Mechanisms of Toxicity

Organochlorides

Neuropoison

Inactivates sodium channel closure

Antagonize GABA receptors

Selective necrosis of zona fasiculata and zona reticularis

Organophosphates

Irreversible inactivation of AChE

Accumulation of ACh

Carbamates

Reversible inhibition of AChE

Pyrethrins, Pyrethyroids and Insectisides

Type I: nerve conduction block by acting on sodium channels

Type II: act on sodium channels in the sensory nerve and interfere with GABA and glutamic acid binding

Amitraz

⍺2 adrenergic agonist and weak monamine oxidase inhibitor

Ivermectin and Milbemycin

Stimulates presynaptic release of GABA

Increases binding of GABA to postsynaptic receptors

Direct GABA agonist effects

Warfarin and Congeners

Vitamin K antagonist

Bromethalin

Loss of sodium-potassium ATPase function

Strychinine

Block inhibitory actions of glycine causing excessive neuronal activity

Arsenic

Interferes with cellular respiration

Lead

Inhibition of free sulphydryl groups involved in heme synthesis= anemia

Inorganic mercury

Direct tissue necrosis and renal tubular necrosis

Inhibits sulphydryl enzymes in microsomes and mitochondria

Organic mercury

Primarily affects the brain
Interferes with metabolic activity, prevents protein synthesis= necrosis