Correction to: Utility of 2-Pyridine Aldoxime Methyl Chloride (2-PAM) for Acute Organophosphate Poisoning: A Systematic Review and Meta-Analysis

Abstract

The original article was corrected. The names of coauthors Roshanak Benabbas and Ian S. deSouza were given incorrectly (as BRoshnak Benabbas^and BIan de Souza^, respectively) in this article as originally published.

Loading and Sustained Release of Pralidoxime Chloride from Swellable MIL-88B(Fe) and Its Therapeutic Performance on Mice Poisoned by Neurotoxic Agents

“…This, in turn, leads to continuous excitation of the central nervous system, respiratory failure, and even death. , As a reactive oxime, pralidoxime chloride (2-PAM) is an antidote for neurotoxic agent poisoning. Detoxification by 2-PAM relies on the reactivation of AChE, which combines with organophosphorus poisons; however, there are strict requirements for the dosage of 2-PAM for treating neurotoxic agent poisoning to ensure a stable 2-PAM concentration in the blood. , If the concentration of 2-PAM in the human body is too low, poisoned AChE cannot be effectively reactivated; if the concentration is excessive, the activity of AChE may be inhibited, resulting in the accumulation of Ach in the human body, which, in turn, leads to side effects such as respiratory failure. , The conventional treatment method is the intravenous administration of a small dose of 2-PAM multiple times. This method tends to generate severe fluctuations of 2-PAM concentrations in blood, resulting in poor therapeutic performance .…”

Penetrating the Blood–Brain Barrier for Targeted Treatment of Neurotoxicant Poisoning by Nanosustained-Released 2-PAM@VB1-MIL-101-NH2(Fe)

“…Nerve agents are a kind of extremely toxic organophosphorus compounds, which could be used by malicious/terrorist actors. , The mechanism of intoxication by nerve agents mainly involves the inhibition of acetylcholinesterase (AChE) by phosphorylation, thereby causing an inability to break down acetylcholine (ACh), and the accumulated ACh overstimulates the muscarinic and nicotinic receptors, , causing cholinergic hyperstimulation and altered neuromuscular function and cognitive function, , leading to respiratory failure, seizures, irreversible brain damage, and even death. The reactivation of AChE in central nervous systems is critical to prevent seizures (which is crucial for survival) and brain damage implied as the cause for long-term cognitive and behavioral neurological impairments observed in organophosphorus poisoning survivors. , The current clinical practice of applied muscarinic receptor antagonist (typically atropine) and AChE reactivators (oximes such as pralidoxime chloride (2-PAM) is most widely used) for the treatment of nerve agents poisoning has been virtually unchanged for more than six decades . Besides, some new promising approaches are emerging, e.g., using catalytic or stoichiometric (bio)­scavenger to prevent the nerve agents concentrations in target tissues or using antinicotinics to antagonize downstream effects of acetylcholine at nicotinic receptors; however, these are still either in an early experimental stages or not available as a licensed medicine …”

“…Pralidoxime chloride (2-PAM) is the most commonly used antidote for nerve agent poisoning, which achieves detoxification by reactivating phosphorylated AChE . Traditionally, 2-PAM is slowly administered intravenously in small amounts or administered per 6 h for about 2 days, but this method is likely to cause fluctuations in blood 2-PAM concentrations. ,, A low concentration of 2-PAM in the human body cannot effectively reactivate the toxic AChE, while excessive administration of 2-PAM may cause accumulation of ACh in the peripheral nervous system and produce side effects, such as headache, tachycardia, increased systolic blood pressure, hyperventilation, decreased renal function, muscular weakness, nausea, and vomiting in humans. − More importantly, the central nervous system including the human brain is the main target of nerve agents, and drugs need to cross the blood–brain barrier before reaching the target .…”

“…The reactivation of AChE in central nervous systems is critical to prevent seizures (which is crucial for survival 7 ) and brain damage implied as the cause for long-term cognitive and behavioral neurological impairments observed in organophosphorus poisoning survivors. 9,10 The current clinical practice of applied muscarinic receptor antagonist (typically atropine) and AChE reactivators (oximes such as pralidoxime chloride (2-PAM) is most widely used 11 ) for the treatment of nerve agents poisoning has been virtually unchanged for more than six decades. 12 Besides, some new promising approaches are emerging, e.g., using catalytic or stoichiometric (bio)scavenger 13 to prevent the nerve agents concentrations in target tissues or using antinicotinics 14 to antagonize downstream effects of acetylcholine at nicotinic receptors; however, these are still either in an early experimental stages or not available as a licensed medicine.…”