• Korean Journal of Fisheries and Aquatic Sciences
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• v.28 no.1
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• pp.87-97
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• 1995

Acute and chronic toxicity of phenol on the mortality, long-term survival and respiration rates of the mysid, Archaeomysis kokuboi adult and juvenile were examined. This experiment was condurted by static bioassay procedure with the different salinity at $25^{\circ}C$ In lethal test, the test animals were exposed to 6 different phenol concentrations to determine $LC_{50}$ and I$LT_{50}$ (median lethal concentration and time) values. The $LC_{50}$ values with the exposure time for the mysid adult ranged from 31.31ppm to 1.49ppm phenol and for the mysid juvenile ranged from 6.90ppm to 0.26ppm in all experimental groups. Mortality was increased with the decrease of salinity, The $96hr-LC_{50}$ values at 16, 24 and $32\%o$ salinity for the mysid adult were 1.49, 2.71 and 4.53ppm phenol, white the values for the mysid juvenile were 0.26, 0.56 and 0.71ppm, respectively. The ratios of $96hr-LC_{50}$ values for the mysid adult to those for the mysid juvenile at 16, 24 and $32\%p$ salinity were 5.73, 4.84 and 6.38, respectively. The mysid juveniles were more sensitive to phenol than the mysid adults. Compared $LT_{50}$ values for the mysid adult with those for the mysid juvenile, the $LT_{50}$ values for the mysid adult ranged from 384.7 to 29.0 hours at 1.7-127ppm phenol concentrations and for the mysid juvenile ranged from 132.2 to 18.7 hours at 0.5~6.Oppm phenol concentrations. The lowest $LT_{50}$ values for the mysid adult and juvenile were showed at the combination of the highest experimental concentration of phenol and the lowest experimental salinity. The mysid juveniles showed lower $LT_{50}$ values than those of adults. The chronic effects of phenol on the mysid at the sublethal effective concentration of phenol were lower in the $32\%o$ salinitr group than 16 or $24\%o$ salinity groups. Oxygen consumption rates of the mysid adult were decreased with the increase of phenol concentration and exposure time, and decreased significantly in lower salinity at the same concentration or phenol.

• Korean journal of applied entomology
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• v.34 no.4
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• pp.360-367
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• 1995

The relative toxicity of abamectin was assessed to the predatory mite Amblyseius womersleyi Schicha and to dicofol-resistant and -susceptible twospotted spider mite (TSM) Tetranychus urticae Koch in the laboratory. Abamectin was much les toxic to the predator than to the spider mite. At 0.12 and 0.6 ppm, all TSM adult females of the tow strains were killed within 48 h after dipping n the solutions. The lower concentrations (0.06 and 0.012 ppm) killed more than 77% of TSM female adults of the two strains at 120 h after treatment. However, abmectin did not significantly affect the survival and mobility of A. womersleyi female adults at a concentration of 0.12 ppm but the mortality was slightly increased up to 20~23% at 0.6 and 6 ppm. Abamectin did not significantly affect hatchability of one-day old TSM eggs at 0.06~0.6 ppm. The Four-day old eggs were much more susceptible to abamectin than one-day old eggs were. Within 0.006-6 ppm, abamectin did not affect the hatchability of A. womersleyi eggs and the development of resulting immature predators. When the predator female adults were dipped in 0.6 and 0.12 ppm solution, their reproduction was not affected, but at 6 ppm it was decreased by 35%. However, the reproduction of TSM reduced significantly at concentrations between 0.006 and 0.6 ppm. The differential toxicity of abamectin between TSM and the predator could be of practical importance in managing spider mite populations in the field. Abamectin at selective sublethal concentrations (i.e., 0.012~0.06 ppm) could be of value in adjusting predator/prey ratios in integrated management of spider mites.

• Radiation Oncology Journal
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• v.31 no.2
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• pp.57-65
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• 2013

Beta-lapachone (${\beta}$-Lap; 3,4-dihydro-2, 2-dimethyl-2H-naphthol[1, 2-b]pyran-5,6-dione) is a novel anti-cancer drug under phase I/II clinical trials. ${\beta}$-Lap has been demonstrated to cause apoptotic and necrotic death in a variety of human cancer cells in vitro and in vivo. The mechanisms underlying the ${\beta}$-Lap toxicity against cancer cells has been controversial. The most recent view is that ${\beta}$-Lap, which is a quinone compound, undergoes two-electron reduction to hydroquinone form utilizing NAD(P)H or NADH as electron source. This two-electron reduction of ${\beta}$-Lap is mediated by NAD(P)H:quinone oxidoreductase (NQO1), which is known to mediate the reduction of many quinone compounds. The hydroquinone forms of ${\beta}$-Lap then spontaneously oxidizes back to the original oxidized ${\beta}$-Lap, creating futile cycling between the oxidized and reduced forms of ${\beta}$-Lap. It is proposed that the futile recycling between oxidized and reduced forms of ${\beta}$-Lap leads to two distinct cell death pathways. First one is that the two-electron reduced ${\beta}$-Lap is converted first to one-electron reduced ${\beta}$-Lap, i.e., semiquinone ${\beta}$-Lap $(SQ)^{{\cdot}-}$ causing production of reactive oxygen species (ROS), which then causes apoptotic cell death. The second mechanism is that severe depletion of NAD(P)H and NADH as a result of futile cycling between the quinone and hydroquinone forms of ${\beta}$-Lap causes severe disturbance in cellular metabolism leading to apoptosis and necrosis. The relative importance of the aforementioned two mechanisms, i.e., generation of ROS or depletion of NAD(P)H/NADH, may vary depending on cell type and environment. Importantly, the NQO1 level in cancer cells has been found to be higher than that in normal cells indicating that ${\beta}$-Lap may be preferentially toxic to cancer cells relative to non-cancer cells. The cellular level of NQO1 has been found to be significantly increased by divergent physical and chemical stresses including ionizing radiation. Recent reports clearly demonstrated that ${\beta}$-Lap and ionizing radiation kill cancer cells in a synergistic manner. Indications are that irradiation of cancer cells causes long-lasting elevation of NQO1, thereby sensitizing the cells to ${\beta}$-Lap. In addition, ${\beta}$-Lap has been shown to inhibit the repair of sublethal radiation damage. Treating experimental tumors growing in the legs of mice with irradiation and intraperitoneal injection of ${\beta}$-Lap suppressed the growth of the tumors in a manner more than additive. Collectively, ${\beta}$-Lap is a potentially useful anti-cancer drug, particularly in combination with radiotherapy.

• Korean Journal of Weed Science
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• v.15 no.2
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• pp.148-153
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• 1995

Glyphosate (N-[phosphonomethyl]glycine) applied to the assimilate-exporting leaves or sprayed to the whole plants of tomato(Lycopersicon esculentum Mil var. Moneymaker) induced the rapid inhibition of 5-enolpyruvyl skimic acid 3-phosphate synthase(EPSP-synthase). It shows that EPSP-synthase activity precedes chlorophyll loss. There is no difference in EPSP-synthase activity between in vivo tomato meristem and cell suspension culture if glyphosate is not applied. The EPSP-synthase activity is in a range of 4 to 6 nkat per mg protein. The inhibition of EPSP-synthase action is induced within 36 h after glyphosate application while the Chl contents were reduced 48 h after the application. In cell suspension culture of tomato and Corydalis (Corydalis sempervirens), a sublethal concentration of glyphosate retards the fresh weight increase and prolonged lag phase. The fresh weight is reached maximal about 14 days after the subculture in the presence of glyphosate. The inhibitory effect of glyphosate on EPSP-synthase is remarkably induced in lag phase.

• Environmental Analysis Health and Toxicology
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• v.15 no.4
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• pp.131-137
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• 2000

The release of hazardous waste materials into the environment poses serious risks in humans and ecosystems. The risk assessment of environmental pollutants including hazardous chemicals requires a comprehensive measurement of hazard and exposure of the chemicals that can be achieved by toxicity evaluation using a biological system such as biomarkers. In this report we have tried to develop a biomarker used to elucidate a molecular basis of, and to monitor abnormal behaviors caused by diazinon in Japanese medaka (Oryzias latipes) as a model organism. First, an attempt was made to clone tyrosine hydroxylase gene from Japanese medaka that would be a candidate for a biomarker for neuronal modulations and behaviors. For monitoring experiments at behavioral and molecular biological levels, the fish were treated under different sublethal conditions of diazinon and their behavioral responses were observed . In this study we have successfully cloned a partial TH gene from the medaka fish through PCR screening of an ovary cDNA library. DNA sequencing analysis revealed that the amplified fragment was 327 bp encoding 109 amino acids. Comparing the DNA sequence of medaka TH with other species, TH gene revealed the DNA sequence was completely identical to that of rat TH. In the RT-PCR, 330 Up of mRNA was consistently amplified in all the treated samples including control There were no significant differences in the TH expression level regardless of treating concentrations (1∼5,000 ppb) and time (0∼48 hr) The reason appeared to be that RT-PCR was not performed using through a quantitative analysis normalized against an actin gene expression. Organ or tissue - specific detection of TH activity and mRNA as biomarkers will be a useful monitoring tool for neurobehavioral changes in fish influenced by toxic chemicals. Furthermore, quantitative analysis of locomotive patterns and its correlation with the neurochemical and molecular data would be highly useful in measuring toxicity and hazard ofvarious environmental pollutants.