Athetosis ; chemically induced ; therapy ; Benzene ; poisoning ; Humans ; Male ; Nitriles ; poisoning ; Pyrethrins ; poisoning ; Young Adult

Adult ; Cause of Death ; Humans ; Male ; Nitriles ; poisoning ; Poisoning ; mortality ; therapy ; Young Adult

Acute Disease ; Animals ; Behavior, Animal ; drug effects ; Female ; Male ; Mice ; Mice, Inbred ICR ; Nitriles ; poisoning ; Rabbits

Accidents, Occupational ; mortality ; Animals ; Cause of Death ; Humans ; Male ; Nitriles ; poisoning ; Rats

Acute Disease ; Adult ; Emergency Nursing ; First Aid ; Humans ; Male ; Nitriles ; poisoning ; Young Adult

OBJECTIVEto investigate the changes of γ-aminobutyric acid (GABA) and glutamate (Glu) in the cerebral cortex following acute bromoxynil intoxication in mice and the protective effect of sodium dimercaptopropane sulfonate (Na-DMPS).

METHODS30 ICR mice were randomly divided into blank control group (10), exposure group (10) and Na-DMPS protection group (10). The levels of GABA and Glu in the cerebral cortex were measured by RP-HPLC. The glutamine (Gln) level and the glutamine synthetase (GS), glutamate decarboxylation enzyme (GAD), γ-aminobutyric acid transaminase (GABA-T) activity in the cerebral cortex were determined by UV colorimetric.

RESULTScompared with the control group [GABA: (3.41 ± 0.12) micromol/g, Glu (14.00 ± 0.16) micromol/g, Gln (1.25 ± 0.19) micromol/g, GAD (13.50 ± 0.25) micromol × g(-1) × h(-1), GABA-T (25.51 ± 0.21) micromol × g(-1) × h(-1), GS(142.19 ± 1.31) U/mg pro], the level of GABA [(3.14 ± 0.14) micromol/g] was decreased (P < 0.05), whereas the level of Glu [(17.54 ± 0.40) micromol/g] and Gln [(3.35 ± 0.27) micromol/g] were increased (P < 0.05), the activity of GAD [(11.93 ± 0.15 micromol × g(-1) × h(-1)], GABA-T [(24.15 ± 0.22) micromol × g(-1) × h(-1)], GS [(140.75 ± 1.01) U/mg pro] was decreased (P < 0.05) in acute intoxication group; Compared with the acute intoxication group, the level of GABA [(3.52 ± 0.30) micromol/g] was increased (P < 0.05), whereas the level of Glu [(14.20 ± 0.32) micromol/g] and Gln [(1.32 ± 0.17) micromol/g] were decreased (P < 0.05), the activity of GAD [(13.01 ± 0.45 micromol × g(-1) × h(-1)], GABA-T [(25.19 ± 0.26) micromol × g(-1) × h(-1), GS [(142.35 ± 1.20) U/mg pro] was increased (P < 0.05); In contrast, the levels of GABA, Glu, Gln and the activity of GAD, GABA-T, and GS in Na-DMPS protection group were not significantly different in comparison with control group (P > 0.05).

CONCLUSIONthe central toxic effects of mice with acute bromoxynil intoxication may be related to the changes of GABA and Glu content in the cerebral cortex;Na-DMPS can protect mice from bromoxynil-induced central toxic effects and GABA and Glu abnormal change in the cerebral cortex.

Animals ; Cerebral Cortex ; drug effects ; metabolism ; Female ; Glutamic Acid ; metabolism ; Male ; Mice ; Mice, Inbred ICR ; Nitriles ; poisoning ; Toxicity Tests, Acute ; Unithiol ; pharmacology ; gamma-Aminobutyric Acid ; metabolism

OBJECTIVE: To establish an animal model in acute poisoned rat by deltamethrin and an analysis method for determination of deltamethrin by gas chromatography-electron capture detector (GC-ECD) and to study the distribution of deltamethrin in rats in order to provide the references for forensic medicine identification about such cases. METHODS: Rats were administered with deltamethrin of different doses(512 and 1,024 mg/kg) and killed 1.5 h later to be dissected rapidly for tissues (blood, hearts, livers, lungs, kidneys and brains etc.). Samples were dehydrated by anhydrous sodium sulfate and extracted with petroleum ether and acetone (V:V=4:1). The level of deltamethrin was determined by GC-ECD. RESULTS: There was a good separate between deltamethrin and endogenous impurities. The limit of quantification for deltamethrin in blood and liver were 0.1 microg/mL and 0.1 microg/g (S/N> or =10), respectively. The recovery rate of deltamethrin in blood was 91.55%-134.37% and both inter-day and intra-day precisions were less than 5.67%. The distribution of deltamethrin in poisoned rats with 512 mg/kg was as follow: lungs > livers > hearts > kidneys > blood > brains and with 1 024 mg/kg dose was lungs > blood > hearts > kidneys > brains > livers (P<0.05). CONCLUSION The GC-ECD method is sensitive for determination of deltamethrin. The distribution of deltamethrin in rats has a dose-dependent manner. The study suggests that samples of blood, hearts, livers, lungs, kidneys and brains are suitable for deltamethrin poisoned analysis.
Animals ; Chromatography, Gas/methods* ; Disease Models, Animal ; Forensic Toxicology/methods* ; Kidney/metabolism* ; Linear Models ; Liver/metabolism* ; Lung/metabolism* ; Male ; Nitriles/poisoning* ; Pyrethrins/poisoning* ; Rats ; Reproducibility of Results ; Sensitivity and Specificity ; Tissue Distribution