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Indication on the involvement of 4-Hydoxynonenal in experimental brain trauma in baboons (Papio Ursinus) (CROSBI ID 464244)

Prilog sa skupa u časopisu | sažetak izlaganja sa skupa | međunarodna recenzija

Žarković, Kamelija ; Žarković, Neven ; Germann, P. ; Waeg, G. ; Schlag, G. Indication on the involvement of 4-Hydoxynonenal in experimental brain trauma in baboons (Papio Ursinus) // Biofactors / Schaur, R.J. (ur.). 1996. str. 93-94

Podaci o odgovornosti

Žarković, Kamelija ; Žarković, Neven ; Germann, P. ; Waeg, G. ; Schlag, G.

engleski

Indication on the involvement of 4-Hydoxynonenal in experimental brain trauma in baboons (Papio Ursinus)

Although intensively studied, pathophisiology of traumatic brain injury is not sufficiently understood. The lack of understanding of the mechanisms of brain injury makes prediction of the outcome (after trauma or insult) and therapy of the injured very difficult and uncertain [1, 2]. Thus, the only parameter of brain injury that is relatively well known are consequences of organ dissfunction often leading to fatal ending. There is an increase of evidence suggesting that oxidative stress could be of particular importance in pathology of brain injury (and recovery) [3]. However, until now, regional distribution of oxidative stress in different parts of the brain was not compared with the morphological (pathoanatomical and pathohistological) changes induced by traumatic brain lesions. Hence, the aim of the pilot experiments performed on anesthetized baboons was to detect possible presence of 4-hydoxynonenal (HNE) as one of the major ”toxic messengers of free radicals” in the brain tissue after standardized experimental mechanical trauma (fluid percussion model) [4]. For that purpose immunohistochemical analysis of the injured brain was performed using novel monoclonal antibodies raised against HNE [5]. In the controls (sham traumatized animals) immunohistochemical positivity to HNE was determined mainly in neurons and astrocytes at the site of implantation of canulla. Slight HNE positivity was noticed in the edematous tissue and leukocytes around the blood vessels. In the injured brain, HNE positive cells were found both at the site of impact (frontal neocortex) and on the opposite side (foliae cerebelli). Both neurons and glial cells were HNE positive in and around the damaged regions of the brain. Soft membranes and subarchnoidal blood vessels were positive, too. Moreover, ependim and plexus chorioideus showed HNE presence, as well as some neurons and glial cells in periventricular diencephalic nuclei, tegmentum pontis and in the periventricular glial cells of corpus callosum. The most interesting was finding of HNE presence in the apparently undamaged (according to the routine HE staining) neurons in these particular regions susceptible to the ”inner cerebral trauma”. These findings indicate that HNE is not generated only at the site of visible traumatic lacerations, but also in the other brain regions that could not be identified by the routine analysis as foci of tissue damage. The results obtained suggest that generation of HNE due oxidative stress is one of the first consequences in traumatic brain injury and that immunohistochemical analysis of HNE distribution in the injured brain might be used to determine very early stage of post-traumatic damage of the brain cells.

injury; brain; oxidative stress; HNE; immunohistochemistry; neuropathology

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Podaci o prilogu

93-94.

1996.

nije evidentirano

objavljeno

Podaci o matičnoj publikaciji

Biofactors

Schaur, R.J.

Graz: KFUniGraz

0951-6433

Podaci o skupu

Oxidative stress

poster

04.07.1996-07.07.1996

Leibnitz, Austrija

Povezanost rada

Kliničke medicinske znanosti

Indeksiranost