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Toxicology > Toxicology - deck II > Flashcards

Toxicology - deck II Flashcards

1
Q

tolerance can be caused either by: (2)

A

Induction of enzymes metabolizing the toxic compound or

Change of the number or binding capacity of specific receptor groups.

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2
Q

Objective Factors influencing the intensity of toxic response (7)

A

Physico-chemical properties of the toxicant
Dose of toxicant

Previous dose(s) of toxicant
Mechanism and ways of action of toxicant

Synergistic or antagonistic effect of other substances (drugs)

Nature of job
Factors connected with job environment

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3
Q

mitochondrial enzyme cytochrome
oxidase

A

is the terminal complex of eukaryotic oxidative phosphorylation in mitochondria.

if cytochrome oxidase is inhibited (such as by cyanide ion) oxygen usage by cells will be prevented -> injury, cell death

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4
Q

Lead accumulates in the –?–, but toxic effect emerges mainly in soft tissues
such as the liver, kidneys, and blood cells.

A

Lead accumulates in the bones, but toxic effect emerges mainly in soft tissues
such as the liver, kidneys, and blood cells.

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5
Q

DDT, which is first of all toxic to the CNS, preferably accumulates in the –?–.

A

DDT, which is first of all toxic to the CNS, preferably accumulates in the adipose tissues.

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6
Q

Paraquat

A

a very toxic
herbicide with a broad spectrum of activity, destroys all green plant
tissues by interfering with the intracellular electron transfer systems,
thereby inhibiting reduction of NADP to NADPH during photosynthesis.

Poisonous to higher organisms as well and a well-characterized pneumotoxicant.

Banned in teh EU.

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7
Q

Toxicants can be classified according to: (min. 5)

A

Chemical structure Usage
Physical state

Physiological effect Biochemical mechanism of toxic effect

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8
Q

phospholipidosis

A

excessive reversible
accumulation of intracellular phospholipids

All chemicals that affect cellular phospholipid metabolism belong to the class
of cationic amphiphilic drugs (CADs)

The mechanism of phospholipidosis is not fully clarified yet, induction of this process
likely occurs by different mechanisms.

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9
Q

how does Acetylsalicylic acid cause biochemical injury

A

aspriin, an NSAID can cause
the death of an organism through a ATP deficiency in several organs, evoking acidosis
and hyperthermia.

Aspirin is converted by esterases (phase I) into main metabolite
salicylic acid, the actual culprit behind aspirin toxicity.

Salicylic acid is an inhibitor of the electron transport chain in mitochondria,
blocks production of ATP, eliciting an increase in the use of oxygen and production of
acidic carbon dioxide (CO2).

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10
Q

The treatment of aspirin intoxication consists of (3)

A
  • a reduction of acidosis by raising the blood pH
  • compensation of the lacking energy by administration of glucose
  • acceleration of elimination of salicylate (urine pH up).
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11
Q

Aneuploidy

A

is a deviation in the multiplicity of single chromosomes, that is,
disappearance or addition of chromosomes.

Many mutagenic carcinogens are aneuploidogens.

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12
Q

Clastogenesis is

A

an addition or reorganization of parts of a chromosome
Known clastogens include acridine yellow, benzene, arsenic, mimosine etc.

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13
Q

Point mutations

A

replacement of one base pair with another in the molecule of DNA.
Most often, bases of the same type are replaced with each other (purine with another
purine or pyrimidine with another pyrimidine; A ↔ G; C ↔ T).

This type of replacement or transition is caused, for example, by nitrous acid (HNO2).

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14
Q

Transversions are

A

a rarer type of point mutation, replacement of a purine with a pyrimidine and vice versa (C/T
↔ A/G). It can render the amino acid code wrong.

A point mutation can be reversed by another point mutation (inverse mutation).
As a result, the initial structure of the nucleotide will be restored.

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15
Q

„frame shift mutation“

A

Insertions add one or more nucleotides to the DNA molecule.

Deletions remove one or more nucleotide groups from DNA molecule.

In the case of insertions and deletions, reading of the whole genetic code becomes
disturbed, “shifted”.

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16
Q

Mutagens are according to their action mechanism, divided into: (3)

A

Destructurating – hydrogen peroxide (H2O2), nitrates, and nitrites. The last two are mutagenic to bacterial but not to mammal cells.

Joining – substances, containing a highly reactive alkylic group like epoxides, dialkyl
sulfates, and lactones-

Replacing, such as nucleic acids.

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17
Q

N-nitrosoamines

A

suspected of causing cancer

e.g. Alcohols induce CYP isoform that activates N-nitrosoamines

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18
Q

what are PAH

A

Polyaromatic hydrocarbons or polycyclic aromatic hydrocarbon, formed from organic material at
barbecuing and smoking

are nonpolar and lipophilic.

Cancer is a primary human health risk of exposure to PAHs & environmental pollutant.

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19
Q

Maillard reaction

A

is a chemical reaction between amino acids and reducing sugars that gives browned food its distinctive flavor.

In food science the Maillard reaction is well known to cause degradation of amino acids and an overall decrease in the nutritional value of foods that have been subjected to heat in processing.

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20
Q

oncogenesis is a multi-step process with the following sequence
of main stages:

A

(1) initiation →
(2) promotion →
(3) transformation →
(4) progression with
neoangiogenesis

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21
Q

Classification of carcinogens, name the 3 groups

A
  1. Genotoxic
  2. Epigenetic
  3. Non-classified
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22
Q

describe genotoxic carcinogens

A

interacting directly with a molecule of DNA

Genotoxic carcinogens can be divided into activation independent (primary) and
dependent (secondary) carcinogens and a heterogenous group with the common
name ‘inorganic compounds’.

Directly DNA-reactive genotoxic carcinogens are of the highest concern because
they do not have a dose below which they are not carcinogenic.

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23
Q

describe epigenetic carcinogens

A

not interacting with DNA

usually act at high contact levels,
leading to prolonged physiological abnormalities, disruption of the hormonal balance,
and tissue damage.

includes: cancer promoters such as various chlororganic pesticides, PCBs and dioxins,

endocrine modificators, immunosupressors such as cyclosporin

etc.

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24
Q

describe nonclassified carcinogens

A

The actual degree of toxicity of various carcinogens in this group is very different.

for example, acrylamide, dioxane, furfural, and sugar
alcohols.

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25
Q

Genotoxic carcinogens can be divided into (2)

A

activation independent (primary) and
dependent (secondary)

carcinogens and a heterogenous group with the common
name ‘inorganic compounds’.

The group of genotoxic carcinogens needing chemical activation is much larger.

Inorganic DNA-reactive carcinogens are, for example, metals such as Cd, Cr, Zn, Ni,
asbestos.

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26
Q

aflatoxin B1

A

the most potent food carcinogen

produced by Aspergillus flavus and -parasiticus.

occurs in foods such as groundnuts, tree nuts, maize, rice etc. as a result of fungal contamination before and after harvest.

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27
Q

the most notorious teratogen

A

thalidomide

scandal happened back in 1961

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28
Q

The homeostatic parameters of the cell are divided into two large groups:

A
  1. Materials the cell needs for energy supply, growth and repair
  2. Environmental factors – osmotic pressure,
    temperature, pH, etc.
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29
Q

Endocrine disruptors are

A

xenobiotics that cause systemic adverse effects to an organism or its offspring by
disturbing functioning of the endocrine system.

Are divided into anthropogenic and natural compounds.

Endocrine disruption is a sophisticated and very insidious mechanism of toxic responses.

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30
Q

name 2 natural endocrine disruptors

A

mycotoxin zearalenone synthesized by microfungi
and

phytoestrogens like genistein from soybean

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31
Q

vitellogenin

A

a protein normally synthesized by female fish as a response to the effect of estrogens.

is a biomarker of endocrine disruption of fish, its synthesis in male fish is caused for example by alkylphenols and synthetic estrogen ethynylestradiol.

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32
Q

Binding of a reactive electrophile to the nucleophilic site (nitrogen bases) of DNA
leads to

A

genotoxicity.

When the frequency of these reactions exceeds the self-repair ability of a cell, such covalent binding can lead to an irreversible formation of a tumor.

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33
Q

alfatoxins produced by?

A

mycotoxins called aflatoxins produced by molds such as Aspergillus flavus and A. parasiticus, aflatoxin B1 (AFB1) being the most toxic and carcinogenic.

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34
Q

Organophosphorus pesticides (OP) and other esters of phosphoric acids and
carbamates bind in the nerve tissue to the active centre of

A

acetylcholinesterase (AChE).

The process results in an inhibition of AChE, leads to an accumulation of ACh and persistance
of the nerve excitation.

Process is accompanied by a number of serious physiological disorders.

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35
Q

What is oxidation?

A

oxidation is joining of a substance molecule with oxygen atom(s)

Oxidation in broader sense - the chemical process where valence electrons move from
one molecule (electron donor) to another molecule (electron acceptor - oxidant)

  • First molecule gets oxidized, the second reduced.
  • Summary of process is a redox reaction.
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36
Q

Various free radicals or molecular particles,
with unpaired valence electrons or a single electron
on one or several atoms, give chain reactions
comprising

A

initiation, propagation and termination.

37
Q

Biological free radicals can be (2)

A
  1. Reactive oxygen species
  2. Reactive nitrogen-oxygen species
38
Q

Oxidative damage of a cell is caused by unstable free radicals
that have

A

one or several non-paired electrons on their electron orbitals.

Such a particle has a tendency to take an electron to its semi-free orbital from another
suitable particle (Nature abhors a vacuum).

As a result, a new particle with an unpaired electron is formed.

39
Q

Oxidants are capable of affecting body systems how? (3)

A
  • (per)oxidate cellular lipids into (per)oxides
  • oxidate and decompose proteins
  • react with molecules of DNA and RNA.

Alterations in the structure of these macromolecules of utmost importance for the cell, they can disturb various cellular systems, such as signal transmission, defence, and repair.

40
Q

Recent studies demonstrate that oxidative stress and oxidative DNA damage may be involved in the cytotoxicity of

A

different pesticides, as well as heavy metals.

41
Q

The antioxidant defense system of a cell,
comprising:

A

 enzymes

 low molecular antioxidants such as ascorbic acid tocoferol
uric acid (most important antioxidant in blood plasma), glutathione.

42
Q

Defense against free radicals can be intensified by feeding

A

antioxidants (incl. free radical scavengers), such as plant polyphenols or antioxidant peptides of fermented meat and dairy products .

43
Q

The action mechanisms of both endogenous as well as exogenous food antioxidants are:

A
  • Retardation of superoxide formation in mitochondria
  • Scavenging of ROS (free radicals) with formation of more stable radicals
  • Chelation or removal of the transition metals (Cu, Fe, Co, Ni, Zn, Mn, Cd, Cr, etc.) from
    the radical formation site
  • Reduction of the already formed hydroperoxides
  • Repair of the injured molecules
44
Q

In order to prove the exposure to a toxic substance and to assess the response and
sensitivity of the organism, respective biomarkers are needed that can be divided into
three interconnected types:

A
  1. Biomarkers of exposure indicate that contact of an organism with a toxicant has
    occurred.
  2. Biomarkers of response (effect) indicate that the organism has somehow responded to the effect of a toxic substance. Significantly more than biomarkers of exposure.
  3. Biomarkers of susceptibility showing a presumed sensitivity to the effect of a toxic
    substance.
45
Q

Biomarkers of presumed susceptibility
can be determined for every single member of a population. Such markers can be:

A
  • Genetic deficiency of an enzyme (for example CYP2D6 or N-acetyltransferase) participating
    in detoxification or metabolism of a xenobiotic.
  • A certain substance reflecting an elevated reactivity of a receptor.
  • A certain substance appearing as a result of a metabolic disorder such as deficiency in
    glucose 6-phosphate dehydrogenase.
46
Q

Toxicogenomics is

A

a new branch of toxicology,
studying the dependence of the structure and activity of the genome on toxic effects of foreign compounds.

Toxicogenomics allows following the defense and compensatory responses
of the cell to the damaging effect of a xenobiotic,
so preceding the formation of a pathological situation.

47
Q

what is nutrigenomics

A

A totally new study area elucidating the effect of foodstuffs on the
genome on the transcriptional level.

48
Q

Nowadays, both designing and execution of animal tests are subjected to the principle of the three R’s

A

replacement, reduction, refinement

Animal tests should be, replaced by in vitro tests as much as possible, their number
should be reduced and their methods refined.

49
Q

Risk =

A

hazard × exposure

50
Q

Chemical hazard is an

A

intrinsic property of a substance to cause adverse effects, arising
from its chemical structure.

51
Q

safety is

A

, a practical certainty that no adverse effects will occur, when a
substance is used in the manner and quantity anticipated for its use.

52
Q

When speaking about toxicological safety, it is always required to

A

indicate
the conditions (test animals, experimental method, etc.),
in which the safety of a compound has been proved.

53
Q

Toxicological safety is

A

the high probability that injury will not result from exposure to
a substance under defined conditions of quantity and manner of use, ideally controlled
to minimize exposure.

54
Q

Risk assessment is based on the principle

A

that in the case of most, but not all, substances,
the adverse response depends on the dose.

55
Q

Risk assessment consists of four basic steps:

A
  • Hazard identification
  • Dose-response relationship demonstration
  • Exposure assessment
  • Risk characterization
56
Q

Therapeutic index (TI) is

A

the ratio of the toxic dose (TD) of a substance to its effective dose (ED) that is necessary for
achieving the expected therapeutic effect.

TI = TD50 / ED50.

57
Q

Most drugs have TI of

A

2 or higher.

A drug with TI of about 2 is still dangerous and the patient must be watched carefully for signs of toxicity (side effects).

TI around of 1 is common for cancer chemotherapeutics.

58
Q

Drugs with TI of 5 or higher are

A

safer.

Some drugs like a few of the antibiotics with great selectivity and minimal toxicity that kill prokaryotic bacteria but have little or no effect on eukaryotic human cells have TIs 50-100.

59
Q

Most often the combined safety factor of

A

10×10=100 is used in the risk assessment.

  • 10 times – considering variability of humans
    in response to a toxic effect
  • 10 times – considering interspecies variability
    (for transition from animals to humans)
60
Q

Risk characterization Meta-analysis is a

A

statistical analysis of a large collection of results from individual
studies, such as experimental studies, opinion surveys and causal models,
for the purpose of integrating the findings to produce a more precise estimate of the
effect of a particular intervention or treatment, with an increased statistical power.

61
Q

The risk-benefit–analysis procedure does what

A

weighs the adverse and beneficial physiological effects that a substance like a food component may have, in order to facilitate more informed management decisions regarding public health issues.

62
Q

the different environmental compartments

A

soil, air, water

63
Q

By identifying the presence of chemicals in the environment, studying their behavior in the different compartments (degradation into metabolites, etc) and measuring their
environmental concentrations, toxicologists obtain

A

the exposure information
necessary to evaluate the likelihood of risk and toxic effects.

64
Q

Concentration of substances in different environmental
compartments are expressed using two differenet systems.

A
  • mg/liter (mg/l) for liquids like water
  • mg/gram (mg/g) for solids
  • mg/cubic meter (mg/m3) for air
    etc.

or

parts per million (ppm) is1 mg/kg = 1 ppm
parts per billion (ppb) is 1 ng/g = 1 ppb
parts per trillion (ppt) is 1 ng/kg

65
Q

Who was Rachel Carson

A

(1907-1964) is the mother of environmental toxicology, as she made it a distinct field within toxicology 1962 with the publication of her conceptional book Silent Spring, which covered the effects of
uncontrolled pesticide use.

66
Q

Environmental toxicology can be defined as

A

the field of science that studies sources, transport,
properties and fate of environmental toxicants and their metabolites
and degradation products in the air, water and soil environments and
in food chains, and their harmful effects on living organisms, as well
as their effects on human health and the natural environment

67
Q

Environmental toxicants can be divided:

A
  • Man-made or anthropogenic (most)
  • Natural toxins, hormones, vitamins, also minerals (arsenic,
    selenium, fluorine)
68
Q

Main exposure routes of humans to environmental toxicants (4)

A

air
soil
surface water
ground water

69
Q

VOC

A

Volatile Organic Compounds (VOC) such as household acetone, formaldehyde,
turpentine

these are harmful environmental toxicants

70
Q

SOC

A

Synthetic organic chemicals (SOC) - organic compounds, created through industrial synthesis that are less volatile than VOLATILE ORGANIC COMPOUNDS.

Some SOCs are volatile, whereas others tend to remain dissolved in water or other solvents.

SOCs are used as pesticides, defoliants, fuel additives and as ingredients for other organic compounds.

these are harmful environmental toxicants

71
Q

radon

A

is an odorless, invisible, radioactive gas naturally released from rocks, soil, and water. Radon can get into homes and buildings through small cracks or holes and build up in the air. Over time, breathing in high levels of radon can cause lung cancer.

72
Q

BPA

A

Bisphenol A is a chemical compound primarily used in the manufacturing of various plastics.

one of the common household environmental toxicants

73
Q

BHA

A

Butylated hydroxyanisole is a synthetic, waxy, solid petrochemical. Its antioxidant properties have caused it to be widely used as a preservative in food, food packaging, animal feed, cosmetics, pharmaceuticals, rubber, and petroleum products.

one of the common household environmental toxicants

74
Q

Non-anthropogenic Sources of environmental toxicants

A

Geochemical pollutants-toxicants that plants absorb from soil and watersuch as arsenic (As), selenium (Se), fluorine (F) ; copper (Cu); vulcanoes

75
Q

Top source of environmental pollution are

A

fossil fuels

In modern societies, oil, gas, coal… are among the most serious sources of environmental pollution.

Combustion of fossil fuels produces extremely high levels
of air pollution, and contributes to soil and water contamination.

76
Q

Non-fossil sources of environmental pollution

A

Uranium in nuclear power plants
Agriculture (livestock)
Trading activities (packaging)
Residential sector (soil & water pollution)

77
Q

Most notable air pollutants
are (min. 5)

A

CO (carbon monoxide),
NO2 (nitrogen dioxide, SO2 (sulfur dioxide,
ozone,
VOC (Volatile Organic Compounds)

and airborne particles containing radioactive pollutants probably among the most destructive ones (specifically when produced by
nuclear explosions).

78
Q

Different events can happen to a chemical
in the period between release to environment and arrival at the biological site of action
in an organism (4)

A
  1. Dissemination (dilution)
  2. Bioaccumulation
  3. Biotransformation
  4. (Bio) degradation
79
Q

Kow

A

is the distribution coefficient of a substance between hydrophobic (non-polar) and hydrophilic (polar) liquid phases measured as the ratio of concentrations of this
substance in those phases in equilibrium state at definite temperature.

80
Q

The higher is Kow, the more

A

hydrophobic (lipophilic) this substance is and
than easier it 1. crosses biomembranes and 2. concentrates in biotic sphere.

81
Q

Fate of pollutants in soil
depends on

A

the soil properties and the physical and chemical
characteristics of pollutant molecules.

Essentially, the uptake of pollutants in the soil is the result of chemical attraction and formed bond strength.

82
Q

what are POP

A

Persistent organic pollutants (POP)
are organic compounds that are resistant to environmental degradation through any chemical, biological or photolytic process.

Application of pesticides over large areas is sustainable if their molecules degrade
naturally, but some organic pesticides are the most widespread POP used in agriculture worldwide.

83
Q

what is the strongest type of chemical bond?

A

a covalent bond is the strongest bond, In such bonding, each of two atoms shares electrons that bind them together.

84
Q

Adsorption of molecules to other chemical components of the soil matrix or soil
biosphere, does what?

A

protects them from both chemical and biological degradation.

Non-adsorbed molecules are bioavailable and therefore exposed to degradation.

85
Q

The bioaccumulation factor depends on

A

molecular size and correlates positively with a lipophilic character measured by the Kow.

86
Q

Adsorption or not of a molecule in the soil is a key step to define what?

A

bioaccumulation.

87
Q

The only efficient policy for recalcitrant molecules that can not be controlled by
remediation is

A

the restriction of their use or banning them altogether.

88
Q

Environmental pollutants are divided into

A

biodegradable and non-biodegradable ones.

Toxicology (6 decks)

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