Effect of exposure to sublethal concentrations of sodium cyanide on the carbohydrate metabolism of the Indian Major Carp Labeo rohita (Hamilton, 1822)

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.

Cyanide Poisoning Deaths Detected at the National Forensic Service Headquarters in Seoul of Korea: A Six Year Survey (2005~2010)

The records of 255 cyanide poisoning deaths obtained from National Forensic Service (NFS) headquarters, located in Seoul of Korea, from 2005 to 2010 were retrospectively reviewed. The mean age was 41.88 +/- 13.09 and range was 6~80 years (unknown in seven cases). The number of deaths of males and females were 200 and 53, respectively (unknown in two cases). The largest number of cases occurred in people aged 40-49 years (81 cases, 31.8%), followed by the age groups 30~39 years (51 cases, 20%), 50~59 years (44 cases, 17.2%) and 20~29 years (43 cases, 16.9%). The total number of deaths among other age groups (below 10, 10~19, 60~69, 70~79, over 80 years and unknown) were 36, representing only 14.1%. Of all cyanide poisoning deaths, 97.3% were due to suicide, and 14.5% of the total number who died received medical treatment. The most frequent site for ingestion was the person's own residence (120 cases, 47.1%) and the route of administration was mainly oral (252, 98.8%). From the total of 255 cyanide poisoning cases, white powders were submitted for analysis in 92 cases. Potassium cyanide and sodium cyanide occupied 51 and 41 cases, respectively. This study showed that poisoning deaths due to cyanide are one of the continuously reported public health problems in Korea. Enforcement of regulations and safety education to prevent cyanide poisoning should be carried out by the government.

Papel del óxido nítrico en la retención de glucosa cerebral post-estimulación de los receptores carotídeos con cianuro de sodio en ratas / The role of the nitric oxide to retain the cerebral glucose post-stimulation of the carotid receptors with sodium cyanide in rats

Se realizó un estudio experimental, con el objetivo de medir la acción del óxido nítrico (NO) en la captación de glucosa cerebral, después de la estimulación con cianuro de sodio (NaCN-5µg/100g) de los receptores del cuerpo carotídeo (RCC). Los experimentos se realizaron en ratas (280-310g) anestesiadas, mantenidas con respiración artificial a una temperatura de 25°C. Los protocolos fueron el control I, la perfusión en cisterna magna (CM) de líquido cefalorraquídeo artificial-LCRa (5 µL/30 s), el control II, la ERC en forma simultánea con la perfusión de LCRa, la perfusión de un donador de NO (nitroglicerina) (NG-3µg/5µL de LCRa) en CM, la ERC en forma simultánea con NG en CM, la perfusión de un inhibidor de NO (L-NAME) (250µg/5µL de LCRa), la ERC en forma simultánea con L-NAME en CM. Los resultados obtenidos indican que la combinación de NG con ERC no altera la retención de glucosa cerebral, mientras que en los controles, la NG sola aumentó la retención cerebral de glucosa. Por el contrario, el L-NAME en combinación con ERC aumentó la captación de glucosa cerebral e indicó que el óxido nítrico desempeña un papel modulador en la respuesta hiperglucemiante en los estados de hipoxia

Effect of Ginkgo Biloba Extract on the Survival of Cultured Human Trabecular Meshwork Cells

PURPOSE: To investigate the effect of Ginkgo biloba extract (GBE, EGb-761) on the survival of cultured human trabecular meshwork cells (HTMC). METHODS: Free radical scavenging activity of GBE was assessed with a DPPH assay. Primarily cultured HTMC were exposed to 10 and 100 microgram/ml of GBE. 0.3 mM sodium cyanide and 100 micrometer hydrogen peroxide were added to the culture medium with GBE for 48 hr. Cellular survival and nitrite production were assessed by MTT assay and Griess assay, respectively. RESULTS: GBE showed free radical scavenging activity. GBE increased the cellular survival of HTMC significantly in a dose-dependent manner under hypoxia or serum-deprived condition, but not to hydrogen peroxide. GBE increased nitric oxide production but not to statistically significant levels. CONCLUSIONS: GBE promotes proliferation and has cytoprotective effects in the context of HTMC exposed to serum-deprived or hypoxic conditions. However oxidative stress induced by hydrogen peroxide did not have an effect on proliferation of HTMC. In addition these effects were not related to the production of nitric oxide.

Effect of Ginkgo Biloba Extract on the Proliferation of Cultured Human Tenon Capsule Fibroblasts

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.

Effect of Prostaglandin F2alpha on the Production of Nitric Oxide in Cultured Ciliary Muscle Cells

PURPOSE: To investigate whether prostaglandin F2alpha (PGF2alpha) affects on the production of nitric oxide (NO) in cultured ciliary muscle (CM) cells. METHODS: Following primary culture of CM cells from porcine eyes, the cells were exposed to PGF2alpha (PhXA85, latanoprost free acid) with and without pretreatments of NO synthase inhibitor (L-NAME, N omega- Nitro-L-arginine methyl ester) and cyclooxygenase inhibitors (indomethacin and dexamethasone) for 3 days. The cellular survivals were also evaluated in serum-deprived and hypoxic conditions induced by sodium cyanide. The cellular survival and nitrite production were assessed by MTT and Griess assay, respectively. RESULTS: PGF2alpha enhanced the production of NO significantly in cultured CM cells in a dose-dependent manner, while various inhibitors abolished this effect. PGF2alpha was not cytoprotective in serum-deprived and hypoxic conditions. CONCLUSIONS: The current results suggest that PGF2alpha potentiates NO production but is not cytoprotective in CM cells. This PGF2alpha-induced NO production in CM cells may be involved in the regulation of uveoscleral outflow.

Protective effect of hydroxysafflor yellow A on experimental cerebral ischemia in rats / 药学学报

<p><b>AIM</b>To investigate the protective effect of hydroxysafflor yellow A (HSYA), a soluble element extracted from Carthamus tinctorius L., on focal cerebral ischemia in rats.</p><p><b>METHODS</b>Focal cerebral ischemia in male Wistar-Kyoto (WKY) rats were induced by permanent middle cerebral artery occlusion (MCAO). Three doses of 1.5, 3.0 and 6.0 mg x kg(-1) of HSYA were administrated to three groups of rats, separately, via sublingular vein injection 30 min after the onset of ischemia. 24 h after ischemia in rats, neurological deficit scores were evaluated and the infarction area of brain was assessed by quantitative image analysis. The in vitro neuroprotective effect of HSYA was tested in cultured fetal cortical neurons exposed to glutamate and sodium cyanide (NaCN).</p><p><b>RESULTS</b>HSYA at doses of 3.0 and 6.0 mg x kg(-1) exerted significant neuroprotective effects on rats with focal cerebral ischemic injury as expressed by neurological deficit scores and reduced the infarct area as compared with saline group, and the potency of HSYA at dose of 6.0 mg x kg(-1) was similar to that of 0.2 mg x kg(-1) of nimodipine. In vitro studies, HSYA significantly inhibited neurons damage induced by exposure to glutamate and NaCN in cultured fetal cortical cells.</p><p><b>CONCLUSION</b>HSYA has potential neuroprotective action against focal cerebral ischemia in rats and cultured rat fetal cortical neurons as well.</p>

Effect of Hypoxia on the Survival and Production of Nitric Oxide in Trabecular Meshwork Cells

PURPOSE: To investigate the effect of hypoxia on the survival and nitric oxide (NO) production of cultured trabecular meshwork (TM) cells. METHODS: After inducing chemical hypoxia with sodium cyanide, the survival and nitrite production of the primarily cultured porcine TM cells were assessed with MTT and Griess assays. The effect of NOS inhibitor, N(omega)-Nitro-L-arginine methyl ester (L-NAME), was also assessed. Flow cytometry using annexin/PI was done to evaluate apoptosis. RESULTS: Chemical hypoxia decreased TM cell survival significantly (p<0.05) with increased NO production. This hypoxia-induced antiproliferative effect was abolished by L-NAME (p<0.05). Flow cytometric analysis revealed that hypoxia induced apoptosis of TM cells, which was inhibited by L-NAME. CONCLUSIONS: Hypoxia decreases the survival of TM cells and induced apoptosis, accompanied by increased NO production. The hypoxia-induced decreased survival of TM cells may be mediated by NO.

Effects of caspases on cerebromicrovascular endothelial cell apoptosis induced by hypoxia / 药学学报

<p><b>AIM</b>To study the effects of caspases on cerebromicrovascular endothelial cell apoptosis induced by hypoxia in vitro.</p><p><b>METHODS</b>The cultured bovine cerebromicrovascular endothelial cells were exposed to NaCN in glucose-free medium. Cell viability was determined by trypan blue staining. Cell apoptosis was defined by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) and flow cytometry. The expression of caspase-3 was detected by immunocytochemical method. Four caspase inhibitors were used to validate the effect of caspases on cell apoptosis.</p><p><b>RESULTS</b>NaCN in glucose-free medium initiated cerebromicrovascular endothelial cell injury markedly and typical apoptotic cells were found in this model. The expression of caspase-3 increased significantly. Four caspase inhibitors decreased the number of injured cells. Selective inhibitor of caspase-1 and -6 reduced expression of caspase-3 significantly.</p><p><b>CONCLUSION</b>The results suggest that caspases family plays an important role in cerebromicrovascular endothelial cell apoptosis induced by NaCN and caspase-3 acts on the downstream of caspase-1 and -6 in protease cascade action to induce apoptosis.</p>

Acetate enhances the chemosensory response to hypoxia in the cat carotid body in vitro in the absence of CO2-HCO3-

To determine if intracellular acidosis enhances hypoxic chemoreception in the absence of CO2-HCO3- at pH 7.4, the effects of sodium acetate (30 mM) were studied on the chemosensory responses of the cat carotid body to hypoxic, stagnant and cytotoxic hypoxia. Carotid bodies were perfused and superfused in vitro with Tyrode's solution, free of CO2-HCO3-, buffered with HEPES-NaOH, pH 7.40, at 36.5 +/d- 0.5 degrees C and equilibrated at PO2 of 125 Torr (perfusate) and < 20 Torr (superfusate). In the absence of acetate, hypoxia (PO2 25 Torr), flow interruption and NaCN (0.01-100 micrograms) augmented the chemosensory discharges. However, in the presence of acetate, the half-excitation time of these responses decreased and their amplitude increased. Thus, acetate enhances the chemosensory response to hypoxic, stagnant and cytotoxic hypoxia. It is suggested that that intracellular acidosis induced by acetate contributes to this potentiation by correcting the alkaline pHi caused by the absence of HCO3-(-)HCO2 in the perfusate

Blood acidification in the swimbladder: mechanisms and metabolic pathways

The metabolism of gas gland cells of the swimbladder epithelium is specialized for the production of acidic metabolites that are released into the blood stream and provoke an increase in gas partial pressure by reducing the effective gas-carrying capacity of the blood. In a subsequent step this initial increase in gas partial pressure is multiplied by back-diffusion of gas molecules from the venous to the arterial side in the countercurrent system, the rete mirabile. Thus, gas partial pressures of up to several hundred atmospheres can be generated in the swimbladder. Measurements of metabolic end products and analysis of the formation of 14C02 from [1-14(superscription) C] glucose and [6-14(superscription) C] glucose revealed that the acidic metabolises are lactic acid, produced in the glycolytic pathway, and also C02, formed in the pentose phosphate shunt. C02 easily enters the blood stream by diffusion. The release of protons from isolated gas gland cells, however, is highly dependent on the extracellular sodium concentration. This sodium dependence can in part be blocked by addition of amiloride, indicating that a Na+/ H+ exchanger is involved in the release of protons. A significant decrease in the rate of proton secretion in the presence of the carbonic anhydrase inhibitor ethoxzolamide indicates that the second major route for the release of protons includes carbonic anhydrase activity and the diffusion of C02.

Consumo de glucosa bajo acción de una cocarboxilasa no degradable, utilizando cianuro como estimulante / Consuption of glucose under the action of a non degradable cocaiboxilase using cyamide as stimulant

Se determinó la variación del consumo de glucosa, por acción de una cocarboxilasa no degradable en animal sano y en animal intoxicado con cianuro como estimulante, midiendo las alteraciones electrofisiológicas de los quimiorreceptores aórticos y carotídeos. La conclusión fue que la cocarboxilasa no degradable inteviene en el metabolismo de la glucosa favorecendo funcional y notoriamente al músculo cardiaco sometido a la anoxia del cianuro, el cual reproduce masivametne los efectos de la isquemia