A comparison of electron-capture GLC, electrolytic-conductivity GLC and UV-absorption HPLC for the analysis of some herbicides in foods. (1/16)

A comparison of gas chromatography with electron-capture or electrolytic-conductivity (nitrogen mode) detection, and high-pressure liquid chromatography (HPLC) with UV-absorption detection (254 nm) was carried out for the analysis of several herbicides in foods. Linuron, propanil, terbacil, benzoylprop-ethyl, and the fungicide DCNA in samples of cabbage, corn, potato, and wheat spiked at 2 and 0.2 ppm were examined. The pesticides were extracted with acetone, partitioned into petroleum ether-methylene chloride, and cleaned up on a 2% deactivated Florisil column before direct chromatographic analysis. Electron-capture gas-liquid chromatography (GLC) was most suitable for DCNA and benzoylprop-ethyl while UV-absorption HPLC was best for terbacil analysis. Linuron and propanil gave similar results for both electron-capture GLC and HPLC. Electrolytic-conductivity GLC could detect all pesticides at the 0.2 ppm level and exhibited the least number of extraneous peaks in the chromatograms.  (+info)

Modeling and predicting selected immunological effects of a chemical stressor (3,4-dichloropropionanilide) using the area under the corticosterone concentration versus time curve. (2/16)

Many chemicals and drugs can induce a neuroendocrine stress response that can be immunosuppressive. Mathematical models have been developed that allow prediction of the immunological impact of such stress responses in mice on the basis of exposure to the important stress-related mediator corticosterone. The area under the corticosterone concentration vs. time curve (AUC) has been used as an indicator of cumulative corticosterone exposure in these modeling studies. 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. Linear relationships between corticosterone AUC values and suppression of the following parameters were noted in B6C3F1 female mice: thymus cellularity and thymus subpopulation percentages, splenic subpopulation percentages, natural killer cell activity, MHC class II protein expression, and IgG1 and IgG2a antibody responses to antigen. Linear models derived in previous studies using mice treated with exogenous corticosterone or with restraint stress effectively predicted the immunological effects of 3, 4-dichloropropionanilide on the basis of corticosterone AUC values. The models derived using immobilization stress were more effective (r(2) for observed vs. predicted = 0.90) than the models derived using mice treated with exogenous corticosterone (r(2) for observed vs. predicted = 0.65). This was expected, because most stressors induce a variety of immunomodulatory mediators, not just corticosterone. These findings have implications for risk assessment in immunotoxicology.  (+info)

In vitro myelotoxicity of propanil and 3,4-dichloroaniline on murine and human CFU-E/BFU-E progenitors. (3/16)

Because of the wide use of pesticides for domestic and industrial purposes, the evaluation of their potential effects is of major concern for public health. The myelotoxicity of the herbicide propanil (3,4-dichloroproprioanilide) and its metabolite 3,4-dichloroaniline (DCA) is well documented in mice, but evidence that pesticides may severely compromise hematopoiesis in humans is lacking. In this study, an interspecies comparison of in vitro toxicity of these two compounds on murine and human burst- and colony-forming unit-erythrocyte (BFU-E, CFU-E) and colony-forming unit-granulocyte/macrophage (CFU-GM) progenitors, has been carried out. Murine bone marrow progenitors and human cord blood cells were exposed to propanil or DCA in doses ranging from 10 micro M to 1000 micro M, and the toxic effect was detected by a clonogenic assay with continuous exposure to the compounds. The results on murine cells indicate that the erythrocytic lineage is the most sensitive target for propanil and DCA. On the other hand, human progenitors seem to be less sensitive to the toxic effects of both compounds than murine progenitors at the same concentrations (IC(50) values are 305.2 +/- 22.6 micro M [total erythroid colonies] and >500 micro M [CFU-GM] for propanil). Propanil was significantly more toxic to human erythroid progenitors than to human CFU-GM progenitors, as was found for the murine cells, emphasizing the role of the heme pathway as the target for propanil. These data confirm the evidence that the compounds investigated interfere with erythroid colony formation at different stages of the differentiation pathway and have different effects according to the dose.  (+info)

Severe propanil [N-(3,4-dichlorophenyl) propanamide] pesticide self-poisoning. (4/16)

BACKGROUND: Propanil pesticide poisoning can produce methemoglobinemia, tissue hypoxia, and depression of central nervous system and respiratory system. It has been recorded only rarely worldwide and most current poison texts consider propanil to be of low toxicity. However, propanil self-poisoning is a significant clinical problem in parts of Sri Lanka and an occasional cause of death. AIM OF STUDY: To report the clinical features and management of severe propanil poisoning. PATIENTS AND METHODS: We report a retrospective case series of patients who were treated in the intensive care unit of and/or died in Anuradhapura General Hospital between 1998 and early 2002. RESULTS: Sixteen patients were identified. Common manifestations of toxicity included confusion, reduced conscious level, cyanosis, and respiratory depression. Marked hemolysis was noted in several patients. Nine deaths occurred due to respiratory depression and cardiorespiratory arrest. Management was difficult given the lack of i.v. methylene blue, inability to measure methemoglobin levels, and paucity of intensive care unit beds. CONCLUSIONS: This series indicates that propanil poisoning can be a severe form of self-poisoning, particularly in resource-poor settings. We have now initiated the establishment of a prospective series of propanil poisoned patients to further describe its clinical features, responsiveness to therapy, and case fatality rate.  (+info)

Modeling and predicting stress-induced immunosuppression in mice using blood parameters. (5/16)

Previous studies have shown that the area under the corticosterone concentration vs. time curve (AUC) can be used to model and predict the effects of restraint stress and chemical stressors on a variety of immunological parameters in the mouse spleen and thymus. In order to complete a risk assessment parallelogram, similar data are needed with blood as the source of immune system cells, because this is the only tissue routinely available from human subjects. Therefore, studies were conducted using treatments for which the corticosterone AUC values are already known: exogenous corticosterone, restraint, propanil, atrazine, and ethanol. Immunological parameters were measured using peripheral blood from mice treated with a series of dosages of each of these agents. Flow cytometry was used to quantify MHC II, B220, CD4, and CD8 cells. Leukocyte and differential counts were done. Spleen cell number and NK cell activity were evaluated to confirm similarity to previous studies. Immune parameter data from mouse blood indicate that MHC II expression has consistent quantitative relationships to corticosterone AUC values, similar to but less consistent than those observed in the spleen. Other immune parameters tended to have greater variability in the blood than in the spleen. The pattern observed in the spleen in which the chemical stressors generally produced very similar effects as noted for restraint stress (at the same corticosterone AUC values) was not observed for blood leukocytes. Nevertheless, MHC class II expression seems to provide a reasonably consistent indication of stress exposure in blood and spleen.  (+info)

The polysaccharide antibody response after Streptococcus pneumoniae vaccination is differentially enhanced or suppressed by 3,4-dichloropropionanilide and 2,4-dichlorophenoxyacetic acid. (6/16)

Propanil (3,4-dichloropropionanilide) and 2,4-D (2,4-dichlorophenoxyacetic acid) are commonly used herbicides that have toxic effects on the immune system. The present study determined the effect of exposure to these chemicals on the immune response to a bacterial vaccine. The antibody responses to the T-independent type 2 antigen, phosphorylcholine (PC) and the T-dependent antigen, pneumococcal surface protein A (PspA) were characterized in C57BL/6 mice after heat-killed Streptococcus pneumoniae (HKSP) immunization and single or mixture herbicide exposure. Propanil exposure significantly increased the number of PC-specific IgM, IgG2b, and IgG3 antibody-secreting B cells (ASC) in the spleen 4-6-fold over control animals in a dose-dependent manner. However, the number of ASC in the bone marrow and serum titers were comparable in control and propanil-treated mice. In contrast, 2,4-D exposure decreased the number of PC-specific IgM and IgG bone marrow ASC 2-3-fold from control animals. The decrease in bone marrow ASC in 2,4-D-treated mice corresponded to a 3-4-fold decrease in PC-specific IgM, IgG2b, and IgG3 serum titers compared to control mice. The number of ASC in the spleens of 2,4-D-treated mice was, however, comparable to control mice. The antibody response to PspA was not affected by any of the treatments. There were no mixture interactions between the two herbicides in any of the responses measured. These results characterize the primary PC-specific antibody response in the bone marrow, spleen, and serum after HKSP vaccination and herbicide exposure. The differential effects of propanil and 2,4-D on the antibody response to a bacterial vaccine demonstrate the potential of chemical exposure to augment or suppress immune responses to vaccines and infectious diseases.  (+info)

Evidence for a novel endocrine disruptor: the pesticide propanil requires the ovaries and steroid synthesis to enhance humoral immunity. (7/16)

Steroid hormones are known to affect the humoral immune response to a variety of antigens. However, the mechanisms regulating these effects are poorly understood. The immunotoxic chemical propanil and estrogen have similar effects on the immune system including augmentation of humoral immune responses. 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. Several experiments were performed to test the hypothesis that propanil increases the response via an estrogenic pathway. Ovariectomy abrogated the effect of propanil on the PC-specific ASC response. Both in vitro and in vivo assays indicate that propanil does not bind either estrogen receptor (ER) alpha or beta. Exogenous estradiol administration in ovariectomized mice failed to restore the effect of propanil on the PC response. Treatment of female mice with a pure ER antagonist, ICI 182,780, or the progesterone antagonist RU486 did not inhibit the increase in ASCs. These data suggest that estrogen and progesterone do not regulate the effect of propanil. However, complete inhibition of steroid synthesis with the gonadotropin-releasing hormone (GnRH) antagonist antide abrogated the increased response in propanil-treated mice, indicating a necessary role for steroid synthesis. Experiments in male mice demonstrated that propanil increased the number of ASCs comparable to female mice. However, orchiectomy did not inhibit this effect, suggesting that androgens do not regulate the amplification of the humoral response. These data suggest a novel role for the ovarian hormones in the regulation of the PC-specific antibody response.  (+info)

Propanil exposure induces delayed but sustained abrogation of cell-mediated immunity through direct interference with cytotoxic T-lymphocyte effectors. (8/16)

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. It is unclear, however, whether PRN also adversely affects cytotoxic T lymphocytes (CTLs) , the primary (1 degrees ) effectors of cell-mediated immunity. In this study we examined both the direct and indirect effects of PRN exposure on 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.  (+info)

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