• Journal of Korean Society on Water Environment
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• v.22 no.3
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• pp.513-520
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• 2006

The effect of chlorination on disinfection byproducts (DBPs) production from bloom-forming freshwater algae including 7 strains of cyanobacteria and 6 strains of diatoms was investigated. The release and degradation of hepatotoxin (microcystins) by the chlorination on Microcystis under differential condition of the chlorination time and dose were also investigated. The disinfection byproducts formation potentials (DBPFP) of cyanobacterial species and diatoms were ranged from 0.017 to $0.070{\mu}mol\;DBPs/mg$ C and from 0.129 to $0.708{\mu}mol\;DBPs/mg$ C respectively. Among three major groups of DBPs, haloacetonitrils (HANs) was major product in most test strains except Aphanizomenon sp. and Oscillatoria sp. Haloacetic acids (HAAs) was less than 5 % of total DBPs. Chloroform and dichloroacetonitril (DCAN) were dominant compounds in trihalomethanes (THMs) and HANs respectively. After 4 hours chlorination of toxic Microcystis aeruginosa under the dose range of 0.5 to $10mg\;Cl_2/L$, the concentration of intracellular microcystins decreased, but dissolved dissolved microcystins concentration increased with the treatment of more than $3mg\;Cl_2/L$. However the total amount of microcystins was almost constant even at $10mg\;Cl_2/L$ of chlorination. To conclude, our results indicate that the chlorination causes algal cell lysis and release of intracellular microcystins in the intact form to surrounding waters.

• BMB Reports
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• v.39 no.2
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• pp.197-207
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• 2006

Cajanus indicus is a herb with medicinal properties and is traditionally used to treat various forms of liver disorders. Present study aimed to evaluate the effect of a 43 kD protein isolated from the leaves of this herb against chloroform induced hepatotoxicity. Male albino mice were intraperitoneally treated with 2mg/kg body weight of the protein for 5 days followed by oral application of chloroform (0.75ml/kg body weight) for 2 days. Different biochemical parameters related to physiology and pathophysiology of liver, such as, serum glutamate pyruvate transaminase and alkaline phosphatase were determined in the murine sera under various experimental conditions. Direct antioxidant role of the protein was also determined from its reaction with Diphenyl picryl hydraxyl radical, superoxide radical and hydrogen peroxide. To find out the mode of action of this protein against chloroform induced liver damage, levels of antioxidant enzymes catalase, superoxide dismutase and glutathione-S-transferase were measured from liver homogenates. Peroxidation of membrane lipids both in vivo and in vitro were also measured as malonaldialdehyde. Finally, histopathological analyses were done from liver sections of control, toxin treated and protein pre- and post-treated (along with the toxin) mice. Levels of serum glutamate pyruvate transaminase and alkaline phosphatase, which showed an elevation in chloroform induced hepatic damage, were brought down near to the normal levels with the protein pretreatment. On the contrary, the levels of anti-oxidant enzymes such as catalase, superoxide dismutase and glutathione-S-transferase that had gone down in mice orally fed with chloroform were significantly elevated in protein pretreated ones. Besides, chloroform induced lipid peroxidation was effectively reduced by protein treatment both in vivo and in vitro. In cell free system the protein effectively quenched diphenyl picryl hydrazyl radical and superoxide radical, though it could not catalyse the breakdown of hydrogen peroxide. Post treatment with the protein for 3 days after 2 days of chloroform administration showed similar results. Histopathological studies indicated that chloroform induced extensive tissue damage was less severe in the mice livers treated with the 43 kD protein prior and post to the toxin administration. Results from all these data suggest that the protein possesses both preventive and curative role against chloroform induced hepatotoxicity and probably acts by an anti-oxidative defense mechanism.

• KSBB Journal
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• v.19 no.1
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• pp.12-16
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• 2004

Recently the measurement of biophoton emission has attracted increasing attention in the study on physiological state of biological systems. We report the measurements of biophoton emission from the mouse fatty liver induced by carbon tetrachloride, CCl$_4$. The hepatotoxin, CCl$_4$ in olive oil, was injected intraperitoneally into two groups of ICR mice which were made of 6 mice in each group. The control groups corresponding to the treated groups were prepared with the injections of olive oil only. After the injections, livers of two groups were extracted and measured biophoton emission in 24 hours and 72 hours later, respectively. We also extracted the plasma in the blood and measured the transaminase activity. Results show that biophoton emission from the livers in 24-hour treated group is 69.3${\pm}$21.2 counts/min/$\textrm{cm}^2$, which is two times more larger than that in 24-hour control group, 29.5${\pm}$5.9 counts/min/$\textrm{cm}^2$ Biophoton emission from the livers in 72-hour treated group is 37.0${\pm}$14.8 counts/min/$\textrm{cm}^2$. These biophoton results correlate with those of the biochemical assays. We conclude that biophoton emission can be used as a biomarker of mouse fatty liver induced by CCl$_4$.

• Journal of Korean Society of Environmental Engineers
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• v.37 no.12
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• pp.657-667
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• 2015

Cyanobacteria frequently dominate the freshwater phytoplankton community in eutrophic waters. Cyanotoxins can be classified according to toxicity as neurotoxin (Anatoxin-a, Anatoxin-a(s), Saxitoxins) or hepatotoxin (microcystins, nodularin, cylindrospermopsin). Microcystins are present within cyanobacterial cells generally, and they are extracted by the damage of cell membrane. It has been reported that cyanotoxins caused adverse effects and they are acculmulated in aquatic oganisms of lake, river and ocean. In natural, microcystins are removed by biodegradation of microorganisms and/or feeding of predators. However, in process of water treatment, the use of copper sulfate to remove algal cells caused extraction of a mess of microcystins. Microcysitns are removed by physical, chemical and biological methods according to reports. The reduction of nutrients (N and P) inflow is basic method of prevention of cyanobacteria bloom formation. However, it is less effective than investigation because nutrients already present in the eutrophic lake. In natural lake, cyanobacteria bloom are not formed because macrophytes invade from coastal lake by eutrophication. Therefore, a coastal lake has to recover to prevent of cyanobacteria bloom formation.