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Institute for Risk Assessment Sciences (IRAS)

is an interfacultary research institute within the faculties Veterinary Medicine, Medicine, Sciences of Utrecht University.

Research in toxicology at IRAS

MSc programmes

Information about the MSc programmes can be found at the website of Utrecht University:


Foreign students enrolled in one of these MSc programmes or students pursuing a PhD education with IRAS possibly can apply for a scholarship: more information is available the website of the IRAS Foundation.


Vpis na univerzitetni program toksikologije na Medicinski Univerzi na Dunaju je še možen.
Dodatne informacije so na:
Cena šolnine je za študente znižana (najnižja med podobnimi programi).

Nekateri pomembni vidiki tega programa:

- Vsa predavanja, materijali in izpiti so v angleščini
- Možen je študij ob delu (66 dni predavanj znotraj treh let)
- Po končanju se pridobi univerzitetni naslov  "Magister znanosti (Toksikologija)"
- Za vse vpisane so mesta garantirana za vseh 15 modulov tekom treh let
- Datumi za izvajanje predavanj so lahko dogovorjeni za več mesecev v naprej
- Možna je udeležba le na posamičnih modulih, če so na voljo prosta mesta

Uspešna pridobitev certifikatov vseh 15 modulov je pogoj za pridobitev naslova Evropsko registriran toksikolog.

Za dodatne informacije se lahko obrnete na Ta e-poštni naslov je zaščiten proti smetenju. Če ga želite videti, omogočite Javascript.

ali direktno na vodjo programa

ao Univ. Prof. Dr. Bettina Grasl-Kraupp
Medical University of Vienna
Dept. of Medicine I
Institute for Cancer Research
Research Unit: Chemical Safety and Cancer Prevention
T +43-1-4277-65137
F +43-1-4277-65159


University course in Toxicology application is still open.
Further information are under:
There are reduced fees especially for students.

Some important advantages of the course are:

- All lectures and course materials are in English
- Extra occupational program (66 lecture days during 3 years)
- University degree as "Master of Science (Toxicology)"
- Guaranteed places for all registered participants throughout the course. Completion within 3 years
- Module dates are agreed with participants if possible and announced in advance
- For continued education: Single modules can be booked if places are available
Contact person:
ao Univ. Prof. Dr. Bettina Grasl-Kraupp
Medical University of Vienna
Dept. of Medicine I
Institute for Cancer Research
Research Unit: Chemical Safety and Cancer Prevention
T +43-1-4277-65137
F +43-1-4277-65159

Zadnjič posodobljeno (Petek, 18 Februar 2011 17:45)



Tetanus toxin and botulinum toxins have very different mechanism of action. Let's find out how.

Tetanus is a highly fatal disease of humans. Mortality rates reported vary from 40% to 78%. The disease stems from a potent neurotoxin (tetanus toxin or tetanospasmin). Clostridium tetani is found in soil, especially heavily-manured soils, and in the intestinal tracts and feces of various animals.

The toxin is produced during cell growth, sporulation and lysis. It migrates through the nerves or is transferred by lymphocytes from a local wound the central nervous system. The clinical pattern of generalized tetanus consists of severe painful spasms and rigidity of the voluntary muscles. The characteristic symptom of "lockjaw" involves spasms of the masseter muscle. It is an early symptom which is followed by progressive rigidity and violent spasms of the trunk and limb muscles. Spasms of the pharyngeal muscles cause difficulty in swallowing. Death usually results from interference with the mechanics of respiration. The toxin has no effect on the mental status, and consciousness is not impaired directly by this illness.

Tetanus toxin is one of the three most poisonous substances known, the other two being the toxins of botulism and diphtheria. The toxin is produced by growing cells and released only on cell lysis. The bacterium synthesizes the tetanus toxin as a single 150kDa polypeptide chain. Tetanospasmin initially binds to peripheral nerve terminals. It is transported within the axon and across synaptic junctions until it reaches the central nervous system. There it becomes rapidly fixed to gangliosides at the presynaptic inhibitory motor nerve endings, and is taken up into the axon by endocytosis. The effect of the toxin is to block the release of inhibitory neurotransmitters (glycine and gamma-amino butyric acid) across the synaptic cleft, which is required to check the nervous impulse. If nervous impulses cannot be checked by normal inhibitory mechanisms, it produces the generalized muscular spasms characteristic of tetanus. Tetanospasmin appears to act by selective cleavage of a protein component of synaptic vesicles, synaptobrevin II, and this prevents the release of neurotransmitters by the cells.

Botulism is mainly food borne intoxication, when botulinum toxin is ingested with food in which spores have germinated. The botulinum toxin type B, which has a molecular mass of 150 kDa, is absorbed by the upper part of the GI tract in the duodenum and jejunum only in a small amount (0.01%). It passes into the blood stream by which it reaches the peripheral neuromuscular synapses. The toxin binds to the presynaptic stimulatory terminals and blocks the release of the neurotransmitter acetylcholine which is required for a nerve to simulate the muscle. This causes the so called flaccid paralysis.

The botulinum toxins are very similar in structure and function to the tetanus toxin, but differ dramatically in their clinical effects because they target different cells in the nervous system. Botulinum neurotoxins predominantly affect the peripheral nervous system reflecting a preference of the toxin for stimulatory motor neurons at a neuromuscular junction. Once damaged, the synapse is rendered permanently useless. The recovery of function requires sprouting of a new presynaptic axon and the subsequent formation of a new synapse. recent evidence suggests that both botulinum toxin as well as tetanus toxin are zinc-dependent endopeptidases that cleave specific proteins that are involved in excretion of neurotransmitters. Both toxins cleave a set of proteins called synaptobrevins. Synaptobrevins are a set of proteins found in synaptic vesicle of neurons, the vesicles responsible for release of neurotransmitters. Presumably, proteolytic cleavage of synaptobrevin II would interfere with vesicle function and release of neurotransmitters.

Additional reading:

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Zadnjič posodobljeno (Petek, 11 Februar 2011 07:52)


Course in Cancer Risk Assessment is organized by Karolinska Institutet, Stockholm, Sweden (May 23-27, 2011). The learning outcomes of the course are to gain knowledge about different methods used for studying carcinogenic properties of chemicals.

More information at