Involvement of decreased neuroglobin protein level in cognitive dysfunction induced by 1-bromopropane in rats

Guo, Ying; Yuan, Hua; Jiang, Lulu; Yang, Junlin; Zeng, Tao; Xie, Keqin; Zhang, Cuili; Zhao, Xianxian

doi:10.1016/j.brainres.2014.12.046

Cited by 11 publications

(18 citation statements)

References 65 publications

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“…Nε‐(hexanoyl) lysine (HEL) is known as a stable marker of lipid peroxidation‐derived protein modification . 4‐Hydroxy‐2‐nonenal (4‐HNE) is also known as a cytotoxic breakdown product generated from lipid peroxidation .…”

Section: Resultsmentioning

confidence: 99%

“…Considering that most reactive oxygen species (ROS) are highly reactive and short‐lived, it is difficult to detect them in biological substances . Therefore, measurement of the end products of lipid peroxidation is one of the most widely accepted approaches for evaluating oxidative damage . 4‐HNE, which is commonly used as a marker of lipid peroxidation, as well as oxidative DNA and/or protein damage, is the major 4‐hydroxyalkenal end product generated by the decomposition of polyunsaturated fatty acids .…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, measurement of the end products of lipid peroxidation is one of the most widely accepted approaches for evaluating oxidative damage . 4‐HNE, which is commonly used as a marker of lipid peroxidation, as well as oxidative DNA and/or protein damage, is the major 4‐hydroxyalkenal end product generated by the decomposition of polyunsaturated fatty acids . HEL has recently been recognised as a useful biomarker of oxidative modification and an early marker of lipid peroxidation .…”

Section: Discussionmentioning

confidence: 99%

“…4‐HNE, which is commonly used as a marker of lipid peroxidation, as well as oxidative DNA and/or protein damage, is the major 4‐hydroxyalkenal end product generated by the decomposition of polyunsaturated fatty acids . HEL has recently been recognised as a useful biomarker of oxidative modification and an early marker of lipid peroxidation . It is generated by the reaction of lysine residues in proteins with 13‐hydroperoxyoctadienoic acid, a lipid hydroperoxide produced from ω‐6 unsaturated fatty acids .…”

Section: Discussionmentioning

confidence: 99%

“…Nε-(hexanoyl) lysine (HEL) is known as a stable marker of lipid peroxidation-derived protein modification. 26,27 4-Hydroxy-2-nonenal (4-HNE) is also known as a cytotoxic breakdown product generated from lipid peroxidation. 28 ONOO − induces tyrosine nitration of proteins, which is detectable by western blotting with an antinitrotyrosine (NT) antibody, and leads to lipid peroxidation.…”

Section: Lipid Peroxidation In the Kidneymentioning

confidence: 99%

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Evaluations of lipid peroxidation and inflammation in short‐term glycerol‐induced acute kidney injury in rats

Nara

Yajima

Abe

et al. 2016

Clin Exp Pharma Physio

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Rhabdomyolysis is characterised by acute kidney injury (AKI) resulting from skeletal muscle injury. Lipid peroxidation-mediated oxidant injury and pro-inflammatory cytokine-mediated inflammatory response play critical roles in the pathogenesis of rhabdomyolysis-induced AKI. The present study aimed to investigate the short-term effects of both lipid peroxidation and inflammatory responses on rhabdomyolysis-induced AKI in a rat model of glycerol-induced rhabdomyolysis. Rhabdomyolysis was induced by the intramuscular injection of 50% glycerol in saline (10 mL/kg) into the hind limbs of rats. Rats were killed 1 or 3 hours after glycerol injection. Time-dependent increases in serum biochemical parameters, including blood urea nitrogen, creatinine, lactate dehydrogenase and creatine phosphokinase levels, were observed 1 hour after glycerol injection. In kidneys, glycerol injection resulted in histopathological changes such as renal tubular injury and renal tubular myoglobin deposition. Levels of Nε-(hexanoyl)lysine-modified, 4-hydroxy-2-nonenal-modified, and nitrotyrosine-modified proteins in rat kidneys were unaltered at 1 hour after glycerol injection, but increased significantly at 3 hours. Increases in renal nitric oxide production and the expression levels of inducible nitric oxide synthase, interleukin-6 and tumour necrosis factor-α in the renal parenchyma were observed at 1 hour after glycerol injection and plateaued at 3 hours. Our findings suggest that the pro-inflammatory cytokine-mediated inflammatory response may cause rhabdomyolysis-induced AKI very shortly after glycerol injection, and lipid peroxidation-mediated oxidant injury may promote the development of these pathophysiological processes.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Lipid Peroxidation In the Kidneymentioning

confidence: 99%

See 3 more Smart Citations

Evaluations of lipid peroxidation and inflammation in short‐term glycerol‐induced acute kidney injury in rats

Nara

Yajima

Abe

et al. 2016

Clin Exp Pharma Physio

View full text Add to dashboard Cite

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Oxidative Stress Mediated Hippocampal Neuron Apoptosis Participated in Carbon Disulfide-Induced Rats Cognitive Dysfunction

et al. 2016

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Occupational exposure to carbon disulfide (CS) exhibits central nervous systems toxicity. But the mechanism is unclear. The present study was designed to investigate the relationship between the CNS damage and cognitive dysfunction caused by CS, and eventually reveal the possible oxidative-related mechanism of hippocampus pathological changes in CS exposed rats. Male Wistar rats were administrated with CS at dosage of 200, 400 and 600 mg/kg for consecutive 20 days, respectively. Cognitive performances were evaluated by Morris water maze tests. Thionin and immunohistochemical analysis were used to investigate the hippocampal neuron damage, and the expression of apoptosis related proteins (cleaved-caspase 3, Bax and Bcl-2) were detected to explore the possible mechanisms of neuronal loss. Oxidative stress parameters were checked by commercial assay kits. Rats exposed to CS displayed cognitive dysfunction manifested as decreased spatial learning ability and memory lesion. Pathological changes and significant neuron loss were observed in hippocampus, especially in CA1 and CA3 sub-regions. Mitochondria-dependent apoptosis pathway was implicated in the CS-induced neuronal loss which was demonstrated by the up-regulation of cleaved-caspase 3 and Bax accompanied with down-regulation of Bcl-2. Furthermore, extensive oxidative stress induced by CS was also revealed by the measurement of ROS, RNS, MDA, GSH&GSSG and antioxidant enzymes (CAT, T-SOD, and GSH-Px). Our study suggested that oxidative stress mediated hippocampal neuron apoptosis might play an important role in CS induced CNS damage and cognitive dysfunction.

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NMDA Receptor Antagonist MK801 Protects Against 1-Bromopropane-Induced Cognitive Dysfunction

Qiu

Wang

et al. 2018

Neurosci. Bull.

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Occupational exposure to 1-bromopropane (1-BP) induces learning and memory deficits. However, no therapeutic strategies are currently available. Accumulating evidence has suggested that N-methyl-D-aspartate receptors (NMDARs) and neuroinflammation are involved in the cognitive impairments in neurodegenerative diseases. In this study we aimed to investigate whether the noncompetitive NMDAR antagonist MK801 protects against 1-BPinduced cognitive dysfunction. Male Wistar rats were administered with MK801 (0.1 mg/kg) prior to 1-BP intoxication (800 mg/kg). Their cognitive performance was evaluated by the Morris water maze test. The brains of rats were dissected for biochemical, neuropathological, and immunological analyses. We found that the spatial learning and memory were significantly impaired in the 1-BP group, and this was associated with neurodegeneration in both the hippocampus (especially CA1 and CA3) and cortex. Besides, the protein levels of phosphorylated NMDARs were increased after 1-BP exposure. MK801 ameliorated the 1-BP-induced cognitive impairments and degeneration of neurons in the hippocampus and cortex. Mechanistically, MK801 abrogated the 1-BP-induced disruption of excitatory and inhibitory amino-acid balance and NMDAR abnormalities. Subsequently, MK801 inhibited the microglial activation and release of pro-inflammatory cytokines in 1-BP-treated rats. Our findings, for the first time, revealed that MK801 protected against 1-BP-induced cognitive dysfunction by ameliorating NMDAR function and blocking microglial activation, which might provide a potential target for the treatment of 1-BP poisoning.

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Involvement of decreased neuroglobin protein level in cognitive dysfunction induced by 1-bromopropane in rats

Cited by 11 publications

References 65 publications

Evaluations of lipid peroxidation and inflammation in short‐term glycerol‐induced acute kidney injury in rats

Evaluations of lipid peroxidation and inflammation in short‐term glycerol‐induced acute kidney injury in rats

Oxidative Stress Mediated Hippocampal Neuron Apoptosis Participated in Carbon Disulfide-Induced Rats Cognitive Dysfunction

NMDA Receptor Antagonist MK801 Protects Against 1-Bromopropane-Induced Cognitive Dysfunction

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