Insecticides Flashcards
Organochlorines Examples
DDT
Organochlorines Target Site
Sodium Channels
Organochlorines Action
Modulation of Sodium Channels
Organochlorines Result
Sustained activation of sodium channels causing hyperactivity of the nervous system - prevents the cell from coming back to its resting potential.
Cell nerver recovers and remains active and functional causing spiking from one stimulus.
Neuron runs out of energy eventually, leading to the death of the insect.
Organochlorines LD50
250 mg/kg (rat) - takes a lot of this drug to have a negative effect on mammals
Pyrethroids Examples
Permethrin and Cypermethrin
Pyrethroids Target site
Sodium Channels
Pyrethroids mode of action
Modulation of sodium channels
Pyrethroids result
Type 1 - repetitive discharge - multiple spikes from a single stimulus
Type 2 - no repetitive discharge, very slow after potential
Both lead to the sustained activation of sodium channels.
Pyrethroids LD50
1500 mg/kg - takes much more of this drug to harm mammals than with DDT
Positives of pyrethroids over organochlorines
Pyrethroids are much less stable compounds and mammals can metabolise them - don’t hang around destroying the environment and humans can digest them if they are ever ingested.
DDT doesn’t degrade so it accumulates in the environment and has negative impacts on the environment.
Phenylpyrazoles examples
Fipronil
Phenylpyrazoles target site
GABA-gated and glutamate-gated chloride channels
Phenylpyrazoles mode of action
Block the transmitter binding to the chloride channels
Phenylpyrazoles result
Chloride influx into the cell causes hyperpolarizing the cell membrane potential keeping it in the resting state - this is lost when using Fipronil.
Loss of post-synaptic inhibition causes hyperexcitation of the CNS.
Can no longer inhibit the action potentials as the chloride ions are blocked to allow the membrane to return to normal.
Positives of phenylpyrazoles?
Glutamate-gated chloride channels are only found in invertebrates so selective toxicity is enhanced.
Not found in mammals.
Neonicotinoids target site
Acetylcholine receptors
Neonicotinoids mode of action
Nicotinic acetylcholine receptor agonist.
Neonicotinoids function
Mimic acetylcholine and binds to Ach receptors (agonists)
Neonicotinoids result
Causes sustained excitation to neurons - hyperexcitation leads to the cell running out of energy and eventually, death.
They have sustained excitation as unlike with acetylcholine, they cannot by hydrolysed by acetylcholinesterases - hence why influx of sodium is sustained as it cannot be stopped.
Organophosphates negatives
They are all derivates of phosphoric acid and they are really toxic.
Organophosphates positives
Oxygen can be replaced by S, C and N to yield diffeent derivatives - means it can produce an incredibly wide range of insecticides.
Organophosphates target site
Acetylcholinesterase
Organophosphates mode of action
Inhibition via phosphorylation of AChE (phosphorylated AChE cannot hydrolyse acetylcholine)
