Relation between both oxidative and metabolic-osmotic cell damages and initial injury severity in bombing casualties

Vučeljić, Marina; Z̆unić, Gordana; Romic, Predrag; Jevtic, Miodrag

doi:10.2298/vsp0606545v

Cited by 10 publications

(7 citation statements)

References 29 publications

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“…The generated free radicals, such as hydrogen peroxide, superoxides, nitric oxide (NO), etc., also cause excitotoxicity and impair the metabolic activity of cells. Further, superoxide radicals generated due to catalytic activity after TBI react with NO to form another potent oxidant peroxynitrite, which impairs cerebrovascular function [ 105 , 106 ]. The ROS possesses an unpaired electron and thus, readily binds to different macromolecules such as protein, nucleic acid, or lipid to cause damage.…”

Section: Oxidative Stressmentioning

confidence: 99%

Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions

et al. 2020

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Studying the complex molecular mechanisms involved in traumatic brain injury (TBI) is crucial for developing new therapies for TBI. Current treatments for TBI are primarily focused on patient stabilization and symptom mitigation. However, the field lacks defined therapies to prevent cell death, oxidative stress, and inflammatory cascades which lead to chronic pathology. Little can be done to treat the mechanical damage that occurs during the primary insult of a TBI; however, secondary injury mechanisms, such as inflammation, blood-brain barrier (BBB) breakdown, edema formation, excitotoxicity, oxidative stress, and cell death, can be targeted by therapeutic interventions. Elucidating the many mechanisms underlying secondary injury and studying targets of neuroprotective therapeutic agents is critical for developing new treatments. Therefore, we present a review on the molecular events following TBI from inflammation to programmed cell death and discuss current research and the latest therapeutic strategies to help understand TBI-mediated secondary injury.

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Section: Oxidative Stressmentioning

confidence: 99%

Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions

et al. 2020

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“…This mechanism is fundamental due to the fact that the brain is highly susceptible to free radical damage because of its oxidative metabolism and its high levels of polyunsaturated lipids [42]. Some studies have demonstrated that superoxide radicals and nitric oxide impair cerebral vascular function after TBI due to their strong oxidative effects [43, 44]. …”

Section: Cellular and Molecular Alterations After Tbimentioning

confidence: 99%

Astrocytes Mediate Protective Actions of Estrogenic Compounds after Traumatic Brain Injury

et al. 2018

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Traumatic brain injury (TBI) is a serious public health problem. It may result in severe neurological disabilities and in a variety of cellular metabolic alterations for which available therapeutic strategies are limited. In the last decade, the use of estrogenic compounds, which activate protective mechanisms in astrocytes, has been explored as a potential experimental therapeutic approach. Previous works have suggested estradiol (E2) as a neuroprotective hormone that acts in the brain by binding to estrogen receptors (ERs). Several steroidal and nonsteroidal estrogenic compounds can imitate the effects of estradiol on ERs. These include hormonal estrogens, phytoestrogens and synthetic estrogens, such as selective ER modulators or tibolone. Current evidence of the role of astrocytes in mediating protective actions of estrogenic compounds after TBI is reviewed in this paper. We conclude that the use of estrogenic compounds to modulate astrocytic properties is a promising therapeutic approach for the treatment of TBI.

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“…Due to the biochemical nature of BOP compared to physical nature of TBI (impact or penetrating injury), subtle molecular changes such as free radical-mediated oxidative stress occur and contribute to the manifestation of BOP-induced brain injury ( 40 , 44 , 110 ). Previous studies have demonstrated that reactive oxygen species such as the superoxide radicals and nitric oxide can form peroxynitrite, a powerful oxidant that impairs cerebral vascular function following blast-induced brain injury ( 46 , 111 ). Cernak et al reported that bilateral vagotomy successfully mitigated bradycardia, hypotension, and apnea caused by blast; prevented extreme metabolic alterations and brain edema; but failed to eliminate oxidative stress in the brain due to blast ( 48 ).…”

Section: Blast Brain Injury and Oxidative Stressmentioning

confidence: 99%

Assessing neuro-systemic & behavioral components in the pathophysiology of blast-related brain injury

Kobeissy

2013

Front. Neurol.

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Among the U.S. military personnel, blast injury is among the leading causes of brain injury. During the past decade, it has become apparent that even blast injury as a form of mild traumatic brain injury (mTBI) may lead to multiple different adverse outcomes, such as neuropsychiatric symptoms and long-term cognitive disability. Blast injury is characterized by blast overpressure, blast duration, and blast impulse. While the blast injuries of a victim close to the explosion will be severe, majority of victims are usually at a distance leading to milder form described as mild blast TBI (mbTBI). A major feature of mbTBI is its complex manifestation occurring in concert at different organ levels involving systemic, cerebral, neuronal, and neuropsychiatric responses; some of which are shared with other forms of brain trauma such as acute brain injury and other neuropsychiatric disorders such as post-traumatic stress disorder. The pathophysiology of blast injury exposure involves complex cascades of chronic psychological stress, autonomic dysfunction, and neuro/systemic inflammation. These factors render blast injury as an arduous challenge in terms of diagnosis and treatment as well as identification of sensitive and specific biomarkers distinguishing mTBI from other non-TBI pathologies and from neuropsychiatric disorders with similar symptoms. This is due to the “distinct” but shared and partially identified biochemical pathways and neuro-histopathological changes that might be linked to behavioral deficits observed. Taken together, this article aims to provide an overview of the current status of the cellular and pathological mechanisms involved in blast overpressure injury and argues for the urgent need to identify potential biomarkers that can hint at the different mechanisms involved.

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Relation between both oxidative and metabolic-osmotic cell damages and initial injury severity in bombing casualties

Cited by 10 publications

References 29 publications

Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions

Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions

Astrocytes Mediate Protective Actions of Estrogenic Compounds after Traumatic Brain Injury

Assessing neuro-systemic & behavioral components in the pathophysiology of blast-related brain injury

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