Objective To investigate the effects of sodium cyanide (NaCN) and hemorrhagic shock on the level of serum oxidative stress in rabbits. Methods A total of 15 Japanese white rabbits were randomly divided into 5 groups: sham operation, hemorrhagic shock (HS), NaCN intoxation, HS+NaCN and HS+NaCN+4-dimethy laminophenol (4-DMAP). The rabbits were anesthetized for left arteria carotis communis cannulation, and connected with three-way tube and RM6240 electronic physiological signal recording system. The models of hemorrhagic shock and/or sodium cyanide intoxation (blood pressure was controlled at 5.3 kPa) were established. At 0.5, 1 and 2 h after the intraperitoneal injection of 2.5 mg/kg NaCN and/or 3.2 mg/kg 4-DMAP, the blood were drawn. The serum superoxide dismutases (SODs), content of malonaldehyde (MDA) and active oxygen (ROS) were detected by spectrophotometric method. Results After HS, NaCN intoxation, HS+NaCN, the SODs decreased significantly (P

Effects of soman on lymphocyte proliferation are investigated in mice. 1 d after soman(154 ?g/kg,sc) poisoning B-lymphocyte reaction to lipopolysaccharide(LPS) is inhibited significantly and is persistent.T-cell proliferation response stimulated by concanavalin(Con A)has a 2-phase changeson the 1st day an increase followed by a dramatical reduction. Both the decreases of T-and B-lymphocyte mitogenic response and the primary increase of T-cell response show a close correlation with the doses of soman in this experiment. It has no relation to the change of the whole blood cholinesterase activity.

Objective To study the toxic effects of Rotenone on glutamate transporter and glutamine synthetase in rat brain.Methods The glutamate levels in the striatum of SD rats were detected by high performance liquid chromatography(HPLC),the expression of glutamate tansporter mRNA and proteins were detected by RT-PCR and Western blotting and the activity of glutamine synthetase was determined by using GS detect kit.Results Rotenone was shown to increase the release of glutamate in rat striatum,the expression of glutamate/aspartate transporter(GLAST)mRNA and protein decreased significantly in 0.6 mg/kg and 1.2 mg/kg Rotenone intoxicated groups,but the expression of GLT-1 and the activity of GS enhanced obviously.Conclusion Down-regulation of GLAST may be responsible for increased Glu level in rat brain induced by Rotenone,but the increased expression of GLT-1 and GS activity may represent a protective mechanism of the brain cells by limiting the neurotoxicity of Glu.

Objective To investigate the apoptotic effect induced by sulfur mustard on the lymphocytes of the rat spleen,and define the role of caspase-3 during the process.Methods Sulfur mustard was given by intraperitoneal injection in a dose of 3.5mg/kg.The animals were anesthetized and the spleens were harvested at different timepoints after intoxication.The histopathogy of spleen was studied with hematoxylin-eosin staining.Caspase-3 mRNA was detected with RT-PCR.Protein expression of caspase-3 was assayed with Western blotting,lymphocytes of rat spleen were isolated and cultured in vitro and they were challenged with sulfur mustard(100?mol/L).The effect of Ac-DEVD-CHO(a specific inhibitor of caspase-3)on sulfur mustard-induced apoptosis of the lymphocytes cultured in vitro was evaluated.Fluorescent probe labeled with Rhodamine 123 was used to study mitochondrial potential.Results The histology of rat spleen was affected after sulfur mustard intoxication,as evidenced by apoptosis of a part of lymphocytes.Protein and mRNA expressions of caspase-3 were increased significantly in the spleens of intoxicated rats as compared with that in control group.DNA ladder and 'sub-G1' peak of lymphocytes which were treated with sulfur mustard in vitro were partially improved by Ac-DEVD-CHO(the specific inhibitor of caspase-3).In addition,mitochondrial potential decreased in a time-dependent manner in the lymphocytes intoxicated by sulfur mustard in vitro compared with that in the control group.Conclusions The spleen is injured in the rat which is intoxicated by sulfur mustard.Lymphocyte apoptosis is one of the mechanisms splenic injury.Caspase-3 may be involved in the process of lymphocyte apoptosis induced by sulfur mustard.

Objective To investigate the effects of hypoxia and sodium cyanide(NaCN)on oxidative stress in rabbit arterial blood.Methods An artificial hypobaric hypoxia chamber was used to simulate 4 000-meter high altitude.Twenty rabbits were randomly divided into 4 groups:hypoxia group with high-or low-dose,non-hypoxia with high-or low-dose.The animals in the non-hypoxia groups were operated under normal circumstances while those in hypoxia groups were subjected to chamber in low pressure for 72 h before receiving the hypoxia experiments.Femoral arterial cannulation was performed on all animals under anesthetization with pentobarbital sodium(30 mg/kg,iv)and NaCN(ip)at the doses of 1.5 mg/kg and 2 mg/kg.Blood samples were collected at 10 min before intoxication,and 5,10,15,20,30,60,120 and 180 min after intoxication and blood seperation was conducted.The activity of superoxide dismutase(SOD),contents of reduced glutathione(GSH)and malondialdehyde(MDA)were determined.Results The MDA content was significantly increased(P

Objective To investigate the relationship of the beneficial effect of CsA on vascular reactivity to Rho-kinase,protein kinase C ( PKC) and mitochondrial permeability transition pore ( MPTP) in traumatic hemorrhagic shock rats. Methods With traumatic hemor-rhagic shock rats and hypoxia-treated vascular smooth muscle cells ( VSMCs) ,the role of Rho-kinase and PKC in CsA-regulating vascular re-activity following shock and their relationship to MPTP was observed. Meanwhile,the effects of CsA on inflammatory mediators including TNF-α, IL-1β and IL-6 were also studied. Results CsA significantly improved the vascular reactivity of superior mesenteric artery following hemor-rhagic shock. Rho-kinase inhibitor Y27632 significantly antagonized CsA-induced increase of vascular reactivity,while PKC inhibitor stauros-porine had no significant influences on the effects of CsA. Further studies showed that CsA and Rho-kinase agonist U46619 inhibited the o-pening of MPTP in hypoxia-treated VSMCs. In addition,shock induced a significant increase of TNF-αand IL-1β,but CsA did not show a sig-nificant inhibitory effect on their level. Conclusion CsA-induced restoration of vascular reactivity following traumatic hemorrhagic shock via inhibiting MPTP opening,and Rho-kinase participate in this process.

Objective To study the toxic effects of rotenone on substantia nigra of rats. Methods Rotenone was given subcutaneously once a day during 28 days. Substantia nigra was dissected. Morphology of dopamine neuron, synapse and myelin sheath were observed. SOD and GSH-Px activity were assayed; MDA and GSH contents were measured. Results Autonomic activities of rats decreased, similar to Parkinson's Symptoms. Morphology of dopamine neuron changed, synapse structures were abnormal, synapse vesicals increased and myelin sheath degenerated. MDA content increased (P

Objective To observe the rotenone induced changes of nitric oxide (NO) concentration and nitric oxide synthase (NOS) activity in rat caudate nuclei and blood plasma. Methods Wistar rats were daily administrated with rotenone at the doses of 0.335, 0.670 and 1.005 mg/kg(sc). Animals were sacrificed on days 30, 60 and 90. The NO concentration and the NOS activity in the caudate nuclei and blood plasma were determined by biochemical methods. Results At each time point of days 30, 60 and 90, rotenone induced significant increases in NO concentration and NOS activity in both the caudate nuclei and blood plasma in dose and time dependent manners. Conclusion Long term exposure to rotenone leads to the increase of nitric oxide and nitric oxide synthase in brain tissues and blood plasma in rat.

Objective To observe the effects of rotenone on the mitochondrial membrane potential and cell cycles in pheochromocytoma (PC12) cells and to explore the injury mechanism of rotenone on dopaminergic neuron. Methods The mitochondrial membrane potential and cell cycles were determined by flow cytometry. Results After treatment with 5.0 ?mol/L rotenone for 12 and 24 h, the percentage of G 0/G 1 phase and S phase in cultured PC12 cells decreased gradually (P

Objective To investigate the changes of autonomic nerve function of coronary heart disease (CHD) patients with panic disorder(PD). Methods All the subjects who met with the diagnostic code of CHD and PD were divided into CHD group(n=40) ,PD group(n=36) ,comorbid CHD and PD group(n=27) ,and 40physical examinee were recruited as normal control group. They had a 24 hours Holter ECG monitoring by time and frequency domain analysis of heart rate variability. ANOVA analysis was utilized to statistic the collected data. Results Compared with normal controls,the patients of others groups had every indexs of HRV were reduced. The indexs of HRV of comorbid CHD and PD were lower than the patients of CHD or PD group. The score of time domain SDNN(70.40 ± 14.74)ms,SDANN(91.72 ± 24.46)ms,PNN50(2.83 ±2.07)%, RMSSD( 15.66 ±7.45)ms,frequency domain LF(647.54 ± 129.24)ms2, HF(596. 16± 127.66) ms2 in comorbid CHD and PD. There were significant differences with others groups(P ＜ 0.05 ). Conclusion The autonomic nervous functional of the patients with CHD and PD were in disorder. The autonomic nervous functional disorder of the patients with comorbid CHD and PD was more severe.