Cyanide poisoning is expected to be antagonized by the administration of oxygen, when it is administered in combination with the conventional cyanide antidote, sodium,thiosulfate. However, the antidotal efficacy and its exact mechanism of oxygen in cyanide poisoning is still a controversial one. To test the effect of oxygen on the antidotal action of thiosulfate ,in cyanide poisoning, author designed this study on the dose-mortality patterns for potassium cyanide in mice. Potency ratios derived from LDso values were compared in groups of mice treated with sodium thiosulfate alone and sodium thiosulfate with oxygen. These results indicated that oxygen enhances the anti-dotal effect of sodium thiosulfate, effectively. This fact demonstrates that oxygen is of importance in the treatment of cyanide poisoning.
Animals ; Mice ; Oxygen* ; Poisoning* ; Potassium Cyanide ; Sodium

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.
Aged ; Eating ; Female ; Humans ; Korea ; Male ; Potassium Cyanide ; Powders ; Public Health ; Retrospective Studies ; Social Control, Formal ; Sodium Cyanide ; Suicide

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.
Fibroblasts* ; Ginkgo biloba* ; Humans* ; Hydrogen Peroxide ; Nitric Oxide ; Sodium Cyanide ; Tenon Capsule* ; Wound Healing

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.
Anoxia ; Ginkgo biloba* ; Humans* ; Hydrogen Peroxide ; Nitric Oxide ; Oxidative Stress ; Sodium Cyanide ; Trabecular Meshwork*

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.
Anoxia* ; Apoptosis ; Cell Survival ; Flow Cytometry ; NG-Nitroarginine Methyl Ester ; Nitric Oxide* ; Sodium Cyanide ; Trabecular Meshwork*

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.
Cyclooxygenase Inhibitors ; Dinoprost* ; Muscle Cells* ; Nitric Oxide Synthase ; Nitric Oxide* ; Sodium Cyanide

AIMTo study the effects of caspases on cerebromicrovascular endothelial cell apoptosis induced by hypoxia in vitro.

METHODSThe 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.

RESULTSNaCN 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.

CONCLUSIONThe 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.

Amino Acid Chloromethyl Ketones ; pharmacology ; Animals ; Apoptosis ; Brain ; blood supply ; Caspase 3 ; Caspase 6 ; Caspase Inhibitors ; Caspases ; metabolism ; Cattle ; Cell Hypoxia ; Cells, Cultured ; Endothelial Cells ; cytology ; metabolism ; Microcirculation ; cytology ; Oligopeptides ; pharmacology ; Sodium Cyanide ; pharmacology

AIMTo investigate the protective effect of hydroxysafflor yellow A (HSYA), a soluble element extracted from Carthamus tinctorius L., on focal cerebral ischemia in rats.

METHODSFocal 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).

RESULTSHSYA 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.

CONCLUSIONHSYA has potential neuroprotective action against focal cerebral ischemia in rats and cultured rat fetal cortical neurons as well.

Animals ; Behavior, Animal ; drug effects ; Brain ; pathology ; Brain Ischemia ; etiology ; pathology ; physiopathology ; Carthamus tinctorius ; chemistry ; Cells, Cultured ; Cerebral Cortex ; cytology ; Chalcone ; analogs & derivatives ; isolation & purification ; pharmacology ; Glutamic Acid ; Infarction, Middle Cerebral Artery ; complications ; L-Lactate Dehydrogenase ; metabolism ; Male ; Neurons ; cytology ; metabolism ; Neuroprotective Agents ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Quinones ; isolation & purification ; pharmacology ; Rats ; Rats, Inbred WKY ; Sodium Cyanide ; antagonists & inhibitors