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Experiments were designed to study in-vivo effects of sodium cyanide on biochemical endpoints in the freshwater fish Labeo rohita. Fish were exposed to two sublethal concentrations (0.106 and 0.064mg/L) for a period of 15 days. Levels of glycogen, pyruvate, lactate and the enzymatic activities of lactate dehydrogenase (LDH), succinate dehydrogenase (SDH), glucose-6-phosphate dehydrogenase (G6PDH), phosphorylase, alkaline phosphatase (ALP), acid phosphatase (AcP) were assessed in different tissues (liver, muscle and gills). Result indicated a steady decrease in glycogen, pyruvate, SDH, ALP and AcP activity with a concomitant increase in the lactate, phosphorylase, LDH and G6PD activity in all selected tissues. The alterations in all the above biochemical parameters were significantly (p<0.05) time and dose dependent. In all the above parameters, liver pointing out the intensity of cyanide intoxication compare to muscle and gills. Study revealed change in the metabolic energy by means of altered metabolic profile of the fish. Further, these observations indicated that even sublethal concentrations of sodium cyanide might not be fully devoid of deleterious influence on metabolism in L. rohita.
Subject(s)
Animals , Sodium Cyanide/administration & dosage , Sodium Cyanide/metabolism , Sodium Cyanide/chemical synthesis , Fishes/growth & development , Fishes/metabolism , MetabolismABSTRACT
PURPOSE: To investigate the effect of Ginkgo biloba extract (GBE) on the proliferation of cultured human Tenon capsule fibroblasts (HTCF). METHODS: Free radical scavenging activity of GBE was assessed with a DPPH assay. Primarily cultured HTCF were exposed to 10 and 100 microgram/ml of GBE, and the effect of this extract on HTCF survival was assessed. Following 48 hr exposure to the media with or without serum, cellular survival and nitrite production were assessed by MTT and Griess assays. To evaluate whether GBE had a cytoproptective effect, HTCF were cultured in a combination of GBE and either sodium cyanide or hydrogen peroxide. RESULTS: GBE showed free radical scavenging activity. GBE increased the cellular survival of HTCF significantly in a dose-dependent manner and provided a cytoprotective effect when cells were exposed to sodium cyanide or were deprived of serum, but not when hydrogen peroxide was added to the medium. GBE decreased nitric oxide production but not to a statistically degree. CONCLUSIONS: GBE promotes proliferation of HTCF and has a cytoprotective effect in serum-deprived or hypoxic conditions. This suggests that GBE may be involved in the regulation of conjunctival wound healing by increasing the survival of HTCF.
Subject(s)
Humans , Fibroblasts , Ginkgo biloba , Hydrogen Peroxide , Nitric Oxide , Sodium Cyanide , Tenon Capsule , Wound HealingABSTRACT
AIM: To study the antidotal effect of N-acetylcysteine(NAC) on acute poisoning with sodium cyanide(NaCN).METHODS:After intraperitoneal(ip) injected of four sulphydryl compounds respectively,the mice which were acutely poisoned by NaCN were observed of the behavioral change,convulsion number and mortality rate(within 72 h).The median lethal dose(LD_(50)) of acutely poisoned mice was detected in NaCN group and NAC protection group.1 min after mice were poisoned by NaCN,the mice were divided into three groups:the first was ip normal saline(NS),the second was ip NAC in combination with sodium thiosulfate(Na_2S_2O_3),the third was ip sodium nitrite(NaNO_2) in combination with Na_2S_2O_3.Then the behavioral change,convulsion number and mortality rate(within 72 h)were observed,recorded,and compared the differences between the mice groups.RESULT: All of the four sulphydryl compounds had protecting effect on acutely NaCN poisoned mice,among them NAC had most prominent effect(P
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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
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Objective To approach the effects of combined plateau hypoxia due to high altitude and sodium cyanide(NaCN)intoxication on the heart function of rats.Methods 84 healthy male SD rats were randomly divided into 2 groups:only NaCN intoxication in plain areas(altitude 308m)(PL group)and combined high altitude(altitude 4 000m)hypoxia and NaCN intoxication(PH group).Rats in PH group were pre-treated with hypoxia for 72h in a plateau hypoxia cabin(simulating altitude 4 000m).12 rats of PH group were anesthetized.NaCN in a dosage of 3.6mg/kg was subcutaneously injected into the back of rats.At the time points of-10min,0min,10min,20min,30min,40min,50min,60min and 90min after NaCN injection,the left ventricular systolic pressure(mLVSP),+dP/dtmax and heart rate(HR)were recorded by physiological functions signal processing system RM6240.The arterial blood were taken from the other 72 rats for myocardium zymogram detection(including AST,LDH,CK,CK-MB)at the time points of 0h,0.5h,1h,2h,4h and 6h after NaCN injection.Results Compared with the PL group,the mLVSP,+dP/dtmax,and HR changed obviously(P
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Objective The aim of present study was to explore the effects of plateau hypoxia on the cyanide ion metabolism and correlative toxicant mechanism.Methods 12 adult rabbits and 72 male SD rats were randomly divided into two groups separately:plain control group with NaCN intoxication and plateau NaCN intoxicant group.2mg/kg NaCN was subcutaneously injected into the back of rabbits,the femoral vein blood was then collected at different designated time points for the measurement of cyanide,hemoglobin and ferrihemoglobin concentrations.Meanwhile 3.6 mg/kg NaCN was subcutaneously injected into the back of rats,the cardiac blood and the hepatic tissue were then collected at the different designated time points for the determination of cyanide ion,cytochrome oxidase activities and for the detection of pathologic changes of hepatic tissue.Results Under the condition of plain and plateau environments,the pharmacokinetics of rabbits induced by NaCN injection was characterized by one-compartment model.The blood cyanide concentration of rats in both plain and plateau groups reached peak value at 30min,and the activity of cytochrome oxidase decreased.Furthermore,the pathologic diagnosis of rats hepatic tissue suggested that liver injury induced by NaCN intoxication at high altitude was more serious than in plain intoxicant.Conclusion Hypoxia could markedly disturb the metabolic process of NaCN in vivo,aggravate the inhibition of cytochrome oxidase activity and lead to serious pathologic injury.
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Objective To investigate the effects of sodium cyanide(NaCN) and /or acute hypobaric hypoxia on the contents of monoamine neurotransmitters in rats' brain.Methods 128 adult male SD rats were divided into normoxic group and acute hypoxia group with 64 animals for each group.An artificial hypobaric hypoxia chamber was used to simulate a 4 000m altitude situation.The acute hypoxic exposure models were established by exposing rats to the hypobaric chamber for 3 days.All the rats were then injected intra-peritoneally with NaCN in a dosage of 3.6mg/kg at sea level and at simulated high altitude at 0,0.5,2 and 6h time points.The rats were sacrificed and the brains were isolated.The brain tissues of hippocampus and striatum corpora were then dissected on ice.Proteins of the brain tissue were extracted by centrifugation.Contents of dopamine(DA),epinephrine(NE) and 5-hydroxytryptamine(5-HT) in the brain tissues were analyzed by HPLC.Results NaCN intoxication did not affect the contents of DA,NE and 5-HT at 0.5h,2h and 6h in the selected brain tissues of the normoxic group.Compared with non-intoxication group,however,NaCN intoxication for 2h or 6h significantly decreased the levels of NE and 5-HT in the hippocampus tissues and the contents of DA,NE and 5-HT in striatum corpora in acute hypobaric hypoxia group.The contents of DA,NE and 5-HT in striatum corpora and the contents of NE and 5-HT in acute hypoxia group were significantly decreased compared with that in normoxic group(P
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Objective To explore the effects of oxidative stress and pulmonary vascular permeability on lung injury in rats treated with sodium cyanide(NaCN) and /or hypobaric hypoxia.Methods A total of 72 male SD rats were randomly divided into 2 groups: the NaCN intoxicated group in 308m altitude and the hypobaric hypoxia combined NaCN intoxicated group in 4 000m high altitude.The animals for the experiment of hypoxia were processed in an artificial hypobaric chamber to simulate the designated high altitude hypoxia(4 000m,61kPa).NaCN was injected subcutaneously to the rats in the both groups at the dosage of 3.6mg/kg.Broncho-alveolar lavage fluid(BALF) and lung tissues were prepared at the time points of 0,0.5,1.0,2.0,4.0 and 6.0h.The activity of SOD,GSH-PX,ACE,LDH,AKP and the content of MDA,GSH,Evan's blue(EB) were detected by spectrophotometric method.Results Combined acute hypobaric hypoxia and NaCN intoxication produced a significant increasing effect on EB content in the rats.The activity of ACE,LDH and AKP in BALF,and the contents of MDA in BALF and lung tissue reached the highest value at 0.5h preparation at the combined hypobaric hypoxia and NaCN intoxicated group,but they were still higher than that of control group(NaCN intoxicated only);correspondingly the activity of SOD,GSH-PX,content of GSH in lung tissue and BALF reached the lowest value at 0.5h preparation at the combined hypobaric hypoxia and NaCN intoxicated group,but they were still lower than that of control NaCN intoxicated group.Conclusion The results suggest that under the condition of hypoxia,NaCN intoxication may produce severe harmful effects on the lungs,increase the pulmonary vascular permeability,and cause severe interference on to the oxidative stress level.