Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
SELECTIVE TOXICITY TO INSECTS HAS BEEN ACCOUNTED FOR BY DIFFERENCES IN METABOLISM. (32)P-MALATHION IS RAPIDLY METABOLIZED IN MICE, RATS, & DOGS, PRINCIPALLY BY HYDROLYSIS OF THE ETHYL ESTER BONDS TO GIVE MALATHION MONOESTER & MALATHION DIACID, WHEREAS IN INSECTS OXIDN TO MALAOXON & CLEAVAGE OF THE PHOSPHATE THIOESTER BOND TO GIVE O,O-DIMETHYL-PHOSPHORODITHIONATE & -PHOSPHOROTHIONATE ARE THE PRINCIPAL ROUTES OF METAB. THE TOXICITY OF MALATHION IS PROBABLY DUE TO ITS OXIDATION TO MALAOXON, WHICH IS SOME 1000 TIMES MORE ACTIVE THAN MALATHION AS AN ANTI CHOLINESTERASE.
MALATHION ... REQUIRES ACTIVATION TO /MALAOXON/ ... TO BECOME AN ACTIVE ANTICHOLINESTERASE AGENT. ... THE CONVERSION OF MALATHION TO MALAOXON IS A REACTION CARRIED OUT BY THE LIVER MICROSOMAL MONOOXYGENASE SYSTEM. COMPETING WITH THE ACTIVATION OF MALATHION ARE ENZYMES RESPONSIBLE FOR ITS DEGRADATION TO NON-TOXIC METABOLITES. THESE ARE ... CHARACTERIZED AS PHOSPHATASES AND CARBOXYLESTERASES OR ALIESTERASES. PRODUCTS OF REACTIONS CATALYZED BY THESE ENZYMES ARE MALATHION MONOESTER, VARIOUS PHOSPHORIC ACIDS & DEMETHYLATED PRODUCT. ... THE DEGRADATION RATE OF MALAOXON EXCEEDS THE ACTIVATION RATE OF MALATHION, SO THERE IS ... LITTLE ACCUMULATION OF THE TOXIC ACTIVATION PRODUCT IN MAMMALIAN SYSTEMS.
STUDIES /SHOWED/ ARTHROBACTER SP ... WAS CAPABLE OF DEGRADING MALATHION. LAB STUDIES IDENTIFIED METABOLITES AS MALATHION HALF ESTER, DICARBOXYLIC ACID, DIMETHYL PHOSPHORODITHIOATE, & DIMETHYL PHOSPHOROTHIOATE.
WHEN LARVAL HOMOGENATES OF MALATHION-RESISTANT & ... SUSCEPTIBLE STRAIN OF INDIAN MEAL MOTH (PLODIA INTERPUNCTELLA HUBNER) WERE TESTED FOR ESTERASE ACTIVITY, RESISTANT STRAIN HAD GREATER ALPHA-NAPHTHYL ACETATE ESTERASE THAN SUSCEPTIBLE STRAIN; LESS CARBOXYLESTERASE & BUTYRYLCHOLINESTERASE; & SIMILAR ACETYLCHOLINESTERASE ACTIVITY.
Metabolite of malathion found in cow feces: dimethyl phosphate. /From table/
Metabolites of malathion in cow, rat, and dog urine and serum are desmethyl malathion and malathion diacid. /From table/
A metabolite of malathion in mouse urine and serum is desmethyl malathion. /From table/
In plants ... /the/ malathion carboxylic acids /malathion mono & dicarboxylic acids/ are ... formed.
Malathion ... is broken down by the mammalian liver. ... Malathion`s selectivity is due to the presence of the carboxyl groups, which are susceptible to mammalian hydrolysis.
Two organophosphorus impurities of technical malathion (insecticide), isomalathion and O,S,S-trimethyl phosphorodithioate, were examined for their effects on the in vivo metabolism of malathion in rats. Both impurities were confirmed to be potent in vivo inhibitors of plasma, liver, and kidney malathion carboxylesterases at relatively low doses. Pretreatment of rats with these impurities followed by administration of (14)C malathion resulted in changes in the quantities of certain malathion metabolites excreted in the urine. Compared to the corn oil pretreated controls, the most notable change in the impurity pretreated animals was in the decrease in the amount of malathion diacid excreted along with a commensurate increase in the amount of excreted malathion alpha monoacid. An increase in malaoxon metabolites in the urine of impurity pretreated rats was indicated, suggesting that more malaoxon was originally produced in these animals.
BY USING HIGH SPECIFIC ACTIVITY MALATHION & ION EXCHANGE CHROMATOGRAPHY, A TOTAL OF 11 METABOLITES WERE ISOLATED FROM THE GERMAN COCKROACH, AMERICAN COCKROACH, & THE COMMON HOUSEFLY, & SEVEN METABOLITES FROM THE WHITE MOUSE. THE PRINCIPAL METABOLITES ISOLATED FROM THE MOUSE WERE MONOETHYL ESTER OF MALATHION (86%), DIMETHYL PHOSPHOROTHIOIC ACID (13%), DIMETHYL PHOSPHORODITHIOIC ACID (5%), 10% OF AN UNKNOWN METABOLITE. RELATIVE AMT OF VARIOUS METABOLITES OBTAINED WERE SIMILAR BETWEEN ROACHES, WHICH IN TURN WERE SLIGHTLY DIFFERENT FROM FLIES. ... LEVEL OF MALAOXON WAS ... GREATER IN COCKROACH THAN IN MOUSE @ ANY TIME AFTER INJECTION, EG, @ 1 HR AFTER INJECTION /OF MALATHION/ THERE WAS 10 TIMES MORE MALAOXON PER G OF ANIMAL. RELATIVE PROP OF METABOLITES INDICATES GREATER PS TO PO ACTIVATION IN INSECTS COMPARED TO MAMMALS ...
The conversion of many organophosphates with a P=S group to P=O is another instance of activation by MFO /mixed function oxidase/ resulting in an incr in toxicity. This process explains the greater toxicity of metabolites like paraoxon, malaoxon, fenitrooxon, etc than that of their parent compounds.
The hydrolysis of malathion by rabbit liver oligomeric and monomeric carboxylesterase results in the formation of a mixture of an alpha and beta monoacid. The oligomeric carboxylesterase produced an alpha/beta ratio of monoacids of 4.55, and the monomeric carboxylesterase produced an alpha/beta ratio of monoacids of 2.33. Kinetic studies demonstrated that the Km values were the same for the corresponding reactions which produced alpha monoacid, or beta monoacid with the same enzyme. Since both carboxylesterases are electrophoretically pure, the kinetic data strongly supports the theory that the reactions which produced alpha and beta monoacids are catalyzed by the same active site.
In man, malathion is metabolized by (1) hydrolytic cleavage of ethyl groups from the succinic acid moiety of the molecule by carboxylesterase enzymes; and (2) hydrolysis of the succinate moiety from the dialkyl thiophosphate.
Plasma and tissue enzymes are responsible for hydrolysis /of organophosphorus compounds/ to the corresponding phosphoric and phosphonic acids. However, oxidative enzymes are also involved in the metabolism of some organophosphorus compounds. /Anticholinesterase agents/
The organophosphorus anticholinesterase agents are hydrolyzed in the body by a group of enzymes known as A-esterases or paraoxonases. These enzymes are found in the plasma and liver and hydrolyze a large number of organophosphorus compounds ... by cleaving the phosphoester, anhydride, P-F, or P-CN bonds. /Anticholinesterase agents/
Absorption, Distribution & Excretion:
THE LESS VOLATILE AGENTS THAT ARE COMMONLY USED AS AGRICULTURAL INSECTICIDES (EG PARATHION, FENTHION, DIAZINON, MALATHION) ARE GENERALLY DISPERSED AS AEROSOLS OR AS DUSTS CONSISTING OF THE ORGANOPHOSPHORUS COMPOUND ADSORBED TO AN INERT, FINELY PARTICULATE MATERIAL. CONSEQUENTLY, THE COMPOUNDS ARE ABSORBED RAPIDLY AND EFFECTIVELY BY PRACTICALLY ALL ROUTES, INCLUDING THE GASTROINTESTINAL TRACT, AS WELL AS THROUGH THE SKIN AND MUCOUS MEMBRANES FOLLOWING CONTACT WITH MOISTURE, AND BY THE LUNG AFTER INHALATION.
... WHEN (14)C-MALATHION ... WAS APPLIED /TO HUMAN SKIN/ 7, 9, & 23% WERE ABSORBED THROUGH FOREARM, ABDOMEN, & FOREHEAD, RESPECTIVELY.
THE INSECTICIDE (14)C-MALATHION WAS ABSORBED & RAPIDLY EXCRETED IN RATS. 8 HR AFTER ORAL DOSE, 44% OF (14)C HAD BEEN EXCRETED IN URINE & 47% STILL REMAINED IN GI TRACT, WHEREAS AFTER 24 HR, 83% HAD BEEN EXCRETED IN URINE, 6% IN FECES, 3% IN EXPIRED AIR, & 8% REMAINED IN GI TRACT. EXCRETION OF (32)P AFTER AN ORAL DOSE OF (32)P-MALATHION TO LACTATING COW WAS LESS RAPID. 69% WAS EXCRETED IN 4 DAY URINE, 8% IN FECES, & 0.2% IN MILK. SINCE EXCRETION OF (32)P WAS VERY SLOW AFTER THAT TIME, ITS INCORPORATION INTO BODY TISSUES HAD PROBABLY OCCURRED, & ITS RELEASE WAS DEPENDENT ON TURNOVER RATES OF THOSE TISSUES.
Percutaneous absorption of chronically applied malathion was determined in man and chronic absorption was compared to single dose absorption. (14)C-Malathion was applied topically to the ventral forearm of human male volunteers. This procedure was followed by repeated administration of non radioactive malathion to the same site. (14)C-Malathion was reapplied on day 8 when urinary excretion of radioactivity from the first application reached minimum detectable levels. Percutaneous absorption from the first admin was 4.48% of the applied dose. Absorption from the second administration was 3.53%. Therefore, the single dose application data are relevant for predicting toxic potential for long term exposure.
EIGHT AUTOPSY SAMPLES FROM AN INDIVIDUAL WHO HAD INGESTED A LARGE AMT OF MALATHION WERE ANALYZED. MALATHION WAS PRESENT IN ALL SAMPLES EXCEPT LIVER. THE HIGHEST CONCN WERE FOUND IN GASTRIC CONTENTS (8621 PPM) & ADIPOSE TISSUE (76.4 PPM). MALAOXON WAS IDENTIFIED IN SOME TISSUES AT VERY LOW LEVELS; A SIGNIFICANT AMT WAS FOUND ONLY IN FAT (8.2 PPM). MALATHION MONOCARBOXYLIC ACID & MALATHION DICARBOXYLIC ACID WERE FOUND IN GREATER ABUNDANCE: 221 PPM IN BILE, 106 PPM IN KIDNEY, & 103 PPM IN THE GASTRIC CONTENTS.
/Measurement was made of/ the ether extractable phosphates in the urine of an adult man who had been administered malathion in a single oral dose of 58 mg (0.84 mg/kg). A total of 23% of the ingested dose was recovered in the ether extractable, urinary phosphate fraction of the urine during the first 16.3 hours. 97% of this recovered dose was excreted in the first 7.5 hours. ... Based on experiments in rats injected ip or fed (32)P-labeled malathion, /it was/ found that an average of 69 and 36%, respectively, of the malathion excreted in the urine to be recoverable in the ether extractable fraction.
... 7% OF TOTAL METABOLITES IN FECES /FROM COW GIVEN MALATHION ORALLY/ WAS CHLOROFORM SOLUBLE, OF WHICH 85% WAS MALATHION & 12% MALAOXON. THE MILK CONTAINED A SMALL AMOUNT OF MALATHION METABOLITES (9.2% OF TOTAL DOSE AFTER 7 DAYS); OF THIS, ONLY 29% WAS EXTRACTABLE OUT OF MILK AND PARTITIONED IN FAVOR OF WATER OVER BENZENE, INDICATING THE ABSENCE OF EITHER MALATHION OR MALAOXON.
No malathion residues were found 24 hr after the exposure of pinfish to 75 ug/l; only malathion monoacid was detected in the gut.
The American cockroach was treated by topical application of (14)C-malathion. The distribution of the label within the body tissues was found to be both rapid and extensive. As much as 40% of the applied label was still present superficially in the cuticle even 24 hr post-application. The overall tissue ranking order for (14)C label was found to be: foregut > digestive tract contents > skeletal muscle > fat body > hidout > midgut > nerve cord > brain > malpighian tubules. Malathion, malaoxon and malathion monoacids were detected in the nerve cord plus brain, the digestive tract, skeletal muscle and fat body at 1, 2 and 24 hr after topical application of the insecticide. At 24 hr post-application a significant proportion of malathion remained unmetabolized in all tissues examined. The highest levels of metabolic transformation were found in the digestive tract and fat body. Insects were prostrate 24 hr after topical application of (14)C-malathion. In these insects the greatest concentration of malathion and monoacids (expressed in relation to unit tissue wt) was found in the digestive tract. On the other hand, the nerve cord and brain contained the greatest concentration of malaoxon. About 18% of applied (14)C-malathion label partitioned into the tissue aqueous phase up to 24 hr after topical application but very little applied label was expired as (14)CO2 or excreted. Although a neurotoxic action may be the cause of prostration and death, the extensive dissemination of malathion and its products belies the concept of any tissue specificity. The haemolymph, after an initial sharp rise in malathion content, maintained a steady malathion level over the 24 hr experimental periods suggesting that the hemolymph is the main distributor of the insecticide to the various body tissues.
Most organophosphate compounds are ... absorbed from skin, conjunctiva, gastrointestinal tract, & lung. /Organophosphate compounds/
The rate of dermal absorption /of organophosphorus pesticides/ may be ... influenced by the solvent used. /Organophosphorus insecticides/
Many of /the organophosphorus insecticides/ are excreted in the milk ... /Organophosphorus insecticides/
Following their absorption, most organophosphorus cmpd are excreted almost entirely as hydrolysis products in the urine. /Anticholinesterase agents/
TOXICANTS CAN BE ABSORBED BY INHALATION, INGESTION, AND SKIN PENETRATION. ... ALL UNDERGO HYDROLYTIC DEGRADATION IN LIVER AND OTHER TISSUES, USUALLY WITHIN HR OF ABSORPTION. DEGRADATION PRODUCTS ARE OF LOW TOXICITY, AND ARE EXCRETED IN URINE AND FECES. /ORGANOPHOSPHATE CHOLINESTERASE-INHIBITING PESTICIDES/
/THEY/ ... ARE RAPIDLY ABSORBED THROUGH MUCOUS MEMBRANE OF DIGESTIVE SYSTEM, RESPIRATORY SYSTEM & THE SKIN, & CONVEYED BY THE BLOOD TO VARIOUS BODY TISSUES. ... THE MAIN ROUTE OF ELIMINATION ... /IS/ THE KIDNEYS. /ORGANOPHOSPHORUS PESTICIDES/
Organic phosphorous insecticides are absorbed by the skin, as well as by the respiratory and GI tracts. Absorption by the skin tends to be slow, but, because the insecticides are difficult to remove, such absorption is frequently prolonged. Skin absorption is somewhat greater at higher temperatures and may be much greater in the presence of dermatitis. /Organic phosphorous pesticides/
Mechanism of Action:
Signs and symptoms of intoxication by anticholinesterase agents /such as malathion/ are caused by the inactivation of the enzyme cholinesterase, which results in the accumulation of acetylcholine at synapses in the neuromuscular system, and secretory glands.
MALAOXON, ACTIVE ANTICHOLINESTERASE METABOLITE OF MALATHION ... HAS ALIESTERASES INHIBITING ACTIVITY.
Organophosphorus derivatives act by combining with and inactivating the enzyme acetylcholinesterase (AChE). ... The inactivation of cholinesterase by cholinesterase inhibitor pesticides allows the accumulation of large amounts of acetylcholine, with resultant widespread effects that may be ... separated into 4 categories: (1) Potentiation of postganglionic parasympathetic activity. ... (2) Persistent depolarization of skeletal muscle ... (3) Initial stimulation following depression of cells of central nervous system ... (4) Variable ganglionic stimulation or blockade ... /Cholinesterase inhibitor pesticides/
The characteristic pharmacological effects of the anti-ChE agents are due primarily to the prevention of hydrolysis of ACh by AChE at sites of cholinergic transmission. Transmitter thus accumulates, and the response to ACh that is liberated by cholinergic impulses or that is spontaneously released from the nerve ending is enhanced. With most of the organophosphorus agents ... virtually all the acute effects of moderate doses are attributable to this action. /Anticholinesterase agents/
The cardiovascular actions of anticholinesterase agents are complex, since they reflect both ganglionic and postganglionic effects of accumulated ACh on the heart and blood vessels. The predominant effect on the heart from the peripheral action of accumulated ACh is bradycardia, resulting in a fall in cardiac output. Higher doses usually cause a fall in blood pressure, often as a consequence of effects of anticholinesterase agents on the medullary vasomotor centers of the CNS. /Anticholinesterase agents/
The main feature of the toxic mechanism of organophosphorus pesticides is inhibition of the esterase enzyme activity, in particular of cholinesterase, which plays an important physiological part. Organophosphorus pesticides can also indirectly interact with the biochemical receptors of acetylcholine. /Organophosphorus pesticides/
... The serum cholinesterase activity of 14 men and 16 women at seven approximately equal intervals throughout one 24 hr day was measured. The lowest average value, ... was 92% of the mean of all values at other sampling times. The next lowest value was 98.7% of the same mean. /It was/ concluded that the small variation observed did not take the form of a regular curve but was entirely individual without correspondence to hour. /Organic phosphorus pesticides/
... There is no change in red blood cell cholinesterase activity in adults associated with age. ... Activity of this enzyme increases progressively during the first year of life, it is higher in children under 3 yr of age than in older children, and it is markedly higher in 5 yr old children than in 3 yr olds. /Organic phosphorus pesticides/
Cholinesterase activity of plasma is significantly higher in men than in women, and this is true no matter which of several choline esters are used as substrate in measuring the enzyme activity. According to some, the difference is confined to young people. There is no sex difference in the red cell enzyme activity. Serum cholinesterase activity of blacks tends to be lower than whites of the same sex. /Organic phosphorus pesticides/
Phosphorylated enzymes, like acetylated acetylcholinesterase, are esters and may be hydrolyzed by nucleophilic agents, including water. The rate at which phosphorylated enzymes are reactivated by water is extremely low, compared to the rate for acetylcholinesterase combined with acetate. When inhibition is by isopropyl phosphate, the rate is essentially zero. /Organic phosphorous pesticides/
Organophosphates poison insects and humans primarily by phosphorylation of the acetylcholinesterase enzyme at nerve endings. /Organophosphate Cholinesterase-inhibiting pesticides/
Interactions:
Of five N-methylcarbamate insecticides tested, only 2-sec-butylphenyl-N-methylcarbamate exhibited marked synergism with malathion when a mixture was tested for the combined acute oral toxicity toward mice. The mixture exhibited less potent synergism toward male rats.
TOXICITY OF MALATHION IS POTENTIATED BY O-ETHYL O-PARA-NITROPHENYL PHOSPHOROTHIOATE, TRI-O-TOLYLPHOSPHATE, & SOME OTHER ORGANOPHOSPHORUS CMPD. IT IS POSTULATED THAT THIS POTENTIATION RESULTS FROM THE INHIBITION OF CARBOXYLESTERASE OR ALIESTERASE ENZYMES RESPONSIBLE FOR DEGRADATION OF MALATHION IN MAMMALS. PRESUMABLY, THIS MECHANISM WOULD LEAD TO INCR FORMATION OF MALAOXON, THE ACTIVATION PRODUCT, BECAUSE THE ENZYMES RESPONSIBLE FOR DEGRADATION OF MALAOXON WOULD BE INHIBITED.
Twelve organophosphorus insecticides were tested for toxicity and mutagenicity in the forward mutation test system (ade6) of the yeast Schizosaccharomyces pombe. Trichlorfon, tested in combination with malathion, produced clearly synergistic effects for toxicity and mutagenicity.
Impurities such as O,S,S-trimethyl phosphorodithioate (TMPD) and the S-methyl isomer of malathion (iso-malathion) strongly potentiated the mammalian toxicity of malathion. The potentiation was attributed to inhibition of mammalian liver and serum carboxylesterase. O,O,S-Trimethyl phosphorothioate (TMP), another impurity present in technical grade malathion, proved to be highly toxic. Rats given a single oral dose of O,O,S-trimethyl phosphorothioate at a level as low as 20 mg/kg died over a period of 3 wk, with death occurring with non cholinergic signs of poisoning. O,S,S-Trimethyl phosphorodithioate also caused similar delayed death in rats, O,O,O-trimethyl phosphorothioate, another impurity in technical malathion, was a potent antagonist to the delayed toxicity of O,O,S-trimethyl phosphorothioate. /Impurities of technical grade malathion/
The disposition and metabolism of pesticides used in combination, especially carbaryl and malathion, is of considerable toxicological importance. Radioactivity was rapidly absorbed from the rat gastrointestinal tract following the administration of 0.25 ml of 10 mg/kg (14)C-carbaryl (0.80 microCi), 10/10 mg/kg (14)C-carbaryl/malathion (0.80 microCi), 10 mg/kg (14)C-malathion (1.03 microCi), or 10/10 mg/kg (14)C-malathion/carbaryl (0.86 microCi). The administration of carbaryl or malathion, individually and in combination, followed a two phase elimination model. The presence of malathion decreased the rate constants of absorption and beta phase elimination of (14)C-carbaryl. In the mean time, the length of the distribution phase and the area under the curve of (14)C-carbaryl were decreased by malathion administration. Although (14)C-malathion's absorption half life was unchanged in the presence of carbaryl, increases were noted in the length of the distribution phase, beta phase elimination half life, and area under the curve for malathion when administered simultaneously with carbaryl. Both combinations caused an increase in (14)C activity to be deposited in the fat as compared to the respectively labeled pesticide. However, only malathion increased the concentration of (14)C-carbaryl remaining in the gastrointestinal tract tissues after the administration of the combined pesticides. The subcellular distribution of the liver indicated that the highest activity was present in the cytosol. These pesticides and their combinations were excreted primarily by the kidney, followed by the lung and the intestinal route. Although there was no alteration in the metabolic pathways due to the combinations, an increase in malaoxon and malathion diacid concentration in urine was observed after the administration of (14)C-malathion/carbaryl as compared to (14)C-malathion. The results from this study revealed that the combination of these pesticides altered fundamental pharmacokinetic parameters, which may explain some of the toxicities associated with exposure to these chemicals in combination.
Pretreatment of rats with chloramphenicol (100 mg/kg, ip) 30 min prior to a single oral LD50 dose of malathion at 340 mg/kg completely protected against malathion induced inhibition of cholinesterase. It appears that the inhibition of malathion toxicity by chloramphenicol pretreatment is attributable to inhibition by chloramphenicol of the metabolic activation of malathion to malaoxon.
Pretreatment with malathion augmented the effect of chlorpromazine and diazepam on learning and retrieval in rats.
The various ne-oils, /such as/ mahua, neem, karanj or pongam, undi, kokum butter, gamboge, dhupa fat and rubber oil generally synergised malathion when malathin and oils, respectively, were tested at 1:1 and 1:5 levels. The synergism is probably because of desulfuration of malathion into malaoxon by ne-oils due to their oxidising nature.
Some phenothiazines may antagonize & some may potentiate the toxic anticholinesterase effects of ... /organophosphorus insecticides/. /Organophosphate cholinesterase inhibitors/
In long term therapy, adrenocorticoids antagonize the antiglaucoma effects of anticholinesterases (incr ocular pressure). ... Anticholinergics antagonize the miotic (antiglaucoma) & other muscarinic effects of anticholinesterases on the autonomic & central nervous systems. Tricyclic antidepressants (anticholinergic effects) antagonize the antiglaucoma (miotic) effects of anticholinesterases in glaucoma. ... Antihistamines with anticholinergic effects antagonize the miotic (antiglaucoma) & CNS effects of anticholinesterases. Anticholinesterases potentiate tranquilizing & behavioral changes induced by antihistamines. The actions of anticholinesterase agents on autonomic effector cells, & to some extent those on CNS, are antagonized by atropine, an antidote of choice. Barbiturates are potentiated by anticholinesterases. ... Dexpanthenol potentiates the effects of anticholinesterases. Fluorophosphate insecticides potentiate the effects of other anticholinesterases. /Anticholinesterases/
BARBITURATES ARE POTENTIATED BY ANTICHOLINESTERASES. ALTHOUGH BARBITURATES MAY BE USED CAUTIOUSLY IN TREATING CONVULSIONS, EXTREME CARE IS ESSENTIAL IN HANDLING POISONINGS DUE TO ANTICHOLINESTERASES, PARTICULARLY ORGANOPHOSPHORUS PESTICIDES. ECHOTHIOPHATE, A CHOLINESTERASE INHIBITOR USED AS MIOTIC, POTENTIATES OTHER SUCH INHIBITORS ... USED FOR OTHER PURPOSES (ADDITIVE EFFECTS) OR POSSIBLY SYNERGISTIC. THOSE EXPOSED TO ORGANOPHOSPHATE INSECTICIDES MUST TAKE STRICT PRECAUTIONS. ... ORGANOPHOSPHORUS INSECTICIDES: ADDITIVE ANTICHOLINESTERASE EFFECTS. HAZARDOUS. PATIENTS ON ANTICHOLINESTERASES (EVEN TOPICAL, SUCH AS EYE DROPS) SHOULD AVOID AREAS WHERE ORGANOPHOSPHORUS INSECTICIDES ... RECENTLY ... USED. /ANTICHOLINESTERASE/
ANTICHOLINESTERASE (ORGANOPHOSPHORUS) INSECTICIDES ANTAGONIZE POLARIZING MUSCLE RELAXANTS. PHENOTHIAZINES /AND THIOXANTHENES/: ... MAY ENHANCE TOXIC EFFECTS OF ORGANOPHOSPHORUS INSECTICIDES. /INSECTICIDES, ORGANOPHOSPHORUS/
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