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1. Propagrin 36
2. Propanide
1. 709-98-8
2. N-(3,4-dichlorophenyl)propanamide
3. Propanide
4. Propanex
5. Dipram
6. Grascide
7. Propanid
8. Stampede
9. Supernox
10. Surcopur
11. Rogue
12. Chem Rice
13. Stam
14. Synpran N
15. Cekupropanil
16. Riselect
17. Herbax
18. Strel
19. Propanamide, N-(3,4-dichlorophenyl)-
20. Prop Job
21. Montrose Propanil
22. 3',4'-dichloropropionanilide
23. Stam M-4
24. N-(3,4-dichlorophenyl)propionamide
25. Wham Ez
26. Propanilo
27. Erbanil
28. Stam F 34
29. Erban
30. Dichloropropionanilide
31. 3,4-dichloropropionanilide
32. Chem-rice
33. Prop-job
34. Stam Lv 10
35. Herbax 4e
36. Crystal Propanil-4
37. Stampede 360
38. Surpur
39. Stam 80edf
40. Bay 30130
41. Fw 734
42. Propionic Acid 3,4-dichloroanilide
43. Propanile
44. Vertac
45. Propionanilide, 3',4'-dichloro-
46. 3',4'-dichlorophenylpropionanilide
47. Nsc 31312
48. S 10165
49. Chebi:34936
50. Nsc-31312
51. Propanil 10 Microg/ml In Cyclohexane
52. F57i4g0520
53. Propanil 10 Microg/ml In Acetonitrile
54. Rosanil
55. Farmco Propanil
56. Stam Supernox
57. Herbax Technical
58. Dsstox_cid_2111
59. Drexel Prop-job
60. Stampede 3e
61. Dsstox_rid_76491
62. Dsstox_gsid_22111
63. Herbax 3e
64. Vertac Propanil 3
65. Vertac Propanil 4
66. Herbax Lv-30
67. Caswell No. 325
68. Propanil [bsi:iso]
69. Bayer 30 130
70. Propanil [iso]
71. Cas-709-98-8
72. Ccris 3009
73. Hsdb 1226
74. Propionic Acid-3,4-dichloroanilide
75. Einecs 211-914-6
76. Epa Pesticide Chemical Code 028201
77. Brn 2365645
78. Propasint
79. Arrosol
80. Dropaven
81. Propanac
82. Ai3-31382
83. Unii-f57i4g0520
84. 3,4-dichloranilid Kyseliny Propionove [czech]
85. Wham Df
86. B-30,130
87. 3,4-dichloranilid Kyseliny Propionove
88. Propanil (dcpa )
89. Spectrum_001807
90. Stam 80 Edf
91. Propanil [hsdb]
92. Specplus_000398
93. Propanil [mi]
94. Spectrum2_001878
95. Spectrum3_000819
96. Spectrum4_000659
97. Spectrum5_001948
98. Cbmicro_000482
99. Wln: Gr Bg Dmv2
100. Cambridge Id 5840989
101. Propionanilide,4'-dichloro-
102. Schembl26871
103. 3',4'-dichloropropioanilide
104. Bspbio_002317
105. Kbiogr_001037
106. Kbioss_002300
107. Spectrum330027
108. Mls002207241
109. Bidd:er0610
110. Divk1c_006494
111. Spbio_001756
112. Propanamide,4-dichlorophenyl)-
113. 3,4-dcpa
114. Chembl1222498
115. Dtxsid8022111
116. Schembl21900164
117. Kbio1_001438
118. Kbio2_002298
119. Kbio2_004866
120. Kbio2_007434
121. Kbio3_001817
122. Lfuleksknzewoe-uhfffaoysa-
123. Zinc362579
124. Hy-b2030
125. Nsc31312
126. Smsf0001373
127. Tox21_201774
128. Tox21_300848
129. Bay-30130
130. Ccg-39416
131. Fw-734
132. Propanil 100 Microg/ml In Methanol
133. Propanil 1000 Microg/ml In Acetone
134. Akos002960411
135. Cb01718
136. Cs-5217
137. Ncgc00094523-01
138. Ncgc00094523-02
139. Ncgc00094523-03
140. Ncgc00094523-04
141. Ncgc00094523-05
142. Ncgc00094523-06
143. Ncgc00094523-07
144. Ncgc00254751-01
145. Ncgc00259323-01
146. As-76229
147. Smr000778058
148. Bim-0000452.p001
149. Db-055477
150. Propionic Acid, 3,4-dichloroanilide
151. Ft-0603505
152. Propanil, Pestanal(r), Analytical Standard
153. 709p988
154. An-652/13319019
155. Q413507
156. S 10145
157. Sr-01000221575
158. Q-201627
159. Sr-01000221575-1
160. Brd-k08618283-001-02-0
| Molecular Weight | 218.08 g/mol |
|---|---|
| Molecular Formula | C9H9Cl2NO |
| XLogP3 | 3.1 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 2 |
| Exact Mass | 217.0061193 g/mol |
| Monoisotopic Mass | 217.0061193 g/mol |
| Topological Polar Surface Area | 29.1 Ų |
| Heavy Atom Count | 13 |
| Formal Charge | 0 |
| Complexity | 187 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Herbicides
Pesticides used to destroy unwanted vegetation, especially various types of weeds, grasses (POACEAE), and woody plants. Some plants develop HERBICIDE RESISTANCE. (See all compounds classified as Herbicides.)
SD rats /were administered propanil/ in a single oral low dose (2.5 mg/kg), multiple oral low dose (2.5 mg/kg for 15 days), single oral high dose (300 mg/kg), or an intravenous dose (0.7 mg/kg in saline). The majority of the radioactivity (78-90%) was excreted in the urine, and 2-13% was excreted in the feces. Most of the radioactivity was eliminated within 24 hours for all except the high oral dose where it took 48 hours to eliminate 90%. For the i.v. data, females excreted 10% in the feces, while males excreted 2%. The carcass contained 0.18-0.71% of the radioactivity, with the liver having the highest residue.
USEPA, Office of Prevention, Pesticides, and Toxic Substances; Revised HED Human Health Risk Assessment for Propanil (709-98-8) (February 2002). EPA Docket No.: EPA-HQ-OPP-2002-0033-0014. Available from, as of May 11, 2012: https://www.regulations.gov/#!home
Repeated inhalation (rat): after exposure to concentrations of 5.6 to 0.2 mg/m3, propanil occurs in the blood, heart and spleen.
IPCS; Poisons Information Monograph 440: Propanil. (April 1990). Available from, as of May 11, 2012: https://www.inchem.org/documents/pims/chemical/pim440.htm
Five minutes after oral administration of single doses (1000 mg/kg, 650 mg/kg) to rats, propanil is detectable in blood and all tissues. Maximum accumulation in lungs, liver, kidneys, spleen, adrenals and heart occurs within 1 to 6 hours of administration.
IPCS; Poisons Information Monograph 440: Propanil. (April 1990). Available from, as of May 11, 2012: https://www.inchem.org/documents/pims/chemical/pim440.htm
Little radioactivity from labeled propanil appeared in tissues in short-duration experiments with rats, mice, & dogs; this indicates that propensity for accumulation of propanil or its metabolites in tissues is slight.
National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 529
For more Absorption, Distribution and Excretion (Complete) data for PROPANIL (6 total), please visit the HSDB record page.
.../It/ is hydrolyzed by... hepatic acylamidase, forming 3,4-dichloroaniline and propionic acid. The enzyme... /is/ present in liver of rats, mice, rabbits, and dogs. Other conversions /occur/... either on propanil... or on dichloroaniline, /producing/... six metabolites in urine. These metabolites constitute about 95% of urinary products.
National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 529
Rainbow trout(Salmo gairdneri) readily metabolize technical grade propanil, forming at least 10 products. One metab recovered from bile was identified as 3',4'-dichloro-2-hydroxypropionanilide or 3',4'-dichloro-3-hydroxypropionanilide. The technical grade contained 0.67 mg/g 3,3',4,4'-tetrachloroazobenzene.
PMID:6847248 Call DJ et al; Arch Environ Contam Toxicol 12 (2): 175-82 (1983)
3,4-Dichloroaniline formed when propanil was added to algal cultures during growth. Experiments showed that some non-axenic algal cultures were very active in DCA formation and that the bacterial contaminants were also active when free of algae. In these studies, the non-axenic Nostoc entophytum and the axenic Polypothrix tenius were active in DCA production.
Menzie, C.M. Metabolism of Pesticides-Update III. Special Scientific Report- Wildlife No. 232. Washington, DC: U.S.Department of the Interior, Fish and Wildlife Service, 1980., p. 461
Red Rice (Oryza sativa Leguminatae) seedlings were the source of an aryl amidase. Studies showed that this enzyme was able to hydrolyze propanil, as well as some analogs. Although active between pH 7.4 to 8.7, the optimum was 8.2. Calculations showed the Km = 2.5X10-5 and that the activity was in the order propanil >>3'Cl > propionanilide > 4'-Cl greater than or equal to 3'5'-dichloro > 2'-Cl.
Menzie, C.M. Metabolism of Pesticides-Update III. Special Scientific Report- Wildlife No. 232. Washington, DC: U.S.Department of the Interior, Fish and Wildlife Service, 1980., p. 461
For more Metabolism/Metabolites (Complete) data for PROPANIL (10 total), please visit the HSDB record page.
In rats given up to 1000 mg/kg orally, blood concentrations are maintained for 24 hr but undetectable after 48 to 72 hr.
IPCS; Poisons Information Monograph 440: Propanil. (April 1990). Available from, as of February 16, 2005: https://www.inchem.org/documents/pims/chemical/pim440.htm
In this study, /investigators/ examined both the direct and indirect effects of /propanil (PRN)/ exposure on /cytotoxic T lymphocytes (CTL)/ activation and effector cell function to gauge its likely impact on cell-mediated immunity. Initial experiments addressed whether PRN alters the class I major histocompatibility complex (MHC) pathway for antigen processing and presentation by antigen-presenting cells (APCs) , thereby indirectly affecting effector function. These experiments demonstrated that PRN does not impair the activation of CTLs by PRN-treated APCs. Subsequent experiments addressed whether PRN treatment of CTLs directly inhibits their activation and revealed that 1 degrees alloreactive CTLs exposed to PRN are unimpaired in their proliferative response and only marginally inhibited in their lytic activity. Surprisingly, secondary stimulation of these alloreactive CTL effectors, however, even in the absence of further PRN exposure, resulted in complete abrogation of CTL lytic function and a delayed but significant long-term effect on CTL responsiveness. These findings may have important implications for the diagnosis and clinical management of anomalies of cell-mediated immunity resulting from environmental exposure to various herbicides and other pesticides.
PMID:16835059 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513295 Sheil JM et al; Environ Health Perspect 114 (7): 1059-64 (2006)
... Previous studies have demonstrated that treatment of the IC-21 macrophage cell line with DCPA resulted in changes of critical macrophage functions, including a decrease in cytokine production, and in the ability to phagocytize and kill bacteria. To understand the mechanism involved in the propanil induced changes, a proteomics analysis was undertaken. For this study, IC-21 cells were exposed to 100 uM propanil or ethanol (vehicle) and stimulated with lipopolysaccharide. After 30 min of exposure, cytosolic fraction was isolated and analyzed by two-dimensional gel electrophoresis. Differential statistical analysis identified 12 spots that were all decreased in the propanil exposed cells compared to vehicle. Mass spectrometry analysis was used to identify the proteins, which was later confirmed by other methods. One of these proteins, Sorting Nexin 6 (SNX6) interacts with the TGF-beta family of receptor serine-threonine kinases and associates with early endosomes during intracellular receptor trafficking. Another protein, H+-ATPase functions as a cytoplasmic pH-regulator promoting acidification of intracellular compartments in macrophages during the respiratory burst. A third protein, fibroblast growth factor regulated-1 (FR-1) protein induced by FGF-1 stimulation is important for enhancement of phagocytosis and plays a role in promoting inflammation. Confirmation of other significantly changed proteins and linking their identity to the alterations in macrophage function is currently in progress. Together the data from toxicoproteomics analysis provides an additional evidence of the mechanism by which propanil suppresses macrophage functions.
Ustyugova IV et al; Toxicol Sci 84 (1-S): 386 (2005)
Stimulation of T cells through the T-cell receptor results in the activation of a series of signaling pathways that leads to the secretion of interleukin (IL)-2 and cell proliferation. Influx of calcium (Ca(2+)) from the extracellular environment, following internal Ca(2+) store depletion, provides the elevated and sustained intracellular calcium concentration ([Ca(2+)](i)) critical for optimal T-cell activation. Our laboratory has documented that exposure to the herbicide 3,4-dichloropropionanilide (DCPA) inhibits intracellular signaling events that have one or more Ca(2+) dependent steps. Herein we report that DCPA attenuates the normal elevated and sustained [Ca(2+)](i) that follows internal store depletion in the human leukemic Jurkat T cell line and primary mouse T cells. DCPA did not alter the depletion of internal Ca(2+) stores when stimulated by anti-CD3 or thapsigargin demonstrating that early inositol 1,4,5-triphosphate-mediated signaling and depletion of Ca(2+) stores were unaffected. 2-Aminoethyldiphenol borate (2-APB) is known to alter the store-operated Ca(2+) (SOC) influx that follows Ca(2+) store depletion. Exposure of Jurkat cells to either DCPA or 50 uM 2-APB attenuated the increase in [Ca(2+)](i) following thapsigargin or anti-CD3 induced store depletion in a similar manner. At low concentrations, 2-APB enhances SOC influx but this enhancement is abrogated in the presence of DCPA. This alteration in [Ca(2+)](i), when exposed to DCPA, significantly reduces nuclear levels of nuclear factor of activated T cells (NFAT) and IL-2 secretion. The plasma membrane polarization profile is not altered by DCPA exposure. Taken together, these data indicate that DCPA inhibits T-cell activation by altering Ca(2+) homeostasis following store depletion.
PMID:18281253 Lewis TL et al; Toxicol Sci 103 (1): 97-107 (2008)
Toxic signs after ip doses of 200 to 800 mg/kg of the herbicide propanil in mice included central nervous system depression, loss of reflex, cyanosis and death at the higher doses. Pretreatment with tri-o-cresylphosphate (triorthotolyl phosphate, TOTP), an esterase inhibitor, prevented cyanosis but slightly enhanced the CNS depressant actions of propanil. Propanil and a probable hydrolytic metabolite, 3,4-dichloroaniline (DCA), produced methemoglobinemia in mice. Comparison of the time- and dose-response relationships for equimolar doses of propanil and DCA showed that DCA was more potent and had a faster onset of methemoglobin production than propanil. The hydrolysis of propanil to yield 3,4-dichloroaniline by liver homogenates was completely inhibited 18 hr after mice were given 125 mg/kg of TOTP. Methemoglobin formation after propanil was inhibited in mice pretreated with 125 mg/kg of TOTP, but TOTP did not affect DCA-induced methemoglobinemia. Inhibition of propanil-amidase activity and propanil-induced methemoglobinemia had similar TOTP dose- and time-response relationships. Pretreatment with SKF-525A inhibited and phenobarbital pretreatment slightly increased both propanil- and DCA-induced methemoglobin formation. Neither pretreatment affected normal liver propanilamidase activity.
PMID:4714336 Murphy SD, Singleton SD; Toxicol Appl Pharmacol 25 (1): 20-29 (1973)
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