Absorption, Distribution and Excretion
Qualitatively, metabolism of dimethoate in mammals is essentially identical to that occurring in insects. There are... quantitative differences. In general, dimethoate, is much more rapidly degraded in mammals and eliminated via urine. For example, 87-90% of oral dose given cattle was found in urine after 24 hr, mainly as hydrolysis products.
...After ingestion of dimethoate, rats eliminate 60% of dose in 24 hr in urine and expired air.
... Dimethoate rapidly penetrated isolated sections of /mouse/ small intestine, colon, and rectum, with the highest rates of penetration occurring in the colon and rectum. The age of the mice had no significant effects on the extent of penetration. /Initial dose not specified/
... Following aerial spraying with 38% dimethoate animal tissues contained higher concentrations of dimethoate than did soil, water or plants. ... The tissue containing the highest concentrations were brain and intially, lung. ...
For more Absorption, Distribution and Excretion (Complete) data for DIMETHOATE (23 total), please visit the HSDB record page.

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Metabolism / Metabolites
... Detoxification pathway ... involves the hydrolysis of carboxyester or carboxyamide linkages in some insecticides by tissue or plasma carboxylesterases (sometimes called aliesterase). Malathion and dimethoate are examples.
Rabbit and rat liver microsomes converted dimethoate to oxygen analog and des-N-methyl derivatives.
After dimethoate was administered to rats, the following compounds were found in urine: 1. dimethoate, 2. dimethoxon, 3. dimethoate carboxylic acid, 4. dimethylphosphorodithioate, 5. dimethyl phosphorothioate, 6. dimethylphosphate, 7. monomethylphosphate, 8. phosphorothioate, 9. formate, and 10. N-methyl 2-glucuronate acetamide.
Oxidative desulfuration of dimethoate to give O-analog took place rapidly in rabbits and rats. Both dimethoate and O-analog underwent subsequent oxidative N-dealkylation coupled with formation of N-hydroxymethyl intermediates.
For more Metabolism/Metabolites (Complete) data for DIMETHOATE (28 total), please visit the HSDB record page.
Dimethoate has known human metabolites that include Omethoate.
Metabolism of organophosphates occurs principally by oxidation, by hydrolysis via esterases and by reaction with glutathione. Demethylation and glucuronidation may also occur. Oxidation of organophosphorus pesticides may result in moderately toxic products. In general, phosphorothioates are not directly toxic but require oxidative metabolism to the proximal toxin. The glutathione transferase reactions produce products that are, in most cases, of low toxicity. Paraoxonase (PON1) is a key enzyme in the metabolism of organophosphates. PON1 can inactivate some organophosphates through hydrolysis. PON1 hydrolyzes the active metabolites in several organophosphates insecticides as well as, nerve agents such as soman, sarin, and VX. The presence of PON1 polymorphisms causes there to be different enzyme levels and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effect of organophosphate exposure.

Toxicity Summary
Dimethoate is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

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Toxicity Data
LC50 = 1,680 mg/m3
LD50: 60 to 387 mg/kg (Oral, Rat)
LD50: 60 mg/kg (Oral, Mouse)
LD50: 400 mg/kg (Oral, Dog)
LD50: 200 mg/kg (Oral, Hamster)
LD50: 300 mg/kg (Oral, Rabbit)
LD50: 350 mg/kg (Oral, Guinea pig)
LD50: 100 mg/kg (Oral, Cat)
LD50: 1000 mg/kg (Dermal, Rabbit)
LD50: 353 mg/kg (Dermal, Rat)
LC50: 1.2 mg/l (Rat)

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Interactions
The effects of various classes of insecticides were studied on N-demethylation of dimethylnitrosamine (DMN) by mouse liver enzymes. Organochlorine insecticides increased the activities of dimethylnitrosamine demethylases I and II. Dimethoate, an organophosphorus cmpd, was the only insecticide tested to inhibit the N-demethylation of dimethylnitrosamine, with more pronounced effect on dimethylnitrosamine demethylase I.
Organophosphates are usually found in the environment with other pesticides and with pollutants of industrial origin can cause combined exposure involving unknown interactions between the agents. In this study, female Wistar rats were given 1/25 LD50 of dimethoate by gavage, combined with the same LD50 fractions of propoxur and cypermethrin or with arsenic (6.66 mg/kg). The doses were given from day 5 to 15 of pregnancy, or that plus for the 4 weeks of lactation, or that plus 8 weeks for the male offspring after weaning. Control rats received distilled water. Electrophysiological recording was done when the male offspring reached 12 weeks of age. Spontaneous activity and evoked potentials from the somatosensory, visual and auditory cortex; and conduction velocity and absolute and relative refractory periods of the tail nerve were measured. The general trend was a shift of the spontaneous cortical activity to higher frequencies and increase in the evoked potential latency. The results showed that combined exposure to several environmental toxicants could be more harmful than the effects of each substance alone ...
Carbon disulfide pretreatment potentiated the anticholinesterase action of parathion and EPN, but suppressed that of dimethoate and diazinon. Carbon disulfide had no significant effect or a slightly suppressive effect on the other compounds. Some of these effects were contrasted with the repeated alteration of the toxicity following phenobarbital pretreatment.

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Non-Human Toxicity Values
LD50 Rat female oral 240-336 mg/kg technical material /From table/
LD50 Mouse subcutaneous 60 mg/kg technical material /From table/
LD50 Hamster male sc 60 mg/kg technical material /From table/
LD50 Rabbit oral 300 mg/kg technical material /From table/
For more Non-Human Toxicity Values (Complete) data for DIMETHOATE (20 total), please visit the HSDB record page.

[1]. Toxic hazard from formulating the insecticide dimethoate in methyl 'Cellosolve'. Nature. 1961;189:507-508.

Dimethoate appears as a white crystalline solid, with a camphor-like odor, white to grayish crystals for technical product. This material is a contact and systemic organophosphate insecticide effective against a broad range of insects and mites when applied on a wide range of crops. It has not been produced in the U.S. since 1982. (EPA, 1998)
Dimethoate is a monocarboxylic acid amide that is N-methylacetamide in which one of the hydrogens of the methyl group attached to the carbonyl moiety is replaced by a (dimethoxyphosphorothioyl)sulfanediyl group. It has a role as an EC 3.1.1.7 (acetylcholinesterase) inhibitor, an agrochemical, an acaricide, an EC 3.1.1.8 (cholinesterase) inhibitor, an insecticide, a xenobiotic and an environmental contaminant. It is an organic thiophosphate and a monocarboxylic acid amide. It is functionally related to a N-methyl-2-sulfanylacetamide.
Dimethoate is a synthetic organic thiophosphate compound and organophosphate acetylcholinesterase inhibitor that is used as a pesticide. It is characterized as a volatile white to gray crystalline solid that has a camphor-like odor, and exposure occurs by inhalation, ingestion, or contact.
Dimethoate is an organophosphate insecticide used to kill mites and insects systemically and on contact. It is used against a wide range of insects, including aphids, thrips, planthoppers and whiteflies on ornamental plants, alfalfa, apples, corn, cotton, grapefruit, grapes, lemons, melons, oranges, pears, pecans, safflower, sorghum, soybeans, tangerines, tobacco, tomatoes, watermelons, wheat and other vegetables. It is also used as a residual wall spray in farm buildings for house flies. Dimethoate has been administered to livestock for control of botflies. Dimethoate is moderately toxic and severe poisoning affects the central nervous system. (L1188)
An organothiophosphorus cholinesterase inhibitor that is used as a systemic and contact insecticide.

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Mechanism of Action
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/
They act principally by inhibition of acetyl cholinesterase (AChE) at the cholinergic synapses. /organophosphorus insecticides/
The signs of poisoning due to organophosphorus cmpd are those due to accumulation of acetylcholine & hence overstimulation of parasympathetic nervous system. It is usual to divide them under 3 headings: muscarinic, nicotinic & central. Muscarinic signs ... consist of hypersalivation, lacrimation, sweating & nasal discharge. Miosis, dyspnea, vomiting, diarrhea & frequency of urination ... Nicotinic effects consist of fasciculation of muscles, weakness & paralysis. Central nervous system effects include nervousness, apprehension, ataxia, convulsions & coma. Death is due to resp failure, or sometimes cardiac arrest. There is little difference between signs produced by different organophosphorus compounds, but route of absorption may influence one system more than another. /Organophosphorus cmpd/
Toxicants of this class phosphorylate almost irreversibly varying amt of acetylcholinesterase enzyme of tissues, allowing accum of acetylcholine at cholinergic neuro-effector junctions (muscarinic effects), & at skeletal muscle myoneural junctions & in autonomic ganglia (nicotinic effects). /Organophosphate pesticides/
For more Mechanism of Action (Complete) data for DIMETHOATE (6 total), please visit the HSDB record page.

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Therapeutic Uses
Medication (Vet): Also used experimentally in many species by many routes (spray, oral, sc, im, pour on, etc), and has shown particular effectiveness against grubs in cattle and reindeer (10 and 30 mg/kg upper safe limits, respectively) and oestrus ovis in sheep (25 mg/kg sc- avoid use in hot or tired animals). Older materials may be more toxic to animals.

C5H12NO3PS2

229.24

228.999

60-51-5

Dimethoate-d6;1219794-81-6

3082

White crystalline solid
Colorless crystals (Tech., white solid pellets)

1.4±0.1 g/cm3

310.3±52.0 °C at 760 mmHg

52-52.5°C

141.4±30.7 °C

0.0±1.5 mmHg at 25°C

1.548

1.32

1

5

5

12

191

0

CNC(CSP(OC)(OC)=S)=O

MCWXGJITAZMZEV-UHFFFAOYSA-N

InChI=1S/C5H12NO3PS2/c1-6-5(7)4-12-10(11,8-2)9-3/h4H2,1-3H3,(H,6,7)

2-dimethoxyphosphinothioylsulfanyl-N-methylacetamide

L-395; Lurgo; Dimethoate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~10.42 mg/mL (~45.45 mM)

Solubility in Formulation 1: 10 mg/mL (43.62 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)