Acute toxicity organophosphorus compounds

Maksimovic M, Boskovic B, Rodovic L et al. (1980). Antidotal effects of bis-pyridinium 2-mono oxime carbonyl derivatives in intoxication with highly toxic organophosphorus compounds. Acute Pharm Jagoslav, 30, 151-160. 

Two factors contribute to the safety of oximes in the treatment of acute poisoning by organophosphorus compounds recommended doses are small, compared with doses likely to cause even mild toxic effects in normal subjects and adverse effects of oximes are reduced in the presence of poisoning by an organophosphorus compound. 

The organophosphorus (OP) and carbamate insecticides are used to control a wide variety of insect pests. The acute toxicity of the OPs and carbamates varies, and many of them have high mammalian toxicity. These compounds react chemically with the active site of acetylcholinesterase, producing a blocked enzyme that cannot degrade acetylcholine. The concentration of acetylcholine then builds up and hyperexcitation occurs. The signs of intoxication include resdessness, tremors, convulsions, and paralysis. Blockage of acetylcholinesterase by OPs is persistent, and recovery of the enzyme takes many hours or even days. The mode of action of the carba-... 

Organophosphorus compounds (OPC) cause two major toxic effects. The first is the well-known acute toxicity initiated by inhibition of acetylcholinesterase (AChE) with subsequent accumulation of acetylcholine at nerve endings. The second effect is organophosphate-induced delayed polyneuropathy (OPIDP) (ataxia and paralysis appearing 2-3 weeks after exposure) associated with inhibi-... 

Table 5. Comparative acute toxicity of nerve agents. Adapted and reproduced from Chapter 34, Organophosphorus compounds as chemical warfare agents , by Maynard RL and Beswick F, in Clinical and Experimental Toxicology ofOrganophosphates (B Ballantyne and TC Marrs, eds),...

An example of absolutely cumulative toxicity is afforded by tri-o-cresyl phosphate or TOCP (figure 2,9). This compound is a cholinesterase inhibitor and neurotoxin. In chickens, an acute dose of 30 mg/kg has a severe toxic effect, which is produced to the same extent by a dose of 1 (mg/kg)/day given for 30 days. This effect may of course be produced by accumulation of the compound in vivo to a threshold toxic level, or it may result from the accumulation of the effect, as it probably does in the case of TOCP. Thus, the inhibition of cholinesterase enzymes by organophosphorus compounds may... 

Organophosphorus and carbamate compounds have come into widespread use in agriculture, since they show low environmental persistence nevertheless, they exert a high acute toxicity. The principal effect of these compounds is the inhibition of the enzyme acetylcholinesterase (AChE), which is essential for terminating the action of the neurotransmitter acetylcholine (ACh). Actually, the intoxication by these compounds results in... 

The acute toxicity of organophosphorus (OP) compounds is usually attributed to their irreversible inhibition of acetylchohnesterase (AChE EC 3.1.1.7). The resultant increase in the level of acetylcholine at cholinergic synapses, particularly in brain and... 

Cholinesterase inhibitor a severely acute toxicant delayed effects may be observed after several hours toxic symptoms similar to other organophosphorus compounds exposure may cause headache, dizziness, blurred vision, and muscle spasms. Other toxic symptoms include vomiting, abdominal pain, diarrhea, seizures, and shortness of breath ingestion of 5-10 g could be fatal to adult humans oral LD50 value (mice) 15 mg/kg, rats 7 mg/kg LC50 inhalation (rat) 69 mg/m /1 h... 

In these laboratory tests, dimethoate is generally used as reference compound due to the high acute toxicity of this organophosphorus insecticide against the honey bee. Thus, the contact LD50 values after 24 and 48 hours of exposure of technical dimethoate to workers are 0.162 and... 

Eldred and Jurs developed a QSAR model for the acute oral mammalian toxicity (LD50) of a set of 54 organophosphorus compounds (67). Feature selec-... 

It is known that human exposure to organophosphorus compounds can result in a variety of acute toxic effects. These arise primarily as a result of the inhibition of acetylcholinesterase. Signs of acute toxicity are due to effects on the central nervous system (anxiety, ataxia, hypotension), to muscarinic effects (wheezing, cough, rhinitis) and to nicotinic effects (muscle weakness, mydriasis and tachycardia). Other acute effects include chest tightness, abdominal cramps, confusion and convulsions. With some organophosphorus compounds, a specific syndrome may develop. This is delayed peripheral neuropathy or OP-induced delayed neuropathy (OPIDN). (For a more detailed discussion on the toxicity of organophosphorus compounds see Chapter 10.)... 

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