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Toxicology > Pesticides > Flashcards

Pesticides Flashcards

1
Q

Give an example of an agricultural crop insectiside

A
  • organophosphates
    = for aphids, grasshoppers, orange wheat blossom midge
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2
Q

Give an example of a Agricultural animal insecticides

A
  • organophosphates
    = for scabies/mites ect or using diazino for sheep dips
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3
Q

List the 4 types of domestic insecticides and give examples

A
  • Garden plant (pyrethroids) for aphids
  • Home (pyrethroids) for flies, ant, woodworm
  • Medical treatment (organophosphates) headlice/scabies
  • Pet flea control (organophosphates) Diazinon flea collars
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4
Q

what is the use of triticonazole

A

stop black spots on plants, mildew

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5
Q

what is the use of ketoconazole

A

Fungicides = dandruff, athletes foot, nail infection

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6
Q

Outline the benefit/risks of using pesticides

A

they are useful because they are harmful
Benefits = improves/protect our healths (control vector borne disease like malaria), allow production of abundant, inexpensive agricultural products
Risk = Toxicity to non-target species, some are pervasive in environment (e.g organochlorines like DDT)

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7
Q

how is the risk associated with pesticides decreased

A
  • using pesticides that are selective for target e.g neonicotinoides
  • regulation to reduce exposure
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8
Q

All insecticides are _ and act by targeting the insect __

A

neurotoxicants
nervous systems

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9
Q

how do isecticides work

A

cause hyperexcitability of nervous system leading to paralysis and death of isects
- by variety of different mechanisms of action
- majority generally non-selective so affect mammalial NS target

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10
Q

what are organophosphates and what some uses barr insecticides

A

Organic derivatives of phosphates, phosphonates or phosphinates (e.g. Diazinon, chlorpyrifos)
OP class is large (100s) and applications diverse
Lubricants e.g. motor oil or hydraulic fluids e.g. aviation due to their viscosity and high pressure and fire resistant properties.
Flame retardants in textiles, furniture etc e.g. triphenyl phosphate

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11
Q

Given an example of organophsosphates nerve agents

A

soman, VX, sarin, tabun, novichok

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12
Q

Despite having different LD50s, most organophosphates induce _

A

same acute toxicity - just depends on dose

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13
Q

what are the symptomology of parasympathetic innervation due to acute toxicity due to organophosphates

A

Lacrimation (tears), Salivation, Sweating, Bronchoconstriction / bronchospasm, Bronchorrhea, Diarrhoea, bradycardia (slow heart rate), miosis
= parasympathetic innervation =

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14
Q

what are the symptomology due neuromuscular junction activation to acute toxicity due to organophosphates

A

Fasiculation (involuntary muscle twitches), tachycardia (fast heart rate), hypertension, muscular weakness

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15
Q

what is the cellular reason for toxicity due to organophosphates

A

Parasympathetic NS = activation of muscarinic cholinergic receptors
Neuromuscular junction = activation of nicotinic cholinergic receptors
CNS = activation of muscarinic and nicotinic cholinergic receptors
↑ Acetylcholine = Hypercholinergic toxicity

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16
Q

what are the symptomology due to CNS activation to acute toxicity due to organophosphates

A

Anxiety, confustion, tremor, convulsion, respiratory depression, coma

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17
Q

How are organophosphates effected by the cells

A

Most OPs are bioactivated.
P=S -> P=O -> potent acetylcholinesterase inhibitors
(some OPs already have P=O bonds e.g sarin)
Phase I metabolism by CYP450 causes this oxidative desulfaration to Oxons

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18
Q

What happens to oxons in the cells

A

Hydrolysed by esterases
1- catalytic hydrolysis by A-esterases (PON1)
2 - non-catalytic hydrolysis by B-esterases (AChE)

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19
Q

How does AChE normally work

A

AChE hydrolysis ACh in the synaptic cleft
However bond between active site on AChE and acetate relatively weak, so AChE recovers quickly and the cycle returns

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20
Q

Hoe does AChE cause acute toxicity when interacting organophosphates

A

AChE hydrolyses OP oxon instead of ACh
Bond between active site on AChE and P of oxon more stable - can take hours/days to break bond
Therefore AChE cannot hydrolyse ACh i.e. inhibited = build up of ACh

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21
Q

How is organophosphates detoxificated

A
  • A-esterases e.g. liver ands plasma PON1 hydrolyse the oxon so AChE reactivated = hydrolysis products excreted
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22
Q

PON1 polymorphisms have _

A

differing catalytic efficiencies towards OPs
Evidence some people are therefore more susceptible to OP toxicity

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23
Q

what is Aging and how does it effect OP acute toxicity

A
  • hydrolysis of one of the alkyl groups
  • if aging occurs AChE is irreversibly inhibited
    = need to make new AChE which takes days
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24
Q

how does oximes work and given an example of one

A

(hydroxylamine derivatives) = pralidoxime (2-PAM)
attaches to AChE, breaking the bonds between the phosphates of oxon and AChE therefore AChE is reactivated
= must occur before aging !

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25
Q

how is organophosphate acute toxicity treated

A

Atropine (muscarinic Rec antagonist) - blocks mAChR stimulation by ACh
Benzodiazepines (GABAa receptor allosteric modulators) - anticonvulsants
Supportive care - clear airways of mucus, oxygen administration and artificial respiration

26
Q

what is organophosphates intermediate syndrome

A
  • develops 24-96h post cholinergic crisis
  • 20-50% of acute poisoning cases
    = weakness/paralysis of muscles innvervation by cranial nerves (neck, intercostals, proximal limbs)
    = respiratory paralysis so need ventilation (no treatment, only support)
    = may lead to death (15-40%), recovery can take up to 30 days
27
Q

what is the toxicological mechanism of intermediate syndrome

A
  • receptor desensitisation at neuromuscular junction from overstimulation
  • muscle damage by localised hypercontractions at the NMJ
28
Q

What OP-induced delayed neuropathy

A

Tend to be OPs with industrial uses (e.g tri-ortho-cresyl phosphate, TOCP)
Develops 2-3 weeks after exposure = Tingling of hands, feet, sensory loss, muscle weakness and flaccidity of muscles at extremities
= Axonpathy = degeneration of axon at distal end and at terminals
- NOT RELATED TO AChE -

29
Q

What is the mechanism behind OP-induced delayed neuropathy

A

Inhibits another esterase = Neuropathy target esterase (NTE) in nerve tissues. NTE phosphorylated by OP but has to age to cause OPIDN
- Mechanism remains obscure -
May be because NTE important for membrane phospholipid homeostasis

30
Q

there is evidence that low level repeated exposure to organophospahtes -

A

1 - Memory and attentional deficits
2- Increased risk of anxiety disorders and depression
Mostly occupational exposures (sheep dippers/field sprayers)
- Contradictory findings = Contentious

31
Q

what is the neuropsychological caused by organophosphates

A
  • 5-HT heavily implicated in aetiology of anxiety and depression
  • Evidence that prenatal exposure alters expression of 5-HT proteins
  • Maybe OPs have another primary mechanism of action besides cholinesterase inhibition? or the effects on 5-HT (proteins, anxiety and behaviour) are secondary neuroadaptations?
32
Q

where in the brain shows the greatest cholineresterase inhibition following in vivo OP exposure

A

dorsal raphe nucleus

33
Q

Using clincial test - what two receptors are responsibel for increase in nueronal activity after organophsopahte application

A

muscarinic
glutamate

34
Q

In vivo diazinion exposure causes what -

A
  • alters 5-HT proteins and increases neuronal activaty in the dorsal raphe nucleus
  • decrease in inhibitory 5-HT1a receptor sensitivity
  • decrease in 5-HT transporter
  • increase in firing rate
35
Q

how is the possible link between OP exposure and depression/anxiety explained

A
  • decrease in inhibitory 5-HT1a receptor sensitivity in dorsal raphe nucleus
  • this is seen in depression and OP exposure
36
Q

what is carbamates

A
  • derivatives of carbamic acid (NH2COOh) e.g aldicarb
37
Q

what is the symptoms of acute toxicity from high levels of carbamates

A

Confusion, headache, restlessness, anxiety, poor concentration, tremor, ataxia, hypotension, respiratory depression, convulsions and coma
= CNS effects the same as OP toxicity
= AChE inhibitors

38
Q

How is carbamylation of AChE different to phosphorylation by OPs

A

carbamylation = short lasting (reversible)
phosphorylation by OPs = irreversible
= rapid regeneration of AChE compareed to inhibition by organophosphate

39
Q

what is the uses of carbamates

A
  • Physostigmine (eserine) = alkaloid of the calabar bean, improves muscle tone in GI tracts to treatment poor gut motility
  • Rivastigmine = used as treatment in Alzheimers disease, improves cholinergic transmission in the CNS to compensate for neurodegeneration
40
Q

what are organochlorines and given examples

A

Organic compunds (contains carbon & hydrogen) that contains at least one covalently bonded chlorine atom CL2
- Chlorinated ethane derivatives e.g. DDT
- Hexachlorocyclohexanes e.g. Lindane
- Cyclodienes e.g. Dieldrin

41
Q

why should organochlorines be carfully observed when in use

A

Are not easily metabolised and very lipophilic so bioaccumulate in humans and animals and in the environment = persistent organic pollutant

42
Q

what is the acute toxicity of DDT

A
  • quite rare
    first sign often hyperesthesia of the mouth followed by paraesthesia
    Headaches, fatigue, tremor, muscle weakness, convulsion
    CNS effect - often reversible
43
Q

very high dose of the organochlorines DDT can cause

A

death due to CNS effects

44
Q

Explain how chronic low level exposure to the organochlorines DDT effects

A

associated with psychological illness, peripheral neuropathy, parkinsonism

45
Q

what is the mechanism linked to chronic low level of the organochlorine DDT toxicity

A
  • increase excitability of CNS
    -slows closure of Na channels so depolarising phase of action potential is prolonged = ↑ probability of repetitive firing
46
Q

In contrast to DDT, lindane are _ _ through _ but do not cause _

A

readily absorbed
skin
tremor

47
Q

how does lindane cause acute toxicity

A

Convulsion
↑ excitability by blocking inhibitory GABAA receptor channel opening

48
Q

how does lindane mechanically cause acute toxicity

A

block GABA receptors channel opening by binding to picrotoxin site

49
Q

how is lindane caused tremor/convulsions treated

A

diazepam

50
Q

what is Pyrethrin

A

extract from the flower heads of chrysathemum

51
Q

what is pyrethroids

A

a synthetic pyrethrins

52
Q

why are Pyrethrin/ Pyrethroids used as a insceticides

A

high insceticidal potency compared to mammalian potency = safer
widely used in people homes

53
Q

what is the symptoms of acute toxicity caused by Pyrethrin/ Pyrethroids

A

tremors, seizures, death
occupational exposure = burning/tingling of the face
(short lived)

54
Q

why was the synthetic analogue pyrethroid developed

A

pyrethrins decomposed rapidly with light

55
Q

what are the toxic signs in rats when exposed to pythrethroids

A

Type 1 - arousal, aggression and fine tremor
Type 2 - profuse salivation, coarse tremors and convulsion

56
Q

what are convulsion caused by pyrethroids thought to be caused by

A

Action of type 2 pyrethrodis at blocking GABAA receptors abeit at much higher concentrations

57
Q

How does pyrethroids thought to cause symptoms

A

The main mechanism of action is at sodium channels
Very similar to ddt, they stop sodium channels from closing – the type 1 , similar time to ddt so cause repetitive firing. Type 2 keep channels open much longer and end up causing depolarization dependent block.
Therefore neurotransmission associated toxicity but evidence of apoptosis

58
Q

how does pyrethroids cause apoptosis

A

activates Na+ channels, leads to repetitive firing
Increase Calcium influx

59
Q

what is the evidence that leads scientist to belive that developmental exposure to pyrethroids increase the risk of ADHD

A

Levels of the pyrethroid metabolite 3-PA measured in urine of children = pyrethroids exposure
Children with 3-PBA levels above limits of detection more likely to be diagnosed with ADHD
Animal study shows exposure to deltamethrin (pyrethriods) causes hyperactivity and impulsive behaviour

60
Q

how, cellularly, does developmental exposure to deltamethrin (pyrethroid) cause ADHD

A
  • Increases dopamine transporter levels in mice
  • subsequent decrease in extracellualr dopamine levels cause compensatory increase in dopamine 1 receptors
  • cause an increase in activity and impulsive behaviour
61
Q

Describe how fungicides may be toxic

A
  • Fungicides tend to have very low acute toxicity in mammals (some exceptions)
  • Fungicides maneb and mancozeb associated with 2-fold increased risk of Parkinson Disease
    Neurotoxicity as mancozeb organometallic pesticide exposure as manganese known to cause neurotoxicity in dopaminergic neurones
62
Q

how may herbicides cause dopaminergic toxicity

A

Generally disrupt the metabolic function and energy transfer in plant cells
But daily subacute paraquat exposure lead to decrease in both muscle function and substantial nigra dopamine level

Toxicology (11 decks)

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