Toxic effects of pesticides
Toxic Effects of Pesticides
Pesticides are widely used in agriculture for the control of weeds, insects or microorganisms leading to exposure to the population through contamination of water and residues in dust and on food, this exposure may lead to adverse health effects (Alavanja, Hoppin & Kamel 2004) and while there are many different agents that are implicated in these effects this discussion will focus on Organophosphate (OP) pesticides and their mechanisms with respect to human health.
The primary target for OP pesticides is the inhibition of acetylcholinesterase (ACheE) (Casarett 2008, p.890) where its normal action is to hydrolyze acetylcholine (ACh), a neurotransmitter which occurs throughout the central (autonomic) nervous system and peripheral (somatic) nervous system where it binds to and stimulates cholinergic receptors, specifically muscarinic and nicotinic receptors (Mileson et al. 1998).
The autonomic nervous system controls visceral functions in the body and ACh acts at muscarinic and nicotinic receptors present at effector organs such as heart, eyes, glands, respiratory and gastrointestinal systems. The somatic nervous system controls all voluntary functions of the body such as movement, posture and respiration, here ACh acts on nicotinic receptors (Mileson et al. 1998).
Therefore inhibition of AChE by OP pesticides leads to an accumulation of ACh at cholinergic synapses producing overstimulation of the muscarinic and nicotinic receptors located in most organs of the body (Casarett 2008, p.890; Mileson et al. 1998) causing signs and symptoms associated with cholinergic overstimulation otherwise known as “cholinergic syndrome” (Casarett 2008; Karami-Mohajeri & Abdollahi 2011). Signs and symptoms associated with cholinergic syndrome or acute OP poisoning please see table 1.
Phosphorylated AChE may be reactivated by nucleophilic oximes such as pralidoxime, as long as the phosphorylated AChE has not aged, aging occurs with the loss of
Pesticides are widely used in agriculture for the control of weeds, insects or microorganisms leading to exposure to the population through contamination of water and residues in dust and on food, this exposure may lead to adverse health effects (Alavanja, Hoppin & Kamel 2004) and while there are many different agents that are implicated in these effects this discussion will focus on Organophosphate (OP) pesticides and their mechanisms with respect to human health.
The primary target for OP pesticides is the inhibition of acetylcholinesterase (ACheE) (Casarett 2008, p.890) where its normal action is to hydrolyze acetylcholine (ACh), a neurotransmitter which occurs throughout the central (autonomic) nervous system and peripheral (somatic) nervous system where it binds to and stimulates cholinergic receptors, specifically muscarinic and nicotinic receptors (Mileson et al. 1998).
The autonomic nervous system controls visceral functions in the body and ACh acts at muscarinic and nicotinic receptors present at effector organs such as heart, eyes, glands, respiratory and gastrointestinal systems. The somatic nervous system controls all voluntary functions of the body such as movement, posture and respiration, here ACh acts on nicotinic receptors (Mileson et al. 1998).
Therefore inhibition of AChE by OP pesticides leads to an accumulation of ACh at cholinergic synapses producing overstimulation of the muscarinic and nicotinic receptors located in most organs of the body (Casarett 2008, p.890; Mileson et al. 1998) causing signs and symptoms associated with cholinergic overstimulation otherwise known as “cholinergic syndrome” (Casarett 2008; Karami-Mohajeri & Abdollahi 2011). Signs and symptoms associated with cholinergic syndrome or acute OP poisoning please see table 1.
Phosphorylated AChE may be reactivated by nucleophilic oximes such as pralidoxime, as long as the phosphorylated AChE has not aged, aging occurs with the loss of
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