Lipid Peroxidation Early after Brain Injury

Scholpp, Joachim; Schubert, Jochen K.; Miekisch, Wolfram; Noeldge-Schomburg, Gabriele

doi:10.1089/0897715041269632

Cited by 14 publications

(6 citation statements)

References 58 publications

(74 reference statements)

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“…Using the same biochemical technique as for plasma TBARS determination, Scholpp et al [18] demonstrated that there was no difference in the levels of this plasma marker for lipid peroxidation between patients with TBI 12 to 24 hours after admission and healthy controls, thus suggesting that it is not a useful biomarker for oxidative stress damage in TBI. However, in this study, the patient sample was relatively small (n = 18), showing a variable degree in TBI severity (GCS between 3 and 13).…”

Section: Discussionmentioning

confidence: 99%

“…Experimental models of TBI in rodents demonstrated that the damage caused by the oxidative stress might vary according to the brain structures, trauma intensity, and time after injury [14]. The role of ROS brain damage in human TBI has been studied; however, the association between its plasma markers and the prognosis in humans remains controversial [15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

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Plasma levels of oxidative stress biomarkers and hospital mortality in severe head injury: A multivariate analysis

Hohl

Gullo

Silva

et al. 2012

Journal of Critical Care

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Plasma levels of oxidative stress biomarkers and hospital mortality in severe head injury: A multivariate analysis

Hohl

Gullo

Silva

et al. 2012

Journal of Critical Care

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“…The presence of superoxide radicals (SORs) in the environment may lead to the synthesis of NO and peroxynitrite and triggers lipid peroxidation. These released SORs may cause oxidative damage through lipid peroxidation [14,15]. Aminoguanidine is a compound that inhibits selectively and competitively inducible nitric oxide synthase and thereby causes reduced nitric oxide formation.…”

Section: Discussionmentioning

confidence: 99%

Investigation of the Efficacy of Aminoguanidine in an Experimental Rat Model with Isolated Bilateral Pulmonary Contusion Due To Blunt Thoracic Trauma

Atik¹

2020

North Clin Istanbul

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Investigation of the efficacy of aminoguanidine in an experimental rat model with isolated bilateral pulmonary contusion due to blunt thoracic trauma Orıgınal Article EMERGENCY MEDICINE Cite this article as: Atik D, Balci Koroglu D, Taslidere B. Investigation of the efficacy of aminoguanidine in an experimental rat model with isolated bilateral pulmonary contusion due to blunt thoracic trauma. North Clin Istanb UNCORRECTED PROOF A mong all trauma cases, chest trauma is the third most common after head and neck and extremity traumas, respectively. Chest trauma is the most common cause of death, especially in the first four decades of life. It occurs due to traffic accidents, occupational accidents, falls and assaults, and constitutes 25% of trauma-related deaths [1]. The mortality rate of isolated chest trauma is 5.5%, but if an additional organ system is injured, this ABSTRACT OBJECTIVE: In severe thoracic trauma, the pulmonary contusions that are almost inevitable and associated with high morbidity and mortality. In this study, we aimed to evaluate the antioxidant activity of aminoguanidine in pulmonary contusion. METHODS: Sixty-three Sprague-male rats were used in this study. Sham and aminoguanidine groups were exposed to isolated blunt thoracic trauma with a force of 1,512 joules. Aminoguanidine was administered intraperitoneally at a dose of 100 mg/kg three hours before the trauma and on the 1. and 2. day after the trauma. The contusion group was exposed to blunt thoracic trauma only. In all groups, arterial blood gas analysis and catalase and NO levels were reported on the 0 th , 1 st , 2 nd and 3 rd days. RESULTS: PO 2 levels were higher in the sham group compared to the contusion group, without statistical significance. On the third day, SaO 2 levels were higher in the AG group compared to the contusion group. SaO 2 levels were comparable in the AG and sham groups on days 1, 2 and 3. There was no difference between the PaO 2 levels of the contusion and sham groups on the 2 nd and 3 rd days. There was no difference between the PaO 2 levels of the AG and sham groups on the 1 st , 2 nd and 3 rd days. We found no difference between the PaCO 2 levels of the contusion and sham groups on the 0-3 days. There was no difference between the PaCO 2 levels of the AG and sham groups on the 1 st , 2 nd and 3 rd days. No difference was observed between the PaCO 2 levels of the AG and contusion groups on the 1 st , 2 nd and 3 rd days. No significant difference was found between the NO levels of the sham and the contusion groups on day 0. There was a significant difference between the sham and contusion groups on the 1 st , 2 nd and 3 rd days. There was no statistically significant difference between the catalase enzyme activities of the sham and AG groups. CONCLUSION: In our study, we showed that the use of aminoguanidine did not significantly reduce the severity of pulmonary contusion and the inflammatory reaction induced by thoracic trauma in rats.

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“…The discrepancy between these earlier studies and ours may be due to a difference in duration of the experiment; it is possible that the antioxidant defense system of the brain was able to withstand tartrazine-induced oxidative stress during the 14-day treatment in this study. An alternative explanation is that lipid peroxidation only occurs in the late stages of oxidative stress [45] and that the markers we examined did not reflect the full effects of tartrazine.…”

Section: Discussionmentioning

confidence: 99%

High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain

Alsalman

Al‐Jafari

Wani

et al. 2019

BioMed Research International

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Tartrazine, an azo dye used in food, cosmetics, and pharmaceuticals with the effects on cell cycle, is not well understood. Therefore, we investigated the toxicity of tartrazine in rat brain with high-dose aspirin. Male Wistar rats (n = 24) were divided into (C) control, (T) tartrazine (700 mg/kg body weight [BW] at weeks 1 and 2), (A) aspirin (150 mg/kg [BW] at weeks 1, 2, and 3), and (TA) aspirin + tartrazine (150 mg/kg [BW] aspirin at weeks 1, 2, and 3 and 700 mg/kg [BW] tartrazine at weeks 1 and 2) groups. The expression of p53, B cell lymphoma-2 extra-large (Bcl-xL), cyclin-dependent kinase 2 (CDK2), p27, and Ki67 was evaluated by quantitative reverse-transcription PCR. A histopathological analysis of brain tissue and oxidative stress level was assessed based on reduced glutathione (GSH), ascorbic acid (AA), and malondialdehyde levels. We found that Bcl-xL, Ki67, CDK2, and p27 were upregulated and p53 was downregulated in the tartrazine-treated group as compared to the control group. Aspirin administration reversed these changes except P53 expression. Tartrazine had no effect on lipid peroxidation but altered AA and GSH levels with no reversal by aspirin treatment. Histopathological analysis revealed that aspirin prevented tartrazine-induced damage including increased perivascular space and hemorrhage. These results indicate that aspirin protects the brain from tartrazine-induced toxicity independent of p53 signaling and antioxidant mechanisms.

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Lipid Peroxidation Early after Brain Injury

Cited by 14 publications

References 58 publications

Plasma levels of oxidative stress biomarkers and hospital mortality in severe head injury: A multivariate analysis

Plasma levels of oxidative stress biomarkers and hospital mortality in severe head injury: A multivariate analysis

Investigation of the Efficacy of Aminoguanidine in an Experimental Rat Model with Isolated Bilateral Pulmonary Contusion Due To Blunt Thoracic Trauma

High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain

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