OBJECTIVE: This study examined the effects on mortality and cell death after biomass charcoal combustion, in which carbon monoxide (CO) emissions were reduced using a biomass combustion improver in mice. METHODS: The biomass (glycerin) charcoal (Biomass CharCoal by Pusan National University, BCCP) was generated in the Power Generation System laboratory, Pusan National University. The effects and molecular mechanisms of biomass charcoal in carbon monoxide poisoning were examined by analyzing the mouse mortality, circulating leukocytes, carboxyhemoglobin (COHb), and expression of the inflammation-related genes, and cleaved capase-3 using enzyme-linked-immunosorbent-assays, real-time polymerase chain reaction, or Western blotting. RESULTS: The mortality rates were lower in the BCCP-exposed mice than in the raw charcoal-exposed mice. The circulating leukocytes were lower in the BCCP-exposed mice than in the raw charcoal-exposed mice. On the other hand, there was no significantly difference in the levels of COHb between both mice. Interestingly, the expression of the apoptosis-related gene, cleaved-capase 3, and the inflammation and tissue necrosis-related gene and receptor for the advanced glycation end products were reduced markedly in the BCCP-exposed mice compared to the raw charcoal-exposed mice. Decreased inflammation and tissue necrotic factors could be molecular mechanisms for the decreased mortality rates after BCCP burning. CONCLUSION: Biomass charcoal (BCCP) reduced the mortality rates and inflammation and tissue necrotic factors by 30%–40%. These results suggest that the biomass charcoal (BCCP) could reduce the incidence of suicide and CO-associated delayed symptoms after charcoal burning. Furthermore, it could extend the time for rescue in suicide attempts using charcoal burning.
Animals ; Biomass* ; Blotting, Western ; Burns* ; Busan ; Carbon Monoxide Poisoning ; Carbon Monoxide* ; Carbon* ; Carboxyhemoglobin ; Cell Death ; Charcoal* ; Glycosylation End Products, Advanced ; Hand ; Incidence ; Inflammation ; Leukocytes ; Mice* ; Mortality* ; Real-Time Polymerase Chain Reaction ; Suicide

PURPOSE: To evaluate the neuroprotective effects of betaxolol (betaxolol hydrochloride) under hypoxic conditions using retinal ganglion cells (RGC-5) and determine whether heme oxygenase-1 (HO-1) expression exerts cytoprotective effects. METHODS: In this study, cultured RGC-5 cells were incubated with different concentrations of betaxolol hydrochloride (0.1 microM, 1 microM or 5 microM) and with 10 microM zinc protoporphyrin (ZnPP), in a hypoxia incubator (1% O2, 5% CO2, 94% N2) for 48 hours and the cell viability of each group was determined. Additionally, cell viability was measured after RGC-5 cells were incubated with 5 microM of brinzolamide (Azopt(R)), brimonidine tartrate (Alphagan(R)) or travoprost (Travatan(R)). RGC-5 cells were divided into three groups and incubated under three different conditions, normoxia group (20% O2, 5% CO2), hypoxia group (1% O2, 5% CO2) and the group with 5 microM of Betoptic S(R) treated under hypoxic conditions (hypoxia, Betoptic S(R)). After incubation for 4, 8, 12 and 24 hours, HO-1 expression was analyzed using Western blotting. RESULTS: Cell viability significantly increased in RGC-5 cells treated with Betoptic S(R) compared with other antiglaucoma agents. Increased levels of HO-1 expression indicate its relevance in cell viability. Furthermore, increased RGC-5 cell viability by Betoptic S(R) was significantly reduced in the HO-1 inhibitor ZnPP-treated group. CONCLUSIONS: We reaffirmed the known cytoprotective effects of Betoptic S(R) and the results suggests that HO-1 expression exerts cytoprotective effects against hypoxia.
Anoxia ; Betaxolol* ; Blotting, Western ; Cell Survival ; Heme Oxygenase-1* ; Heme* ; Incubators ; Neuroprotective Agents* ; Retinal Ganglion Cells ; Zinc ; Brimonidine Tartrate ; Travoprost

PURPOSE: In order to determine whether the Tonicity responsive enhancer binding protein (TonEBP) is expressed by hypertonic and hyperosmolar stress, TonEBP expression was investigated in the retinal ganglion cell (RGC) line, RGC-5 cells. METHODS: After RGC-5 cells were cultured by Staurosporine, TonEBP expression was measured with Western immunoblotting analysis and real-time reverse transcription-polymerase chain reaction in 50 mM NaCl, 100 mM mannitol, 50 mM glucose, or 100 mM glucose at 3, 6, 12, and 24 hours after exposure to each environment. RESULTS: In this study, the protein expression of TonEBP was determined to be statistically significantly checked in 50 mM NaCl after 3, and 6 hours, in 100 mM mannitol after 6 hours, and in 100 mM glucose after 3, and 6 hours. TonEBP messenger Ribonucleic acid (mRNA) expression was determined to be statistically significantly checked in 50 mM NaCl after 3 hours, in 100 mM mannitol after 3, and 24 hours, and in 50 mM glucose after 3, and 24 hours. CONCLUSIONS: These results suggested that TonEBP was expressed by hypertonic and hyperosmolar stress at the protein and mRNA levels. Further studies are nedded to determine the role of TonEBP and the mechanism of expression and regulation of TonEBP.
Blotting, Western ; Glucose ; Mannitol ; NFATC Transcription Factors ; Osmotic Pressure ; Retinal Ganglion Cells ; RNA ; RNA, Messenger ; Staurosporine

PURPOSE: To investigate the production of long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmic reticulum (ER) stress and its role in ER stress-associated cell death, PTX3 expression was evaluated in the human retinal pigment epithelial cell line, ARPE-19. METHODS: PTX3 production in ARPE-19 cells was analyzed in the absence or presence of tunicamycin treatment by enzyme-linked immunosorbent assay. PTX3 protein and mRNA levels were estimated using western blot analysis and real-time reverse transcription-polymerase chain reaction, respectively. Protein and mRNA levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and ARPE-19 cell viability were measured in the presence of tunicamycin-induced ER stress in control or PTX3 small hairpin RNA (shRNA)-transfected ARPE-19 cells. RESULTS: The protein and mRNA levels of PTX3 were found to be significantly increased by tunicamycin treatment. PTX3 production was significantly decreased in inositol-requiring enzyme 1α shRNA-transfected ARPE-19 cells compared to control shRNA-transfected cells. Furthermore, pretreatment with the NF-κB inhibitor abolished tunicamycin-induced PTX3 production. Decreased cell viability and prolonged protein and mRNA expression of CHOP were observed under tunicamycin-induced ER stress in PTX3 shRNA transfected ARPE-19 cells. CONCLUSIONS: These results suggest that PTX3 production increased in the presence of tunicamycin-induced ER stress. Therefore, PTX3 could be an important protector of ER stress-induced cell death in human retinal pigment epithelial cells. Inositol-requiring enzyme 1α and the NF-κB signaling pathway may serve as potential targets for regulation of PTX3 expression in the retina. Therefore, their role in PTX3 expression needs to be further investigated.
Anti-Bacterial Agents/pharmacology ; Apoptosis ; Blotting, Western ; C-Reactive Protein/biosynthesis/*genetics ; Cells, Cultured ; Endoplasmic Reticulum Stress/*drug effects/genetics ; Enzyme-Linked Immunosorbent Assay ; *Gene Expression Regulation ; Humans ; Polymerase Chain Reaction ; RNA, Messenger/*genetics ; Retinal Pigment Epithelium/*metabolism/pathology ; Serum Amyloid P-Component/biosynthesis/*genetics ; Tunicamycin/*pharmacology