Absorption, Distribution and Excretion
Diuron is readily absorbed through the gastrointestinal tract in rats and dogs. The concentration of diuron in tissues is positively correlated with dose. No significant storage of diuron in tissues was observed… Diuron is also partially excreted unchanged in feces and urine. The absorption of 14C-diuron in solution by roots was investigated. …Small amounts of monomethyl and demethyl derivatives were found in nutrient solutions from soybean, oat, and corn leaves. Diuron is most readily absorbed through roots; followed by leaves and stems. Transport primarily occurs upwards through the xylem. Five dairy cows were fed diuron at concentrations ranging from 0–550 ppm. Approximately 50% of diuron was detected in urine, 10% in feces, and 5% in blood. Diuron was not detected in milk samples. The concentrations of diuron products in urine and blood were positively correlated, while those in urine and feces were negatively correlated. This suggests that the remaining diuron may be absorbed by the body or degraded into undetectable metabolites. High-dose dietary diuron is carcinogenic to the bladder of rats. The mechanism of action of diuron is believed to be urothelial toxicity and necrosis, followed by regenerative urothelial hyperplasia. The urothelial toxicity induced by diuron is not caused by urinary solids. Diuron is extensively metabolized; in rats, N-(3,4-dichlorophenyl)urea (DCPU) and 4,5-dichloro-2-hydroxyphenylurea (2-OH-DCPU) are the major urinary metabolites; lower concentrations of metabolites include N-(3,4-dichlorophenyl)-3-methylurea (DCPMU) and trace amounts of 3,4-dichloroaniline (DCA). In humans, there have been cases of product abuse, and DCPMU and DCPU have been detected in urine. To help elucidate the mechanism of action of diuron and assess the metabolites that cause diuron bladder cytotoxicity, we investigated the concentrations of metabolites in the urine of male Wistar rats treated with 2500 ppm diuron, their in vitro urothelial cytotoxicity, and their gene expression profiles. The concentration of DCPU detected in rat urine was significantly higher than the in vitro IC50 value and induced more gene expression changes than other tested metabolites. The concentration of 2-OH-DCPU in urine was approximately half the in vitro IC50 value, while the concentrations of DCPMU and DCA in urine were significantly lower than their IC50 values. We believe that DCPU is the major metabolite causing urothelial cytotoxicity in diuron-induced rat bladder, with 2-OH-DCPU also contributing. This study supports the mechanism of action of diuron-induced rat bladder effects, including metabolism to DCPU (and a small amount of 2-OH-DCPU), urinary concentration and excretion, urothelial cytotoxicity, and regeneration and proliferation. This study aims to investigate the biotransformation and distribution of diuron… The only metabolic pathway detected by liquid chromatography/mass spectrometry in human liver homogenate and liver microsomes from seven mammals, including human liver microsomes, was the demethylation of the terminal nitrogen atom. No other phase I or II metabolites were observed. The order of N-demethyldiuron production in liver microsomes based on intrinsic clearance (V(max)/K(m)) was: dog > monkey > rabbit > mouse > human > miniature pig > rat. All tested recombinant human cytochrome P450 (P450) enzymes catalyzed N-demethylation of diuron, with CYP1A1, CYP1A2, CYP2C19, and CYP2D6 exhibiting the highest activity. Based on the mean abundance of P450 enzymes in human liver microsomes, the relative contributions of human CYP1A2, CYP2C19, and CYP3A4 to hepatic diuron N-demethylation were approximately 60%, 14%, and 13%, respectively. Diuron exhibits strong inhibitory activity only against CYP1A1/2 (IC50: 4 μM). 3,4-Dichloroaniline (3,4-DCA) is a metabolite of diuron, as well as two other pesticides, linuron and pretilachlor. However, the EPA's Metabolic Assessment Review Committee (MARC) concluded that 3,4-dichloroacetic acid (3,4-DCA) residues should not be included in risk assessments of diuron, linuron, and pretilachlor because 3,4-DCA is a significant residue of pretilachlor but not itself a significant residue of diuron or linuron. Although analytical methods used to quantify significant diuron residues convert all residues to 3,4-DCA for convenience, 3,4-DCA is not a significant residue in any metabolic or hydrolysis study.
...1-(3,4-dichlorophenyl)-3,3-dimethylurea, 3-amino-1,2,4-triazole, 1-(3,4-dichlorophenyl)-3-methylurea, and 1-(3,4-dichlorophenyl)urea were isolated from the urine of a woman poisoned with diuron. The urine may have contained trace amounts of 3,4-dichloroaniline, but no unmetabolized herbicide was detected.
For more complete metabolite/metabolite data on diuron (12 metabolites in total), please visit the HSDB record page.
Known human metabolites of diuron include N-desmethyldiuron.

Toxicity Summary
Identification and Uses: Diuron is a solid. Diuron is a photosynthesis inhibitor primarily used for weed control in non-cultivated land. It has also been used for selective control of broadleaf and grass weeds in sugarcane, citrus, pineapple, cotton, asparagus, and in temperate regions, as well as in trees and shrubs. Additionally, it can be used as a soil disinfectant. Human Studies: Diuron may irritate the skin, eyes, or nose. In vitro studies have shown that diuron is cytotoxic to human cells, and oxidative stress exacerbates its toxicity. A suicide attempt victim did not show symptoms of poisoning after taking diuron and aztreon preparations. Animal Studies: Diuron can irritate the eyes and mucous membranes of rabbits, but a 50% aqueous paste is non-irritating to intact skin in guinea pigs. High doses (2500 ppm) of diuron induced bladder hyperplasia in rats after 20 weeks of exposure. The study also found that rats exposed to high doses (1250 ppm and 2500 ppm) of diuron showed upregulated expression of genes related to the aryl hydrocarbon receptor signaling pathway. In a two-year bioassay, high doses (2500 ppm) of diuron induced a high incidence of bladder cancer in rats, while the incidence of renal pelvis papilloma and carcinoma was low. The mechanism of action of this herbicide on the rat urothelium is believed to be: its metabolism activates into metabolites, which are excreted and concentrated in the urine, ultimately leading to cytotoxicity, urothelial cell necrosis and shedding, regenerative proliferation, and eventually tumor formation. At a concentration of 2500 ppm for two years, both rats and dogs exhibited growth retardation, mild anemia, abnormal pigmentation, increased erythropoiesis, and hemosiderin deposition in the spleen. Some rats developed splenomegaly, and dogs developed hepatomegaly. A concentration of 750 ppm of diuron induced toxicity in male offspring, but these changes were not permanent, and no abnormalities were observed in the reproductive system of adult rats. A three-generation rat study showed that a dietary concentration of 125 ppm of diuron had no adverse effects on reproduction. In rat developmental studies, 500 mg/kg diuron reduced the average fetal weight, while 250 mg/kg diuron increased the number of malformed fetuses. In zebrafish studies, diuron significantly altered zebrafish behavior, such as reducing spontaneous coiling movements in embryos and decreasing wall-to-wall tropism in juveniles. In vitro endocrine disruption assays demonstrated the activity of diuron. Diuron was tested in Salmonella strains TA1535, TA97, TA98, and TA100, with metabolic activation at concentrations of 0, 10, 25, 50, 100, or 250 μg/plate, and no activation at concentrations of 0, 0.5, 1, 2.5, 5, or 10 μg/plate. No increase in reversal rate was reported. Cytotoxicity was observed in strain TA1535. Ecotoxicity studies: Diuron metabolites have estrogen-like effects, potentially mediated by enhanced estradiol biosynthesis and accelerated ovarian development in female Nile tilapia. Further research indicates that the bioconversion of diuron into its active metabolites alters central nervous system signaling pathways, potentially affecting androgen levels and stress responses, as well as behaviors required for social dominance, growth, and reproduction in fish. Oysters are frequently exposed to diuron concentrations common in the wild during gametogenesis, which can impact offspring and potentially impair their adaptation. Diuron exacerbates the negative impact on oyster reproduction by inducing structural and functional alterations in DNA. Furthermore, parental exposure to diuron affects the DNA methylation patterns of their offspring. This study assessed the effects of the herbicide diuron using a circulating multicompartmental algae, Daphnia magna, and bacterial microecosystem. Results showed that a diuron concentration of 0.2 ppm was lethal to Daphnia magna populations. Diuron also affects newborn larvae, preventing them from maturing. Diuron has been associated with severe and widespread wilting in the dominant mangrove species Avicennia marina (Forsk.) Vierh. var. . In three adjacent estuaries in the Mackay region of northeastern Australia, canopy conditions of Eucalyptifolia (Val.) NC Duke (Avicennia genus) have declined, and seedling health has deteriorated. This wilting may lead to deterioration of coastal water quality, increased turbidity, increased nutrient and sediment deposition, and further diffusion of toxic chemicals. Diuron has been reported to bind to androgen receptors. This suggests that diuron may block the receptors, leading to reproductive toxicity. Interactions: Both diuron and antimycin A act between cytochrome b and c1 in the respiratory chain. The inhibition rate of diuron showed a hyperbolic kinetic relationship with concentration, while the inhibition curve of antimycin A was S-shaped. The combined effects of antimycin A and diuron on yeast mitochondrial state 4 respiration and the apparent Ki value of diuron were significantly reduced in the presence of antimycin A. The interaction coefficient between antimycin A and diuron was 0.4, indicating that antimycin A induces a conformational change in the β-cl fragment of the respiratory chain, allowing diuron to bind more tightly to its site of action.

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Non-human toxicity values
Oral LD50 in male rats: 3400 mg/kg
Oral LD50 in rats: 1017 mg/kg

According to the U.S. Environmental Protection Agency (EPA), diuron may be carcinogenic. Diuron is a white crystalline solid, a wettable powder. Its main hazard is environmental pollution. Immediate measures should be taken to limit its spread in the environment. It can cause illness through inhalation, skin absorption, and/or ingestion. Diuron is used as a herbicide. Diuron belongs to the 3-(3,4-substituted phenyl)-1,1-dimethylurea class of compounds, which are urea compounds in which two hydrogen atoms on one nitrogen atom are replaced by methyl groups, and one hydrogen atom on the other nitrogen atom is replaced by a 3,4-dichlorophenyl group. It is a photosystem II inhibitor, an exogenous substance, an environmental pollutant, a mitochondrial respiratory chain inhibitor, and a urea herbicide. It is a dichlorobenzene and 3-(3,4-substituted phenyl)-1,1-dimethylurea. Diuron, also known as DCMU (3-(3,4-dichlorophenyl)-1,1-dimethylurea), is a urea herbicide that inhibits photosynthesis. It was introduced by Bayer in 1954 under the trade name diuron. DCMU is a highly specific and sensitive photosynthesis inhibitor, the process by which plants use light, water, and carbon dioxide from the atmosphere to synthesize plant sugars and cellulose. Diuron blocks electron transport at a key point in this process. It blocks the plastoquinone binding site of photosystem II, thereby preventing electrons from flowing from the source of photosystem II to plastoquinone. This interrupts the photosynthetic electron transport chain in photosynthesis, thus reducing the plant's ability to convert light energy into chemical energy (ATP and reduction potential).
A pre-emergence herbicide.

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Mechanism of Action
Chlorophyll fluorescence measurements showed that electron transport in intact soybean leaves was significantly inhibited after 1 hour of treatment with a 40 mM diuron solution.
The potent inhibitory effect of substituted urea compounds on the plant photosynthetic mechanism is achieved by inhibiting the Hill reaction, i.e., the release of oxygen in the presence of living chloroplasts and suitable hydrogen acceptors. Substituted urea compounds

C9H10CL2N2O

233.09

232.017

330-54-1

Diuron-d6;1007536-67-5

3120

White, crystalline solid
Colorless crystals
White powder

1.3±0.1 g/cm3

362.3±52.0 °C at 760 mmHg

158-159°C

172.9±30.7 °C

0.0±0.9 mmHg at 25°C

1.565

2.88

1

1

1

14

211

0

CN(C(NC1=CC(Cl)=C(Cl)C=C1)=O)C

XMTQQYYKAHVGBJ-UHFFFAOYSA-N

InChI=1S/C9H10Cl2N2O/c1-13(2)9(14)12-6-3-4-7(10)8(11)5-6/h3-5H,1-2H3,(H,12,14)

3-(3,4-dichlorophenyl)-1,1-dimethylurea

HW 920; Dirurol; Diuron

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

DMSO : ~250 mg/mL (~1072.55 mM)

Solubility in Formulation 1: ≥ 6.25 mg/mL (26.81 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 62.5 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 6.25 mg/mL (26.81 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 62.5 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 6.25 mg/mL (26.81 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 62.5 mg/mL clear DMSO stock solution to 900 μL corn oil and mix evenly.

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