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Selected Publication:

Type of publication: Baccalaureate Thesis
Type of document:

Year: 2015

Authors: Hatami, Jasmin

Title: Determination of activities of enzymes of the heme degradation pathway in different brain regions of rats following global ischemia.

Other title: Bestimmung der Enzymaktivitäten de Häm-Abbaus in verschiedenen Hirnregionen von Ratten nach anschließender globalen Ischämie

Source: Bakkalaureatsarbeit, Vet. Med. Univ. Wien, pp. 51.


Duvigneau Catharina

Högler Sandra

Vetmed Research Units:
Institute for Medical Biochemistry

Global ischemia as a consequence of cardiac arrest (CA) results in acute neuronal damage which is followed by regenerative and degenerative processes. Neurodegenerative diseases affect the heme degradation pathway, involving heme oxygenase (HO) and biliverdin reductase (BVR) in sensitive brain regions. Both, HO and BVR are considered as important antioxidative defense systems providing cytoprotections in conditions of enhance cell stress. In neurodegenerative diseases (Alzheimers desease etc.) two specific brain regions, namely hippocampus and cortex exhibited augmented HO activity. Recently, some findings indicate also a role for BVR in neurodegeneration. In several experimental models of brain ischemia, profound changes of inflammatory and cell stress markers were observed short after the acute insult. It is known that acute brain damage also results in long term changes involving repair and degenerative processes, which all impact on restoration of the proper function of the affected brain areas. Since,- neurodegenerative diseases were shown to be associated with changes in the heme degradation pathway, it is possible that these mechanisms are also operating in the long term processes induced by brain damage following global ischemia. The aim of the current work was to determine activities of HO and BVR in samples of both hippocampus and motor cortex of rats after two weeks following global ischemia, as a consequence of CA. Samples of brain tissue (motor cortex, hippocampus) from sham operated control animals (n=9) and animals subjected to global ischemia (cardiac arrest for 6 and 8 min; n=7 and 5) that had been stored at -80°C, were used. In order to prevent induction of biases, brain areas were homogenized and distributed into droplets of a defined volume. The droplets were used to determine the activities of HO and BVR by an optimized photometric enzyme-coupled assay. Activities were expressed as extracted amount of bilirubin normalized for the underlying protein concentration in droplet samples. In animals subjected to CA activity of HO was consistently lower in motor cortex (p<0.01 in 6min CA; p<0.01 in 8min CA) and hippocampus (p<0.05 in 6min CA; p<0.05 in 8min CA). No activities of BVR were affected by CA. Our findings suggest HO-activity as possible marker for neuronal regenerative/degenerative processes occurring long term after CA.

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