Disease relevance of propanil

• These data suggest that human exposure to propanil may be monitored in the absence of observable toxicity by the analysis of propanil metabolites bound to hemoglobin [1].
• Propanil-induced methemoglobinemia and hemoglobin binding in the rat [1].
• Role of metabolites in propanil-induced hemolytic anemia [2].
• Oral exposure to propanil also caused splenomegaly and thymic atrophy in animals in much the same manner as animals exposed via the i.p. route [3].
• In the present study, we investigated the effect of propanil on IL-2 expression and production in the murine lymphoma T cell line, EL-4 [4].

High impact information on propanil

• Our previous studies demonstrated that both in vivo and in vitro 3,4-dichloro-propionanilide (propanil) exposure inhibited interleukin-6 (IL-6) and tumor necrosis factor (TNF) production by adherent thioglycollate-elicited peritoneal cells (macrophages) after lipopolysaccharide (LPS) stimulation [5].
• Propanil exposure induces delayed but sustained abrogation of cell-mediated immunity through direct interference with cytotoxic T-lymphocyte effectors [6].
• The postemergent herbicide propanil (PRN ; also known as 3,4-dichloropropionanilide) is used on rice and wheat crops and has well-known immunotoxic effects on various compartments of the immune system, including T-helper lymphocytes, B lymphocytes, and macrophages [6].
• Evidence for a novel endocrine disruptor: the pesticide propanil requires the ovaries and steroid synthesis to enhance humoral immunity [7].
• The immunotoxic chemical propanil and estrogen have similar effects on the immune system including augmentation of humoral immune responses [7].

Chemical compound and disease context of propanil

• We examined the metabolism of propanil and 3,4-dichloroaniline in rat liver microsomes to identify metabolites that may be involved in propanil-induced methemoglobinemia [8].
• These data indicate that N-hydroxy-3,4-dichloroaniline mediates propanil-induced hemolytic anemia, and that occupational exposure to propanil may result in an increased risk of hemolytic episodes [2].
• Propanil enhances the number of phosphorylcholine (PC)-specific IgG2b, IgG3, and IgM antibody-secreting cells (ASCs) in the spleen four- to sixfold 7 days after vaccination of female C57BL/6 mice with heat-killed Streptococcus pneumoniae [7].
• Exposure to 150 mg herbicide/kg body weight of propanil or 2,4-D alone had no effect on thymus weight [9].
• However, similar levels of corticosterone were induced after exposure to 50, 100, or 150 mg propanil/kg body weight, and 50/50 or 100/100 mixture treatments, doses that did not produce thymic atrophy or cell loss [9].

Biological context of propanil

• Nuclear run-on assays determined that the transcription rate of the IL-2 gene was decreased approximately 50% in the presence of 20 microM propanil, indicating that it was able to interfere with signal transduction [4].
• Modeling and predicting selected immunological effects of a chemical stressor (3,4-dichloropropionanilide) using the area under the corticosterone concentration versus time curve [10].
• In the present study, an immunotoxicant known to induce a stress response, 3,4-dichloropropionanilide (propanil), was evaluated to determine if corticosterone AUC values are related to suppression of immunological parameters in mice treated with this chemical [10].
• Propanil and its metabolites are transported within characteristic ditch ecosystems in the production landscape of northeast Arkansas. Runoff from these ditch ecosystems is further transported to a river or other water body supplied by the Mississippi River Alluvial aquifer [11].
• 1. The uptake, elimination and tissue distribution of total radioactivity derived from the herbicide, [14C]propanil (3,4-dichloropropionanilide) and its metabolites were examined in individual farm-raised Channel Catfish which were exposed for 24 h to water containing 1 ppm of 14C-propanil under static conditions [12].

Anatomical context of propanil

• Altered AP-1 (activating protein-1) activity and c-jun activation in T cells exposed to the amide class herbicide 3,4-dichloropropionanilide (DCPA) [13].
• However, the number of ASC in the bone marrow and serum titers were comparable in control and propanil-treated mice [14].
• Propanil inhibits tumor necrosis factor-alpha production by reducing nuclear levels of the transcription factor nuclear factor-kappab in the macrophage cell line ic-21 [15].
• EROD, BROD, and 7-pentoxyresorufin-O-dealkylase activities were slightly increased in microsomes from propanil- and 3,4-dichloroaniline-pretreated rats, which suggests that these compounds may be weak inducers of cytochrome P450 isozymes [16].
• When labeled erythrocytes were exposed in vitro to propanil or 3,4-dichloroaniline and then readministered to rats, no decrease in erythrocyte survival was observed, which indicated that these compounds were not direct-acting hemolytic agents [2].

Associations of propanil with other chemical compounds

• In vitro myelotoxicity of propanil and 3,4-dichloroaniline on murine and human CFU-E/BFU-E progenitors [17].
• LPS-stimulated primary mouse macrophages produced less TNF-alpha protein and message after treatment with the herbicide propanil (Xie et al., Toxicol. Appl. Pharmacol. 145, 184-191, 1997) [15].
• Ovariectomy abrogated the effect of propanil on the PC-specific ASC response [7].
• A liquid chromatography/electrospray ionization/mass spectrometry method was reported for the compliance analysis of seven phenylurea compounds and two related herbicides (tebuthiuron and propanil) in drinking water [18].
• Four herbicides, namely propanil, maleic hydrazide, glyphosate, and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), were investigated for genotoxicity in the wing spot test of Drosophila melanogaster [19].

Gene context of propanil

• Further studies demonstrated a marked reduction in the nuclear levels of the stimulatory p65 subunit of NF-kappaB after propanil treatment, as measured by fluorescence confocal microscopy and Western blot analysis [15].
• Both oral and i.p. propanil exposure resulted in up to a 60-70% reduction in IL-6 and TNF-alpha production by the LPS-stimulated macrophages, depending on the route, postexposure time, and dose of propanil administered [3].
• Pulsing normal spleen cell cultures with propanil for up to 8 h before T-cell activation resulted in reduced IL-6 but not IL-2 or IFN-gamma production [20].
• The p50 subunit of NF-kappaB was not found to be reduced after propanil exposure by Western blot [15].
• In vitro exposure to propanil also significantly reduced macrophage cytokine production [3].

Analytical, diagnostic and therapeutic context of propanil

• The amide-class herbicide, propanil, causes numerous immunomodulary effects in animal models [4].
• Northern blot analysis demonstrated that the message levels of these cytokines were reduced by approximately the same percentage as the protein levels in propanil-treated macrophages, indicating a possible transcriptional or pretranscriptional target(s) for propanil [3].
• When supernatants of cells stimulated with phorbol 12-myristate 13-acetate in the presence of propanil were assessed by enzyme-linked immunosorbent assay, IL-2 levels were dose-dependently decreased by 20 and 50 microM of propanil but not at 10 microM [4].
• Chronic toxicity tests were carried out using sublethal propanil concentrations (0.07, 0.10, 0.21 and 0.55 mg/l) during 21 days [21].
• Using HPLC, the objective of this experiment was to analyze the fate of cyhalofop-butyl in barnyardgrass tissue when applied alone and in combination with halosulfuron, propanil, or triclopyr [22].

References