Midterm practice Flashcards

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1
Q

One can reduce scombroid poisoning symptoms by cooking fish and using antihistamines.
True or False?

A

True.
Cooking does not destroy histamine, but the use of antihistamines can help alleviate the symptoms.

Cooking causes inactivation of histamine-producing spoilage bacteria. However, histamine is heat resistant, so it can remain intact in cooked products.

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2
Q

One can reduce scombroid poisoning symptoms by cooking fish or using antihistamines.
True or False?

A

False.
Cooking does not destroy histamine, but the use of antihistamines can help alleviate the symptoms.

Cooking causes inactivation of histamine-producing spoilage bacteria. However, histamine is heat resistant, so it can remain intact in cooked products.

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3
Q

Caffeine’s rapid absorption is responsible for its quick stimulant effect.
True or False?

A

True.

After ingestion, caffeine is quickly absorbed into the bloodstream, leading to its stimulating effects on the central nervous system.

Trimethylxanthine

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4
Q

Caffeine’s slow absorption is responsible for its delayed stimulant effect.
True or False?

A

False.

After ingestion, caffeine is quickly absorbed into the bloodstream, leading to rapid stimulating effects on the central nervous system.

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5
Q

Environment Canada, CFIA, and Fisheries and Oceans Canada all have some authority to control PSP outbreaks.
True or False?

A

True.

Environment Canada, the Canadian Food Inspection Agency (CFIA), and Fisheries and Oceans Canada all have roles in controlling paralytic shellfish poisoning (PSP) outbreaks. These agencies work together to monitor and manage marine toxin outbreaks, including PSP, to ensure public health and food safety.

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6
Q

DDT and related non-polar pesticides enter plasma blood pool from fat deposits.
True or False?

A

True.

DDT and related non-polar pesticides are lipophilic, meaning they can accumulate in fat deposits. Over time, they can enter the bloodstream from these fat stores and circulate through the plasma blood pool.

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7
Q

DDT and related non-polar pesticides are unable to enter plasma blood pool from fat deposits.

True or False?

A

False.

DDT and related non-polar pesticides are lipophilic, meaning they can accumulate in fat deposits. Over time, they can enter the bloodstream from these fat stores and circulate through the plasma blood pool.

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8
Q

Maximum level of saxitoxin present in shellfish should not exceed 80 μg/100g shellfish.
True or False?

A

True.

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9
Q

Maximum level of saxitoxin present in shellfish should not exceed 0.8 μg/100g shellfish.

True or False?

A

False.

Maximum level of saxitoxin present in shellfish should not exceed 80 μg/100g shellfish.

0.8 μg/100g tetrodotoxin is the regulatory limit for pufferfish poisoning.

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10
Q

Maximum level of tetrodotoxin present in pufferfish should not exceed 0.8 μg/100g tissue.
True or False?

A

True.

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11
Q

Maximum level of tetrodotoxin present in pufferfish should not exceed 80 μg/100g tissue.

True or False?

A

False.

Maximum level of tetrodotoxin present in pufferfish should not exceed 0.8 μg/100g tissue.

Maximum level of saxitoxin present in shellfish should not exceed 80 μg/100g shellfish.

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12
Q

Maximum level of domoic acid present in shellfish should not exceed 20 ppm.
True or False?

A

True.

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13
Q

Maximum level of domoic acid present in shellfish should not exceed 0.8 μg/100g shellfish.

True or False?

A

False.

Maximum level of domoic acid present in shellfish should not exceed 20 ppm.

0.8 μg/100g shellfish is the regulatory limit for tetrodotoxin.

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14
Q

Maximum level of domoic acid present in shellfish should not exceed 0.8 ppm.

True or False?

A

False.

Maximum level of domoic acid present in shellfish should not exceed 20 ppm.

Maximum level of brevetoxin present in shellfish should not exceed 0.8 ppm (20MU/100g).

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15
Q

Maximum level of brevetoxin present in shellfish should not exceed 0.8 ppm.

True or False?

A

True.
0.8 ppm (20 MU/100g)

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16
Q

Maximum level of brevetoxin present in shellfish should not exceed 20 ppm.

True or False?

A

False.

Maximum level of brevetoxin present in shellfish should not exceed 0.8 ppm (20MU/100g).

Maximum level of domoic acid present in shellfish should not exceed 20 ppm.

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17
Q

Migraines are sometimes generated by biogenic amine containing foods.

True or False?

A

True.

Migraines can sometimes be triggered by foods containing biogenic amines, such as histamine, tyramine, and phenylethylamine. These compounds are found in certain aged, fermented, or processed foods and can cause vasodilation, potentially leading to migraines in sensitive individuals.

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18
Q

Migraines are never generated by biogenic amine containing foods.
True or False?

A

False.

Migraines can sometimes be triggered by foods containing biogenic amines, such as histamine, tyramine, and phenylethylamine. These compounds are found in certain aged, fermented, or processed foods and can cause vasodilation, potentially leading to migraines in sensitive individuals.

19
Q

Caffeine competitively binds to […]

A

adenosine receptors, resulting in indirect release of norepinephrine, dopamine, seratonin, and GABA.

20
Q

[…] competively binds to adenosine receptors, resulting in […]

A

Caffeine competitively binds to adenosine receptors, resulting in indirect release of norepinephrine, dopamine, seratonin, and GABA.

21
Q

Domoic acid

A

Amnesic shellfish poisoning

22
Q

Amnesic shellfish poisoning

A

Domoic acid

23
Q

Sucralose is a […]

A

non-caloric sweetener

24
Q

LD50

A

Degree of toxicity

LD50 is the amount of a material, given all at once, which causes the death of 50% (one half) of a group of test animals.

25
Q

Food traceability is […]

A

a requirement of food safety

26
Q

Teratogenic

A

Non-lethal, abnormal changes to the fetus

27
Q

Non-lethal, abnormal changes to the fetus

A

Teratogenic

28
Q

Ricin

A

Toxic non-edible lectin

29
Q

Toxic non-edible lectin

A

Ricin

30
Q

Any substance foreign to the living system

A

Xenobiotic

31
Q

Xenobiotic

A

Any substance foreign to the living system

32
Q

Describe in one or two clear sentences, what factors would influence the subject variability to toxicity responses on exposure to multiple low doses of the aflatoxin B-1.

A
  • Subject variability to toxicity responses on exposure to multiple low doses of aflatoxin B-1 can be influenced by factors such as genetic differences in detoxification enzyme activity (e.g., cytochrome P450), age, nutritional status, immune function, and cumulative exposure to other environmental toxins.
  • These factors can alter the body’s ability to metabolize and excrete the toxin, leading to variable susceptibility.
33
Q

Describe the difference between biotransformation and bioaccumulation. Give 2 examples in your answer.

A

Biotransformation is the process by which a substance, typically a toxin, is chemically altered by the body’s metabolic system, often in the liver, to make it easier to excrete. This occurs through two phases.

  • Phase I reactions involve the modification of the toxin through processes like oxidation, reduction, or hydrolysis, typically mediated by enzymes such as cytochrome P450. These reactions introduce or expose functional groups (e.g., hydroxyl groups) on the toxin to make it more reactive or water-soluble. An example is the oxidation of aflatoxin B-1 by cytochrome P450.
  • Phase II reactions follow Phase I, where the modified toxin from Phase I undergoes conjugation with molecules like glucuronic acid, glutathione, or sulfate. This makes the compound even more water-soluble and easier to excrete. An example is the conjugation of benzo[a]pyrene (a polycyclic aromatic hydrocarbon) with glucuronic acid for easier elimination from the body.

Bioaccumulation, refers to the gradual build-up of a substance in an organism’s tissues over time, usually because the substance is absorbed faster than it can be excreted, or because there is an imbalance in phase I and II enzymes. An example of bioaccumulation is the build-up of DDT in the fatty tissues of animals, or mercury accumulating in the tissues of fish.

34
Q

Why is a deficiency in phase II enzymes dangerous?

A
  • A deficiency in Phase II enzymes is dangerous because it limits the body’s ability to detoxify and excrete harmful substances effectively.
  • After Phase I reactions, many toxins are converted into reactive intermediates, which can be more harmful than the original substance.
    • For example, a deficiency of glutathione S-transferase can lead to a carcinogenic reaction forming nucleic acid adducts.
  • Without adequate Phase II enzyme activity, these reactive intermediates accumulate, increasing the risk of cellular damage, oxidative stress, and mutagenesis, which may lead to diseases such as cancer.
35
Q

What is a nucleic acid adduct?

A
  • Nucleic acid adducts are abnormal chemical compounds that form when a reactive chemical, often a metabolite of a toxin, binds covalently to DNA or RNA.
  • These adducts are significant because they can cause mutations by disrupting the normal structure and function of the nucleic acid.
  • If the body fails to repair these adducts, they can lead to errors during DNA replication, which may cause mutations, potentially leading to cancer or other diseases.

For example, when there is a deficiency of glutathione S-transferase (phase II enzyme), aflatoxin B-1 secondary metabolites can form a DNA adduct with guanine, leading to mutations that can initiate cancer.

36
Q

Use a diagram to illustrate how phase I and phase II enzymes biotransform aflatoxin B-1.

A
37
Q

Use a diagram to illustrate how phase I and phase II enzymes biotransform brevetoxin.

A
38
Q

What are the major qualitative and quantitive DOPER activities that need to be considered to evaluate the toxicity of a food contaminant?

A

Detection (D) – Qualitative and Quantitative: This step involves identifying the presence of the contaminant in food using various methods (e.g., chromatography, bioassays). It also includes quantifying the contaminant’s concentration to assess exposure risk.

Occurrence (O) – Qualitative and Quantitative: This refers to understanding how frequently and where the contaminant is found in food sources. Data on its distribution in the food chain, geographical prevalence, and seasonal trends help evaluate the likelihood of exposure.

Properties (P) – Qualitative: Understanding the physical and chemical properties of the contaminant, such as its solubility, stability, and chemical structure, is essential to predict how it behaves in food and the body.

Effects (E) – Qualitative and Quantitative: This involves studying the toxic effects of the contaminant on health, including dose-response relationships. Qualitatively, this includes the types of damage (e.g., carcinogenesis, mutagenesis). Quantitatively, it includes metrics like LD50 (lethal dose for 50% of a population) to determine the potency of the toxin.

Regulations (R) – Quantitative: This refers to the established legal limits and safety thresholds for the contaminant in food. Regulatory bodies set permissible levels based on risk assessments, ensuring consumer protection.

39
Q

This diagram provides you with the major qualitative and quantitative DOPER activities that need to be considered to evaluate the toxicity of a food contaminant.

How would you apply the activities identified to accurately assess the toxicity, or hazard, of:

Aflatoxin - half-life

A
  • Half-life is defined as the time required for some measure of a toxicant in the body to decrease to half its concentration value observed at the initiation evaluation interval.
  • To assess the half-life of aflatoxin, I would use quantitative metabolism to determine the elimination rate constant.
  • I would administer a dose of aflatoxin to a mouse and measure the serum concentration of aflatoxin initially and then again at 6 – 10-time intervals.
  • Then I would plot the log[aflatoxin] vs. time to obtain a line via first order kinetics whereby the slope equals -k/2.303 (-k = elimination rate constant).
  • Then I could calculate the half-life of aflatoxin using the equation t1/2=0.693/k.
40
Q

This diagram provides you with the major qualitative and quantitative DOPER activities that need to be considered to evaluate the toxicity of a food contaminant.

How would you apply the activities identified above to accurately assess the toxicity, or hazard, of:

Lipid oxidation, reactive epoxides - mutagenic activity assessment

A
  • Mutagenesis is the induction of genetic damage (i.e., mutations).
  • To assess the ability of reactive epoxides from lipid oxidation to cause mutagenesis, I would use qualitative metabolism to determine the types of reactive epoxides formed.
  • I could do this using LC-MS and/or NMR to identify exactly which types of epoxides are formed, and determine their structure, which will be crucial to identify mutagenic potential.
41
Q

This diagram provides you with the major qualitative and quantitative DOPER activities that need to be considered to evaluate the toxicity of a food contaminant.

How would you apply the activities identified to accurately assess the toxicity, or hazard, of:

Artificial trans fats - NOEL

A
  • No observable effect level refers to the dose below which no measurable biological effects occur.
  • To assess the NOEL of artificial trans fats I would use hepatocytes in vitro to measure the metabolic activity and toxic effects on the cells at different concentrations of trans fats.
  • By identifying the highest concentration where no harmful effects occur (e.g., changes in enzyme activity or cell viability), I could determine the NOEL.
42
Q

This diagram provides you with the major qualitative and quantitative DOPER activities that need to be considered to evaluate the toxicity of a food contaminant.

How would you apply the activities identified above to accurately assess the toxicity, or hazard, of:

Saxitoxin - mouse bioassay

A
  • The mouse bioassay measures survival time in minutes to give MU.
  • HPLC-MS methods are available to quantitate all the PSP toxins in samples, and many workers have relied on the analytical methodology as, at least a first step in assessing risk.
  • With HPLC, you can quantify the amount of toxin and from records on MB results you can predict pretty well if the amount quantified has a serious health risk.
  • Nowadays, that is almost good enough and only on rare occasions where there is a possibility of lethality at a “high” concentration, will the testing go beyond to include a mouse bioassay to confirm lethality.

Notwithstanding all this, the MB is still considered the official method for PSP detection.

43
Q

This diagram provides you with the major qualitative and quantitative DOPER activities that need to be considered to evaluate the toxicity of a food contaminant.

How would you apply the activities identified above to accurately assess the toxicity, or hazard, of:

Caffeine - genotoxicity

A
  • Genotoxicity is similar to mutagenicity, but refers to the induction of DNA damage, which can include adduct formation or breakages, in addition to mutations.
  • To assess the genotoxicity potential of caffeine I would use physiologically based kinetic models to predict tissue concentrations of caffeine and its metabolites.
  • In this way, I could predict realistic exposure scenarios to assess the potential of caffeine to cause DNA damage.