• Molecular & Cellular Toxicology
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• v.3 no.3
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• pp.172-176
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• 2007

Butylated hydroxytoluene (BHT) is widely used antioxidant food additives. It has been extensively studied for potential toxicities. BHT appears adverse effects in liver and thyroid. In this study, we evaluated the genetic toxicity of BHT with more advanced methods, in vitro mouse lymphoma assay $tk^{+/-}$ gene assay (MLA) and in vivo mouse supravital micronucleus (MN) assay. BHT did not appear the significantly results in the absence and presence of metabolic activation system with MLA. Also, in vivo testing of BHT yielded negative results with supravital MN assay. These results suggest that BHT itself was not generally considered genotoxic.

• BMB Reports
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• v.42 no.5
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• pp.299-303
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• 2009

In this study, we use promoter analysis to show that interaction between Jab1 and p53 induces suppression of p53 activation in U2OS and H1299 cells. Interaction between p53 and Jab1 was further confirmed by immunoprecipitation and immunofluorescent analyses. In particular, Jab1 was able to induce nuclear export of p53 as previously reported. When Jab1 was overexpressed in U2OS cells followed by etoposide or hydrogen peroxide ($H_2O_2$), cell death induced by such stresses was protected against. On the contrary, when the level of Jab1 was suppressed in U2OS cells, cytotoxicity imposed by etoposide and $H_2O_2$ was dramatically increased, suggesting a cell protective role for Jab1. These results indicate that Jab1 is a negative regulator of p53 and a plausible oncogene.

• Food Science and Biotechnology
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• v.14 no.5
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• pp.572-575
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• 2005

The effects of cooking method, cooking time and various food ingredients on the formation/ inhibition of heterocyclic aromatic amines (HAAs) in pork products were investigated. Three HAAs, 2-amino-3,8-dimethylimidazo [4,5-f] quinoxaline ($MeIQ_x$), 2-amino-3,4,8-trimethylimidazo [4,5-f] quinoxaline ($DiMeIQ_x$) and 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP) were measured in pork products using solid-phase extraction and HPLC. Pork patties were boiled, oven-broiled and pan-fried to internal temperatures of 71, 77 and $88^{\circ}C$. Generally, HAA concentrations increased with increasing internal temperature, and HAA formation was greatest with pan-fried. Selected food ingredients (vitamin E, sodium nitrite, sodium tripolyphosphate, sodium ascorbate, Nanking cherry tissue and cherry tissue extract) inhibited HAA formation in pork patties fried at $225^{\circ}C$ for 10 min/side, with the greater inhibition provided by cherry tissue and its methanolic extract.

• Journal of Food Hygiene and Safety
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• v.9 no.2
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• pp.67-74
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• 1994

This study was aimed to find out the comparative effects between non-irradiated, and 5kGy-10kGy of gamma-irradiated Panax Ginseng Radix powder on the genotoxicity for identification of possibility of DNA damage causing cancer. Four different short-term mutagenicity tests were used: (1) Salmonella typhimurium reversion assay (Ames test) (2) Chromosome aberration test in cultured Chinese hamster lung (CHL) fibroblast cells. (3) Micronucleus test in ddY mouse (4) Somatic mutation and recombination test in the wing cells of Drosophila melanogaster.Gamma-irradiated Panax Ginseng Radix powder revealed negative results in these four mutagenicity tests. This means gamma-irradiated ginseng could be safe on the genotoxic point of view.

• Environmental Mutagens and Carcinogens
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• v.26 no.2
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• pp.45-47
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• 2006

The reactive oxygen species (ROS) caused the damage of macro molecules, many degenerative disease and cancer, which was produced in process of the aerotropic metabolic pathway as well as in response to the various genotoxic stresses. Recently, redox systems including the number of antioxidant proteins such as catalase, glutathione peroxidase, heam-containing peroxidase, peroxiredoxin and superoxide dismutase (SOD) has been reported to have chemopreventive effects. Antioxidant proteins has been known to have the activity directly removing ROS and affecting the protein-protein interaction and cell signaling to induce the cellular responses. We need to understand the mechanism of antioxidants prevent DNA damage from oxidative stresses for researching the cancer prevention and providing the development of cancer therapeutic drug.

• Korean Journal of Environmental Biology
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• v.31 no.3
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• pp.189-191
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• 2013

Mycotoxins such as aflatoxin B1 (AFB1), ochratoxin A (OTA) and zearalenone (ZEA) are widespread contaminants of food and feedstuffs. It is very likely, that humans and animals are always exposed to mixtures of mycotoxins rather than to individual compounds. Therefore, risk assessments should consider mixture toxicity data. In the present study the combination of AFB1, OTA and ZEA was tested for genotoxicity in rat bone marrow and blood leukocytes after 15, 30 and 60 days treatment. The level of DNA damage was determined by the comet assay. The tail intensity and Olive tail moment in leukocytes and bone marrow cells were significantly higher than in controls. At the same time, the level of DNA damage in bone marrow cells was higher than in leukocytes. The data suggests that prolonged exposure to mycotoxins combination through food consumption can induce DNA damage contributing to the harmful effects in vivo.

• Toxicological Research
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• v.24 no.3
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• pp.161-167
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• 2008

Recently, arsenic-toxicity has become the major focus of strenuous assessment and dynamic research from the academy and regulatory agency. To elucidate the cause and the mechanism underlying the serious adverse health effects from chronic ingestion of arsenic-contaminated drinking water, numerous studies have been directed on the investigation of arsenic-toxicity using various in vitro as well as in vivo systems. Neverthless, some questions for arsenic effects remain unexplained, reflecting the contribution of unknown factors to the manifestation of arsenic-toxicity. Interestingly, very recent studies on arsenic metabolites have discovered that trivalent methylated arsenicals show stronger cytotoxic and genotoxic potentials than inorganic arsenic or pentavalent metabolites, arguing that these metabolites could play a key role in arsenic-associated disorders. In this review, recent progress and literatures are summarized on the metabolism of trivalent methylated metabolites and their toxicity on body systems including cardiovascular system in an effort to provide an insight into the future research on arsenic-associated disorders.

• Environmental Mutagens and Carcinogens
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• v.25 no.3
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• pp.97-103
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• 2005

The genotoxic effect of antimalarial drugs amodiaquine (AQ), mefloquine (MQ) and halofantrine (HF) was investigated in.at liver cells using the alkaline comet assay. AQ, MQ and HF at concentrations between $0-1000{\mu}mol/L$ significantly increased DNA strand breaks of rat liver cells dose-dependently. The order of induction of strand breaks was AQ>MQ>HF. The rat liver cells exposed to AQ and HF (200 and 400 ${\mu}mol/L$) and treated with (Fpg) the bacterial DNA repair enzyme that recognizes oxidized purine showed greater DNA damage than those not treated with the enzyme, providing evidence that AQ and HF induced oxidation of purines. Such an effect was not observed when MQ was treated with the enzyme. Treatment of cells with catalase, an enzyme inactivating hydrogen peroxide, decreased significantly the extent of DNA damage induced by AQ, and HF but not the one induced by MQ. Similarly quercetin, an antioxidant flavonoid at $50{\mu}mol/L$ attenuated the extent of the formation of DNA strand breaks by both AQ and HE. Quercetin, however, did not modify the effects of MQ. These results indicate the genotoxicity of AQ, MQ and HF in rat liver cells. In addition, the results suggest that reactive oxygen species may be involved in the formation of DNA lesions induced by AQ and HF and that, free radical scavengers may elicit protective effects against genotoxicity of these antimalarial drugs.

• Journal of the Korean Society of Food Science and Nutrition
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• v.27 no.1
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• pp.57-62
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• 1998

This study was designed to demonstrate the antigenotoxic potential of methyl alcohol extracts from Auricularia mesenterica and Gyrophora esculenta against the frequency of micronucleate polychromatic erythrocyte(MNPCE) produced by benzo($\alpha$) pyrene in vivo. We used the mouse bone marrow test system to measure the effect of single and multiple treatments of each sample. Genotoxicity of benzo ($\alpha$) pyrene(150mg/kg, i.p.) as positive control was the highest at 36 hours. However, each sample per dose was not genotoxic, showing MNPCE values in the range of the control level. Treatments of methyl alcohol extracts both of Auricularia mesenterica and Gyrophora esculenta showed significant decreased frequencies of NMPCE induced by benzo($\alpha$) pyrene within 12 hours by single treatment(100mg/kg, oral). And also, the MNPCE level produced benzo($\alpha$) pyrene was decreased by the treatment of benzo($\alpha$) pyrene(5 to 200mg/kg, oral) of each sample, but significantly different redults were obtained with 100mg/kg. In the multiple treatment, the highest antigentoxic effects were demonstrated with 20mg/kg in the each sample, a range which induced inhibition indices of 54.2 and 56.3%, respectively.

• Molecular & Cellular Toxicology
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• v.1 no.3
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• pp.172-178
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• 2005

[ $21{\alpha}$ ]- and ${\beta}$-Methylmelianodiol were isolated as the inhibitor of IL-5 bioactivity from Poncirus tripoliata. To develope as an anti-septic drug, the genotoxicity of $21{\alpha}\;-and\;{\beta}-methylmelianodiol$ was subjected to high throughput toxicity screening (HTTS) because they revealed strong IL-5 inhibitory activity and limitation of quantity. Mouse lymphoma thymidine kinase ($tk^{+/-}$) gene assay (MOLY), single cell gel electrophoresis (Comet) assay in mammalian cells and Ames reverse mutation assay in bacterial system were used as simplified, inexpensive, short-term in vitro screening tests in our laboratory. These compounds are not mutagenic in S. typhimurium TA98 and TA100 strains both in the presence and absence of metabolic activation. Before performing the comet assay, $IC_{20}$ of $21{\alpha}-methylmelianodiol$ was determined the concentration of $25.51\;{\mu}g/mL\;and\;21.99\;{\mu}g/mL$ with and without S-9, respectively. Also $21{\beta}-methylmelianodiol$ was determined the concentration of $24.15\;{\mu}g/mL\;and\;\;22.46\;{\mu}g/mL$ with and without S-9, respectively. In the comet assay, DNA damage was not observed both $21{\alpha}-methylmelianodiol\;and\;21{\beta}-methylmelianodiol$ in mouse lymphoma cell line. Also, the mutant frequencies in the treated cultures were similar to the vehicle controls, and none of $21{\alpha}\;-and\;{\beta}-methylmelianodiol$ with and without S-9 doses induced a mutant frequency over. twice the background. It is suggests that $21{\alpha}\;-and\;{\beta}-methylmelianodiol$ are non-mutagenic in MOLY assay. The results of this battery of assays indicate that $21{\alpha}\;-and\;{\beta}-methylmelianodiol$ have no genotoxic potential in bacterial or mammalian cell systems. Therefore, we suggest that $21{\alpha}\;-and\;{\beta}-methylmelianodiol$, as the optimal candidates with both no genotoxic potential and IL-5 inhibitory effects must be chosen.