications

Heat generates oxidized linoleic acid metabolites that activate TRPV1 and produce pain in rodents

Heat generates oxidized linoleic acid metabolites that activate TRPV1 and produce pain in rodents

Activation of TRPV1 in the spinal cord by oxidized linoleic acid metabolites contributes to inflammatory hyperalgesia

Evaluation of Acute Oxidative Stress Induced by NiO Nanoparticles In Vivo and In Vitro

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