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Summary Toxicology NWI-MOL054 Kayleigh $3.89
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Summary Toxicology NWI-MOL054 Kayleigh

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 7 keer verkocht
  • Vak
  • Toxicology (NWIMOL054)
  • Instelling
  • Radboud Universiteit Nijmegen (RU)
  • Boek
  • Principles of Biochemical Toxicology

This is a detailed summary of all the lectures' content of the course Toxicology at the Radboud university. All the compounds and principles that are covered in the lectures are covered in great detail in this summary.

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Document informatie

  • Onbekend
  • 21 oktober 2020
  • 21 oktober 2020
  • 39
  • 2018/2019
  • Samenvatting

Onderwerpen

  • toxicology
  • radboud university
  • nwi mol054

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  • Radboud Universiteit Nijmegen (RU)
  • Moleculaire Levenswetenschappen
  • Toxicology (NWIMOL054)
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Voorbeeld van de inhoud

Summary Toxicology 2018 Kayleigh Schouren


Let’s start with the definition of Toxicology as being ‘the study of adverse effects of chemicals on
health’. It is often in the news, like the Fipronil-incident of a few months ago. Toxic compounds can
also be used during war, which is very cruel. However not all toxic compounds need to be avoided,
they often have useful applications in the medical world. Botulinum toxin can be used as a cosmetic
and a muscle relaxant for people with spasms, whereas it is one of the most powerful toxins on
earth. The fact that toxic compounds can have medical applications relays on the statement : ‘all
Ding sind Gift und nichts ohn Gift; allein die Dosis macht, dass ein Ding kein Gift ist’. Meaning that
everything is toxic depending on its dose.




The severity of the intoxication depends on several factors:
- The toxicity of the substance
- Exposure (route, type, size, duration and frequency)
- The organism (species, sex, age, nutritional status)
- Interactions (physical, environmental, simultaneous or successive exposure to another toxin)

There are several phases that must be elaborated when trying to investigate the risk a certain
compound poses.
In the exposition phase one studies the behavior of a compound in the environment, and in which
way it is possible for the compound to be administered to a person.
Then the toxicokinetic phase comprises everything that the body does to the compound. So
absorption, distribution, biotransformation and excretion (ADME)
Eventually in the toxicodynamic phase, the effects of the compound on the body will be examined.
Does it interact with certain receptors, or is it damaging DNA and proteins?

To determine the actual effect a compound will have on a person, knowledge about several things is
required:
- Which substance was involved
- The structure and properties of the compound
- Toxicity of the compound
- What is known about the exposure
- What is the dose-response relationship
- What is known of the mechanism

The reason why we speak here of biotransformation instead of metabolism, is that the term
‘biotransformation’ is specifically meant for the metabolism of xenobiotics. Metabolism could also be
the energy house-holding in your body.

Xenobiotics are metabolized to remove them from the body as quickly as possible. Because they are
‘xeno’ they are not something that the body wishes to keep. Excretion is a lot more easy when a
compound is more polar, because then it is easily excreted by the kidneys, whereas apolar
substances are easily reabsorbed. Biotransformation pathways are thus focused on increasing the
polarity of a compound, these pathways can be divided into two phases:
Phase I reactions, in which often a functional group is added to the compound (OH, NH2, SH or
COOH). These functional groups are important for the phase II reactions.

,Summary Toxicology 2018 Kayleigh Schouren


In the phase II reactions, hydrophilic substrates will be coupled to a functional group of the
xenobiotic in order to make the compound hydrophilic as well. Groups that are commonly used for
conjugation are: glutathione, sulphate, acetyl and glucuronide.

Oxidation by cytochrome P450 is one of the most important phase I reactions.
They can also oxidize N, O and S atoms by dealkylating
them.
Oxidation often takes place via epoxidation. These
epoxide-metabolites can then cause damage when they
are not detoxicated quickly enough.




Glucuronidation is a very important phase II
reaction, which very much occurs during the
biotransformation of aspirin.
There are many differences between the
possible biotransformation routes between
species. The major detoxication route of
paracetamol in humans is via glucuronidation.
This pathway ensures that another pathway
leading to a toxic intermediate, is less
represented. Cats however, do not have this
glucuronidation pathway and therefore
produce a lot more of the toxic intermediate,
eventually leading to the death of the animal.

Differences in metabolism also exist within species, only
then the differences are much more due to quantitative
than qualitative effects. Meaning that some people
metabolize a certain compound faster than others do,
detoxicating the compound more quickly or creating a toxic
metabolite more rapidly.

Different drugs or food habits can lead to different
metabolism as well. Some foods and drugs are known to
enhance the function of certain enzymes. Or some drugs
may enhance the expression of enzymes. St. John’s Wort for
example increases the activity of CYP3a4, leading to rapid
metabolism of administered drugs, whereas grapefruit
reduces the expression of CYP3a4 leading to unexpected
high drug concentration and AUC.

When we want to predict the toxicity of a certain compound, we need to know how much a person
has been exposed to the compound. This exposure is determined by the metabolism and the

, Summary Toxicology 2018 Kayleigh Schouren


transport of the compound through the body, toxicokinetics. A compound can for example travel
through the whole body, resulting in systemic exposure. Another option is to contact only specific
organs, leading to tissue exposure. The toxicokinetics are thus of importance in predicting the effects
that a certain compound will have on the body.
Of course it starts with the way the toxin enters our body, via the lungs, gastrointestinal tract or skin.




When a compound is ingested, it must first survive the acidic attack of the stomach. Once it is in the
intestines it depends on several properties whether the compound is taken up or not.
- Lipophilicity (the more lipophilic the more easily it is absorbed)
- The size (smaller compounds are taken up more readily)
- Molecular mimicry (when the compound resembles another compound for which a special
transporter is expressed, it can be absorbed by means of this special transporter)
Absorption via the lungs also very much depends on the size of the particles. Smaller particles can
travel further into the airways, ending in the alveolar sacs. Here they can cause irritation or be taken
up and delivered to the blood. Lipophilicity naturally plays a role as well, because the compounds still
need to pass through a membrane in order to be absorbed. Also the ventilation rate is of importance,
someone who is sporting breathes more and more deeply and could therefore have a higher
exposure to a compound than a person who is watching in the same room.
The intestines and the lungs have one thing in common, and that is their large surface area, making
contact with a compound more likely.
The skin, in contrast, has a relatively small surface area (2-3 m2). Molecules must pass multiple cell
layers before they reach the blood stream, during this process compounds can cause irritation and
sensitization of the skin. There are many differences in exposure via the skin between individuals,
and even between different body parts.

For all these routes of absorption there are four basic mechanisms that are involved in the transport
of xenobiotics through the membrane:
Diffusion, this is only possible for very small and lipophilic compounds
Facilitated diffusion, this is a passive process which involves carriers or channels
Active transport, they make use of ATP or concentration gradients
Endocytosis, large molecules or particles that are invaginated by the plasma membrane


Once inside the body, a certain compound can be trapped inside a specific organ due to changes in
pH for example. The liver is often target of adverse effects of chemical compounds. This is due to a
few reasons:

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