Mycotoxins
22 important questions on Mycotoxins
Do micro-toxins only propose a risk in humid climates? Like Thailand
- some mycotoxins (pe aflatoxins): especially present in crops from warm countries; they enter EU by importation
- others (pe thrichothecenes, fumonisins, ochratoxin A): indigenous in EU crops
What are the 3 major groups of micro toxins?
- Aspergillus mycotoxin
- Penicillium mycotoxin
- Fusarium mycotoxin
Do micotoxins producing aflatoxin grow in the netherlands?
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What are the mycotoxins produced by EU crops?
- trichothecenes
- fumonisins
- ochratoxin A
Are mycotoxins avoidable and what kind of limits do they have?
TDI (Tolerable Daily Intake) and ALARA (as low as reasonably achievable) or MOE (margin of Exposure)
Do microorganisms only produce 1 type of toxin?
Different microorganisms might produce the same type of toxins.
The fungus might have died but the microtoxens are still present.
What are the 4 naturally occurring afla-toxins and which one is the most toxic?
B has a blue fluorecent colour
G has a green fluorecent colour.
B1 and G1 is the most cargiogenic due to the double bond on the side of the molecule. Most is published about B1 since it occurs most.
What is AF M1 and AF M2?
This happens in milk!
Cows receiving 300 ng/g AFB1 in feed milk 24 h later with 1-3 ng/ml AFM1
What is the effect of acute toxicity of aflatoxins?
- Hepatocyte necrosis starting in zone 3 (high P450 content; low GSH) extending to zone 1
- Reduced blood clothing and increased capillary fragility resulting in haemorrhages and eventually death (ED50 0.3 - 9 mg/kg bw)
In other words cells in the liver will die.
This is really a concern for people. The chronic exposure is however.
What is the chronic toxicity of aflatoxins?
- reduced weight gain
- reduced milk yields
- reduced feed intake and feed conversion
- liver necrosis
- liver chirrhosis
- hepatomas (liver tumors)
Is is group 1 carcinogenic for man. Rear since this is not often proven because you can not test people.
What are the different groups of cancer risk compounds classified by the international agency for research on cancer (IARC)?
Group 2A: probably carcinogenic to man; should be forbidden
Group 2B: possibly carcinogenic for man
Group 3: compound cannot be classified because of lack of sufficient data
Group 4: proven to be non-carcinogenic for man
based on scientific arguments and conservative
How do they now that aflatoxins causes liver cancer?
How does aflatoxins cause cancer?
What is the order of carcinogenicity of aflatoxins?
What does the p53 tumoer suppressor gene do?
- Normally controls cell replication cycle
- Detects DNA damage
- Stops replication
- Promotes repair
- If repair is not possible it will let the cell die.
- Mutations can allow cancerous cells to proliferate
Why is a ALARA still of use for aflatoxin?
This is far under 10 000
It is probably not achievable to get values under 10 000 so therefore it is important to keep it as low as possible.
What is the best approach to reduce aflatoxin exposure worldwide?
EXAMENVRAAG!
- prevention based on good agricultural practice (educate farmers and production chain)
- Regulation and Control (contaminated batches should be taken out)
Are the regatory limits for aflatoxin safe?
There reason why these regulation limits are set is because you can not measure lower limits of aflatoxins.
What is the risk characterization of sterigmatocystine?
However they did a reversed calculation. So from the BMDL10 they ditermen how much sterigmatocystine you can eat every day before getting sick.
The highest observed dose was under this level.
From what do you get kidney cancer?
Does ochratoxin A have a TDI?
It causes cancer by cellular oxidative damage. This damages the tissue and therefore more and more new cells will be made causing cancer.
You need a specific amount of molecules to do this. Therefore a TDI can be obtained.
How can you calculate the TDI form a LOAEL?
This happens in the case of ochratoxin A (OTA)
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