etters

S168 Abstracts / Toxicology L

of mucosa and further symptoms. By morphometric measurementthere was found out, that in parenchyma of testes in experimen-tal animals in comparison with control group occurred decreaseof relative volume of seminiferous epithelium about 27% and atthe same time increase of relative volume of interstitial tissue. Inthe experimental group also the average thickness of seminiferoustubules decreased to 250.22 ± 21.9 �m in comparison with controlgroup (343.76 ± 27.5 �m). Differences were significant (P < 0.01).Disorders of spermiogenesis showed a great variability. Most fre-quently was damaged zone of meiosis and metamorphosis; in somecases the aspermatic tubules were found. Damage of testicularparenchyma and spermiogenesis negatively influenced also fertil-ity of males (decreasing from 100% at the beginning of experimentto 22.2% at the end of experiment).

doi:10.1016/j.toxlet.2008.06.266

S13Atropine but not methylatropine corrects paraoxon-inducedrespiratory disturbances

Pascal Houzé ∗, Laetitia Pronzola, Maya Kayouka, Fréderic Baud

INSERM U705, Paris, France

Objective: Diethylparaoxon (PO) induces respiratory toxicity but themechanism is still unclear. We previously showed that atropine (A)induced a complete correction of the respiratory toxicity. The aimof this study was to compare the effects of A and methylatropine toclarify the origin of the respiratory toxicity.

Methods: Male Sprague–Dawley rats were given PO(0.215 mg kg−1, sc) and treated with A (base: 10 mg kg−1, sc)or equimolar MeA (base: 5.42, 54.2, and 542 mg kg−1, sc) 30 minafter PO. Respiratory function was assessed using whole bodyplethysmography and central temperature using infra-red teleme-try. Results are expressed as mean ± S.E.M. Statistical analysis usedANOVA tests.

Results: PO induced a significant decrease in temperature 30 minafter injection lasting 90 min. This effect was partially correctedby A, but not by MeA. PO induced an increase in expiratory timeand tidal volume, and a decrease in respiratory rate. Comparing theeffects of equimolar doses, A completely reversed the PO-inducedrespiratory alterations while MeA had no significant effect. Using10 and 100-fold higher dosages, MeA still had no significant effect.

Discussion: In contrast with A which can cross the blood-brain

barrier and modify both peripheral and central muscarinic effects,MeA does not cross the blood-brain barrier. PO poisoning inducedhypothermia was partially corrected by A but not by MeA. Acompletely reversed respiratory disturbances, while MeA had nosignificant effect at any dosages. We conclude that PO respiratorytoxicity is primarily mediated by disrupted muscarinic signaling inthe central nervous system.

doi:10.1016/j.toxlet.2008.06.267

S14TEA pretreatment induces significant increasing of pralidoximeantidotal activity

Pascal Houzé ∗, Maya Kayouka, Patricia Risède, Frédéric Baud

INSERM U705, Paris, France

Objective: The efficiency of pralidoxime methylsulfate (PRX), usedas an antidote to organophosphate poisoning is depends on itsplasma concentrations. In rats, we have previously shown that apretreatment by tetraethylammonium (TEA) significantly modi-

180S (2008) S32–S246

fies the pharmacokinetics of PRX, increasing the beta half-life anddecreasing the clearance without modification of the volume ofdistribution. The aim of this study is to determine if TEA-delayedPRX elimination modify the oxime antidotal activity regarding thediethylparaoxon-induced respiratory effects.

Methods: Male Sprague–Dawley rats were intoxicated withdiethylparaoxon (PO) (50% of DL50, SC). Tetraethylammonium(75 mg/kg IM) and PRX (50 mg/kg, IM) were injected 15 and 30 minafter PO administration, respectively. Respiratory function wasassessed using whole body plethysmography. Results are expressedas mean ± S.E.M. Statistical analysis used Student’s t test andANOVA tests with p < 0.05.

Results: Compared to control group, PO administration induceda significant decrease in respiratory rate, an increase in expi-ratory time and the tidal volume with no modifications of theinspiratory time. The effects were maximal 30 min post PO andplateaued through the study. At the maximal PO effects, PRX injec-tion induced a rapid (<5 min), complete but transient (<30 min)reversal of paraoxon-induced respiratory effects. In TEA-pretreatedgroup, PRX induced a complete and prolonged (180 min) reversionof all respiratory effects.

Conclusion: This preliminary study shows that the decreasing ofPRX elimination enhances and prolongs its antidotal activity. Thisresult proves the necessity to maintain high plasma PRX concen-trations during organophosphate poisoning therapy.

doi:10.1016/j.toxlet.2008.06.268

S15Extraction and identification of Aldicarb (Temik) from post-mortem tissues samples

khaled Ibrahim 1,∗, Madiha Zakhary 2, Abd-Elmonem 3, Abd-Elmoty 3

1 Forensic chemist at Assuit Chemical Laboratory of Medico-legalDepartment, Ministry of Justice, Egypt, 2 Biochemistry Department,Faculty of Medicine, Assiut University, Assiut 71516, Egypt, 3 Head ofAssiut Chemical Laboratory, Medico-legal Department, Ministry ofJustice, Egypt

Keywords: Temik; Tissue sample; TLC and HPLC

Aldicarb is a potent inhibitor of cholinesterase and has a highacute toxicity. This means that it acts as a nerve poison by dis-

rupting nerve impulses. In this submitted work, the extractionand identification of Temik in stomach content from autopsycases. The analytical protocol includes grinding these tissues withdichloromethane at pH 5.7. The reaction products was tested byT.L.C. on silica gel precoated plates and dichloromethane:ethylacetate:chloroform (65:25:10) mobile phase, a violet spots areformed after irradiation by U.V. light. Also, colored spots appearwhen sprayed by Dragen droff or furfural reagents. This was themethod has been confirmed by sharp peak by HPLC measurement.

doi:10.1016/j.toxlet.2008.06.269

S16Roles of detoxification enzymes in pyrethroid resistance of Heli-coverpa armigera from Turkey

Metin Konus 1,∗, Sakine Ugurlu 2, Mesude Iscan 3

1 Graduate Program of Biochemistry, Middle East TechnicalUniversity, Ankara, Turkey, 2 Plant Protection Central ResearchInstitute, Ankara, Turkey, 3 Department of Biological Sciences, MiddleEast Technical University, Ankara, Turkey