• KSBB Journal
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• v.14 no.2
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• pp.192-197
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• 1999

marine bacterium Pseudomonas sp. CHCS-2 produced the biosurfactant in the culture broth which contained 2%(w/v) arabian light crude oil and the productivity of biosurfactant was increased with the addition of glucose. The crude oil in the culture broth was degraded by this strain and carbon chain of $_nC_{12}~_nC_{22}$ was completely degradaded during the incubation for 196 h. The crude biosurfactant was purified by Amberlite XAD-7, Sepharose CL-4B and DEAE-Sepharose CL-6B column chromatography. Therefore, 0.21g/L of the purified biosurfactnat was obtained. The purified biosurfactant was a type of lipoprotein and the molecular weight was estimated as 67kDa by SDS-PAGE. The lipid composition was identified as octadecanoic acid by gas chromatography/mass spectrometry. And then, the N-terminal amino acid sequence of the protein was determined as Ser-Val-lle-Asn-Thr-lle-X-Met-lle-Gly-Gln-Gln- and the sequence did not show homology to any other known lipoprotein. Therefore, the purified lopoprotein was predicted novel biosurfactant.

• Environmental Analysis Health and Toxicology
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• v.20 no.4 s.51
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• pp.365-374
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• 2005

Ambient air particulate matters are classified into two distinct modes in sire distribution, namely the coarse and fine particles. Correlation between high particulate concentration and adverse effect on human populations has long been recognized. However, the toxicology of these adverse efforts has not been clarified. We investigated the genotoxic effect of PM 2.5 collected from urban area in Seoul by comet assay (A549 cells), CBMN assay (CHO-K1 cells) and EROD-microbioassay (H4IIE cells). Results from in vitro micronucleus assay and comet assay showed that PM 2.5 samples collected from traffic area, residential area and indoor air induced chromosomal damage and DNA breakage in a non-cytotoxic dose. The complex mixture effect of these PM 2.5 extracts was quantified by EROD-microbioassay in terms of its bio-TEQ (biologiral -TCDD equivalent concentration) which was 70.87$\pm$28.07, 93.55$\pm$21.80 and 14.31 $\pm$ 1.10 ng/g-PM 2.5 in traffic area, residental area and indoor air samples, respectively. Conclusively, we suggested that PM 2.5 collected from traffic area and residential area contains CYPIA inducer and genotoxic materials.

• Environmental Analysis Health and Toxicology
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• v.25 no.1
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• pp.85-94
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• 2010

Platycodon grandiflorum, Doraji as Korean name, is one of the most widely used traditional oriental medicine for bronchial diseases and also used as a folk remedy for geriatric diseases and inflammatory diseases. In recent studies, it has been reported that some effect of P. grandiflorum is derived from its antioxidant activity, although there is still a lack of evidence to establish its oxy-radical scavenging activity. In this study, total oxy-radical scavenging capacity (TOSC) assay was used to evaluate antioxidant activity of total extracts (T-PG), polysaccharide fraction (Po-PG), and saponin fraction (Sa-PG) isolated from P. grandiflorum against peroxyl radicals and peroxynitrites. And MTT assay was taken to assess cyto-protective effects of T-PG, Po-PG and Sa-PG in H4IIE cells treated with hydrogen peroxide and tert-butylhydroperoxide. In the TOSC assay, Sa-PG showed strong oxy-radical scavenging capacity compared with T-PG and Po-PG. In cell-based assay, T-PG and Po-PG protected cells from oxidative stress, but Sa-PG did not protect cells because of cytotoxicity of Sa-PG. These results suggest that the saponin components of P. grandiflorum have relatively strong antioxidant capacity and cytotoxicity in rat hepatoma cells.

• Toxicological Research
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• v.23 no.3
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• pp.263-269
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• 2007

Although taurine (2-aminoethanesulfonic acid) can inhibit oxidative stress in both animal and epidemiological studies, it is obscure whether taurine directly scavenges oxy-radicals or indirectly regulates oxidant production and/or antioxidant defense system. The reason for this discrepancy remains unknown but may be due, in part, to the lack of a validated assay system for evaluating oxy-radical scavenging capacity. The antioxidant activities of taurine and hypotaurine (2-aminoethanesulfinic acid), a precursor of taurine, against peroxyl radicals, hydroxyl radicals and peroxynitrites were determined by the total oxy-radical scavenging capacity (TOSC) assay and cell-based assay using H4IIE cells. tert-Butylhydroperoxide or hydrogen peroxide-induced cell toxicity determined by MTT assay was markedly inhibited by 10mM taurine or hypotaurine. The tert-butylhydroperoxide- or hydrogen peroxide-induced changes in oxidative stress markers, such as cellular glutathione and malondialdehyde, were ameliorated by 10mM taurine or hypotaurine. However, specific TOSC values calculated from the slope of the linear regression for taurine against peroxyl radicals, hydroxyl radicals or peroxynitrites were all less than 1 TOSC/mM. On the other hand specific TOSC values for hypotaurine against peroxyl radicals, hydroxyl radicals or peroxynitrites were 48, 2096, or 69 TOSC/mM, respectively. These results suggest that taurine protects cells against oxidative insults, which is not ascribed to directly scavenging activity of taurine against oxy-radicals. These results support the idea that the oxidation state of sulfur in antioxidants may be a determinant of oxy-radical scavenging capacity.

• Toxicological Research
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• v.23 no.2
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• pp.143-150
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• 2007

Although animal and epidemiological studies have suggested oxidative stress as an etiological factor in pathogenesis including cancer, inflammation, sepsis, fibrosis, cardiovascularlneurodegenerative diseases and aging-related disorders, conflicting results have been obtained in clinical trial with antioxidants. The reason for this discrepancy remains unknown but may be due, in part, to the lack of a validated assay system for evaluating antioxidant capacity. The antioxidant activity of a series of sugar alcohols against peroxyl radicals, hydroxyl radicals and peroxynitrites was determined by the total oxy-radical scavenging capacity (TOSC) assay and cell-based assay using H4IIE cells. Specific TOSC values calculated from the slope of the linear regression for erythritol, xylitol, sorbitol or mannitol against peroxyl radicals was $2.1{\pm}0.2,\;3.7{\pm}0.3,\;9.1{\pm}0.3$ or $8.7{\pm}1.1$ TOSC/mM, respectively. Specific TOSC values for erythritol, xylitol, sorbitol or mannitol against peroxynitrite was $1.9{\pm}0.3,\;3.9{\pm}0.4,\;7.8{\pm}0.7$ or $7.7{\pm}0.5$ TOSC/mM, respectively. These results suggest that oxy-radical scavenging capacity is dependent on the number of aliphatic hydroxyl group in sugar alcohols of monosaccharide. Tert-butylhydroperoxide (t-BHP)-induced cell toxicity determined by MTT assay was marginally attenuated by 10 mM erythritol, but completely inhibited by 10 mM xylitol, 2 mM sorbitol or 0.75 mM maltitol, a disaccharide alcohol. Oxidative stress markers, such as glutathione (GSH) and malondial-dehyde (MDA) levels, were measured in t-BHP-treated cells using HPLC equipped with a fluorescence detector and a reverse phase column. Erythritol did not change the levels of GSH and MDA in H411E cells treated with t-BHP. The t-BHP-induced changes in cellular GSH and MDA levels were ameliorated by 10 mM xylitol and completely blocked by 10 mM sorbitol and maltitol. These results indicate that sugar alcohols protect cells against oxidative stress via scavenging oxy-radical and suggest that TOSC assay in conjunction with cell-based assay is a valid method for evaluating antioxidant capacity of natural and synthetic chemicals.

• Korean Journal of Food Science and Technology
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• v.39 no.6
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• pp.688-693
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• 2007

The hepatoprotective effects of water extracts composed of Adenophora triphylla var japonica Hara (ATJH) on acetaminophen (APAP)-induced hepatotoxicity were investigated in vivo and in vivo. The effects of ATJH on liver toxicity induced by APAP were assessed by blood biochemical and histopathological analyses. APAP treatment (350 mg/kg) caused severe liver injury in mice as indicated by their significantly elevated plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Pretreatment with ATJH for 3 or 7 days attenuated the increases in ALT and AST when challenged with APAP. The reductions in viability caused by high dose of APAP (450 mg/kg) in vivo were reversed by pretreatment with ATJH. These protective effects of ATJH against APAP-induced toxicity were consistent with the results from the histopathological examinations. We next examined the effects of ATJH on the gene expression of glutathione S-transferases (GSTs) that detoxify the metabolic intermediates of APAP in H4IIE cells. The hepatic GST protein levels [$\alpha$ class (GSTA2, GSTA3/5)] were significantly elevated in a dose-dependent manner by ATJH treatment. In summary, ATJH is effective at protecting against APAP-induced hepatotoxicity by GST induction, implying that ATJH should be considered a potential chemopreventive agent.