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Hans Zischka, PhD - "Mitochondrial Toxicology"

Institute of Molecular Toxicology and Pharmacology (HMGU) and Institute of Toxicology and Environmental Hygiene (Technical University Munich), Munich, Germany
When Nov 29, 2019
from 02:00 PM to 03:00 PM
Where Tigem, Vesuvius Auditorium
Contact Name
Contact Phone 081-19230659
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Abstract
Our group studies mitochondrial destruction upon diverse aspects of cell-toxic conditions. As an example we will present our latest research results concerning mitochondrial impairments in Wilson disease (WD) and related animal models.
In Wilson disease (WD) functional loss mutations in the ATP7B gene cause dramatic liver copper overload leading to acute liver failure. In the LPP(-/-) rat, an established animal model for WD, massive liver copper accumulation causes hepatitis that rapidly progresses to liver failure and animals’ death.
In search of the lethal cause in these animals, we find that the progressive copper accumulation in the hepatocyte’s mitochondrial compartment is paralleled by severe mitochondrial structural and functional impairments, similar to alterations observed in WD patients, finally culminating in mitochondrial destruction. In a collaborative effort with the group of Roman Polishchuk at TIGEM, we could recently show that the hepatocytes aim to overcome this mitochondrial dysfunction by activating mitophagy.
Importantly, reduction of the mitochondrial copper load by Methanobactin, a small peptide with an exceptionally high copper affinity, is associated with the reestablishment of normal mitochondrial structure and function, as well as with liver restoration and the avoidance of acute liver failure.
Therefore, depleting the devastating mitochondrial copper burden is a prime requirement for an efficient treatment strategy against acute liver failure in this disease.


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