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BIO367 - Forensic Toxicology > WEEK 7-12 OBJECTIVES > Flashcards

WEEK 7-12 OBJECTIVES Flashcards

1
Q

Outline the mechanism of action of caffeine.

A

Adenosine receptors
- G protein-coupled receptors with adenosine as endogenous ligand
- Caffeine is an antagonist at the A1 and A2A receptors

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2
Q

Caffeine will lead to

A

increased heart rate and decreased inhibition of the central nervous system
- Decreasing inhibition of the CNS will increase levels of neurotransmitters such as dopamine and hence it is a stimulant

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3
Q

Adenosine receptors are also involved in

A

sleep-wake cycle (desired effect to stay awake)

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4
Q

Caffeine depency

A
  • Generally defined as consumption of over 1000 mg of caffeine every day
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5
Q

Symptoms of caffeine dependency

A

irritability, restlessness, insomnia, headache and heart palpitations

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6
Q

Caffeine dependency and cancer/ and other disease or disorder

A
  • Gives a lower overall risk of cancer, but may increase the risk of some specific cancers
    o May also protect against cardiovascular disease, type 2 diabetes and liver disease
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7
Q

Caffeine overdose

A
  • Ingestion of over 500 mg caffeine at one time can lead to toxicity
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8
Q

initial symptoms of caffeine toxicity

A

anxiety, insomnia, muscle twitching, heart palpitations

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9
Q

extreme doses of caffeine can lead to

A

mania, depression, hallucination and breakdown of muscle tissues

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10
Q

LD50 of caffeine

A

LD200, so about 100 cups of coffee

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11
Q

death cause by (caffeine)

A

cardiac arrhythmia and arrest

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12
Q

Briefly outline the potential risks linked to food preservatives and colourings.

A
  • Artificial preservatives and colouring are controversial, and many have been linked with toxic effects
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13
Q
  1. What is meant by the term ‘protein substitution’?
A

Adulterated foods to artificially inflate protein content into a food product

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14
Q

Point of protein substitution

A

o Protein content in food is a highly desirable nutritional quality
o It is also very expensive to produce
o Other nitrogenous non-protein compounds can be added
o These can have potential toxic effects

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15
Q

What is the toxic mechanism of action of melamine?

A
  • Metabolism of melamine produces metabolites which crystallise in the kidney and bladder
    o The tubules of the kidney become blocked
    o These cause obstructive urolithiasis (stones), which can lead to renal failure
    o Can also cause bladder cancer and reproductive damage with chronic exposure
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16
Q
  1. What is meant by the terms ‘surrogate’ and ‘denatured’ alcohols?
A

o Surrogate alcohols – high level of ethanol (up to 95%)
o Denatured alcohols – ethanol that contains additives to make it poisonous or to give it a foul taste or smell to discourage recreational consumption (10% ethanol)

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17
Q

Methanol is a CNS

A

depresseant

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18
Q

methanol affects activity of

A

NS and brain

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19
Q
  1. Outline the mechanism of action of methanol.
A

Stimulation of some inhibitory neurotransmitters (GABA, glycine) and inhibition of stimulatory neurotransmitters

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20
Q

What are the two main toxic effects of methanol?

A

1) stimulation of inhibitory neurotrans and inhibition of simulatory neurotrans
——decrease HR, loss of consciusness
2) Toxication reaction in the liver
——methanol interacts with enzyme alochol dehydrogenase

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21
Q

what happens in the toxication reaction of methanol

A
  • In the liver, methanol interacts with the enzyme alcohol dehydrogenase
    o This converts the methanol into formaldehyde
    o Formaldehyde interacts with aldehyde dehydrogenase
  • This converts the formaldehyde into formic acid

toxiccc

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22
Q

Formic acid toxicity

Formic acid has two main toxic effects:

A
  1. Inhibition of cytochrome c oxidase
    o This causes cellular hypoxia; inhibits ATP production
    o Causes cell death, can target specific cell types such as the optic nerve
  2. Metabolic acidosis
    o Production of excess acid in the body that cannot be removed by the kidneys
    Blood pH will drop (< 7.35) leading to coma and death
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23
Q
  1. What are the two mechanisms of action of thujone?
A

1) Thujone is an antagonist at the GABAA receptor
2) Thujone also activates 5-aminolevulinic acid synthase

24
Q

1) Thujone is an antagonist at the GABAA receptor

A
  • This prevents inhibition, meaning that the CNS is more sensitive
  • While this will have effects throughout the body, the most apparent are muscle spasms and convulsions
    o May also contribute to psychoactive symptoms
  • In mice, the LD50 is 45 mg/kg
25
Q

2) Thujone also activates 5-aminolevulinic acid synthase, which catalyses this reaction:

A

succinyl CoA + glycine ———-> 5-aminolevulinic acid + CO2 + CoASH
- 5ALA is the first compound in the synthesis of porphyrins, e.g. haem
- Accumulation of porphyrins can lead to porphyria
o Symptoms include seizure, pychosis, weakness and extreme pain

26
Q

toxicity of ethylene glycol is not due to the molecule itself, but its

A

metabolites

26
Q

toxicity of ethylene glycol is not due to the molecule itself, but its

A

metabolites

27
Q

What are the three main toxic effects of ethylene glycol

A

1) Metabolic acidosis - CNS and cardiovascular dysfunction

2) Oxalic acid binds and inhibits the action of succinate dehydrogenase - **shut down **TCA cycle **

3) Associates with Ca2+ to form calcium oxalate - renal failure and CNS dysfunction

28
Q

Be sure to describe the physiological consequences of methanol toxicity

A
  • Symptoms occur in three stages:
    1. CNS: intoxication, followed by drowsiness or coma; seizures possible (death in 24 hours if dose high)
    2. Metabolism: acidosis
    3. Kidneys: acute renal failure (death in 2 weeks)
29
Q

how is diethylene glycol different from ethylene glycol in its effects

A
  • Metabolite that causes toxicity is 2-hydroxyethoxyacetic acid (HEAA)
  • It is likely the HEAA causes metabolic acidosis as well as damage to the kidney and liver
  • Symptoms occur in three phases:
    1. Gastrointestinal: nausea, vomiting; also some CNS symptoms (depression, altered mental status)
    2. Metabolic acidosis: leads to renal failure
    3. CNS dysfunction: lethargy, paralysis, coma
30
Q

What are the host factors that affect metal toxicity

A

1) interaction with essential metals
2) formation of metal-protein complexes
3) age and stage of development
4) lifestyle
5) immune status

31
Q

what are the important metal-binding proteins

A

1) metallothioneins
2) transferrins
3) ferritin
4) chelation

32
Q

Metallothioneins

A

o Cysteine-rich proteins attached to Golgi
- Bind and regulate physiological metals (Zn, Cu)
- Also bind toxic metals (Cd, Hg, Ag, As)
o Increased expression on metal exposure
o Provide some protection from toxic metals

33
Q

Transferrins

A
  • Plasma iron-binding proteins
  • Control level of free iron in body fluids
  • Bind to transferrin receptors and release iron into cell
34
Q

Ferritin

A
  • Intracellular iron-binding protein
  • Binds to other toxic metals, provides protection
35
Q

Chelation

A
  • Some organic compounds will bind with metals
    o Used for treatment of metal poisoning
  • These are called chelating agents
    o British anti-Lewisite (BAL)
    o Dimercaptosuccinic acid (DMSA)
    o Pencillamine
    o Ethylenediamine tetraacetic acid (EDTA)
    o Deferoxamine/deferasirox
36
Q

Toxic mechanism of arsenic

A

binds to thiols (CoA), inhibits pyruvate dehydrogenase (shuts down TCS and leads to ATP depletion, necrosis)

37
Q

Toxic mechanism of lead

A

binds to sulfhydryl groups (modifies enzyme activity especially neuronal and kidney cells), hijacks Ca transporter (nephrotoxic, degrades myelin sheath of neurons)

38
Q

Toxic mechanism of mercury

A

irreversibly inhibits selenoenzymes, can also inactivate S-adenosyl-methionine

39
Q

Describe the toxic mechanism of cadmium. Which other metals have the same basic mechanism?

A
  • Inside the cell, Cd causes high levels of H2O2
    o Causes oxidative stress
  • Particularly affects lungs and kidneys
    o Death usually due to kidney failure
    o Also causes bones to become soft
    o Chronic exposure causes cancer
  • Chromium, copper, copper, iron, nickel
40
Q
  1. How does zinc toxicity differ from that caused by cadmium?
A
  • Zinc will cause oxidative stress in cells
  • Zinc reacts with stomach acid to form corrosive zinc chloride
  • Nerve receptors in the nose are susceptible
    o Can cause anosmia
    o Excess zinc suppresses iron absorption
41
Q

Toxic mechanisms of cobalt

A

stabilises hypoxia inducible factor (HIF) so mimics effects of hypoxia, causes cell damage and necrosis

42
Q

Toxic mechanism of magnesium

A

overdose can cause electrolyte imbalance and kidney disorder, can cause cardiac arrest

43
Q

mechanism of action of chlorine gas

A
  • It reacts with water in the lungs to form hydrochloric acid
44
Q

How can chlorine gas be toxic

A

destroys lung tissue and causes death by asphyxiation

45
Q

mechanism of action of phosgene gas

A

acts on proteins in the alveoli of the lungs

46
Q

how can phoshene be toxic

A
  • It reacts with the amine groups of the proteins and creates urea-like cross-linkages
  • This disrupts the blood-air interface, reducing the ability of the lungs to exchange O2 and CO2
  • Death is caused by asphyxiation
  • It also produces HCl which damages lung tissue
47
Q

mechanism of action of mustard gas

A
  • Highly lipophilic, so readily absorbed into the skin
    o Forms a cyclic sulfonium ion that is very reactive
    o This ion alkylates guanine nucleotides in DNA, preventing cell division and triggering apoptosis or tumourigenesis
    o It also causes oxidative damage to the cell
48
Q

toxicity of mustard gas due to

A

the ion alkylates guanine nucleotides in DNA, preventing cell division and triggering apoptosis or tumourigenesis

It also causes oxidative damage to the cell

49
Q

mechanism of lewisite gas

A
  • Arsenite binds to pyruvate dehydrogenase and prevents conversion of pyruvate to acetyl CoA
50
Q

toxicity of lewisite gas

A

1) shuts down TCA cycle and aerobic respiration
2) lack of ATP leads to weakness and restlessness

51
Q

mechanism of action of nerve gases

A

AChE inhibitors

52
Q

how nerve gases lead to toxic effects

A

o It binds to the active site and inactivates the enzyme
o Without AChE, ACh builds up in the synapse, preventing the muscle from relaxing

then loss of bodily function, spasms, death by respiratory paralysis

53
Q

Two broad types of nerve gas

A
  1. G-series: initially developed in Germany
    o First developed was tabun
    o Discovered by the Allies after WWII
    o Example: sarin
  2. V-series: developed by UK, US and Russia
    o Example: VX gas
54
Q

mechanism of action of dioxins

A
  • Dioxins interact with a specific receptor, the aryl hydrocarbon receptor (AHR)
    o AHR is a transcription factor, regulating gene expression
    o Binding of dioxins to AHR induces expression of a group of cytochrome P450 enzymes that break down foreign compounds
    o These enzymes can also break down important endogenous compounds
55
Q

key effects of dioxins include

A

1) Immunotoxicity
2) Endocrine disruption
3) Tumour promotion

BIO367 - Forensic Toxicology (3 decks)

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