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염산 DDB-S가 랫드의 생식독성에 미치는 영향에 관한 연구
김현우,박진홍,문서현,유국종,김화,김준성,박종하,조현선,강가미,황성희,김판기,문전옥,이치호,조명행 한국독성학회 2003 Toxicological Research Vol.19 No.1
A teratogenic study of dimethyl dimethoxy biphenylate derivative (DDB-S) was carried out on Sprague-Dawley rats. DDB-S dissolved in saline was administered to male and female rats by intravenously injection at daily doses of 50 mg/kg, 75 mg/kg, and 100 mg/kg. A half of dams were sacrificed at 20th day of gestation to scrutinize the pregnant performances and fetal development. And the remaining dams were allowed to deliver. The growth, reflex, behaviour and reproductive function of F1 offsprings were examined. There was no treatment-related difference in body weight, food consumption and necropsy findings of dams. No gross, skeletal and visceral abnormalities was observed in F1 fetuses from dams treated with DDB-S. F1 offsprings did not show any treatment-related difference in growth, reflex, behaviour and reproductive performance. At caesarean section of F1 dams, no growth retardation and gross abnormality was observed in F2 fetuses. In conclusion, DDB-S did not show any potential teratogenic effect in rats.
조명행,김민영,김현우,박진홍,김준성,진화,문서현,유국종,강가미,김윤신,김영철,Hae Yeong Kim,이기호,조현선 대한수의학회 2004 Journal of Veterinary Science Vol.5 No.4
Potential toxicological interactions of 4-(N-methyl-Nnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and/or dibuthyl phthalate (DBP) on ozone were investigated after 32- and 52-wk exposures using hprt mutation assay. Male and female B6C3F1 mice exposed to ozone (0.5 ppm), NNK(1.0 mg/kg), DBP (5,000 ppm), and two or three combinations of these toxicants 6 h per day for 32- and 52-wk showed increases in the frequencies of TGr lymphocytes comparedto the control groups. Additive interactions were noted from two combination groups compared to the ozone alone in both sexes of 32- and 52-wk studies. The most common specific mutation type in the hprt genes of test materials-treated male and female mice was transversion with very few transition. The results indicate that such dominant transversion may be responsible for toxicityand combined exposure to ozone, NNK, and DBP induces additive genotoxicities compared to ozone alone. Potential toxicological interactions of 4-(N-methyl-Nnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and/or dibuthyl phthalate (DBP) on ozone were investigated after 32- and 52-wk exposures using hprt mutation assay. Male and female B6C3F1 mice exposed to ozone (0.5 ppm), NNK(1.0 mg/kg), DBP (5,000 ppm), and two or three combinations of these toxicants 6 h per day for 32- and 52-wk showed increases in the frequencies of TGr lymphocytes compared to the control groups. Additive interactions were noted from two combination groups compared to the ozone alone in both sexes of 32- and 52-wk studies. The most common specific mutation type in the hprt genes of test materials-treated male and female mice was transversion with very few transition. The results indicate that such dominant transversion may be responsible for toxicity and combined exposure to ozone, NNK, and DBP induces additive genotoxicities compared to ozone alone.
조명행,김민영,송경석,박건호,장승희,김현우,박진홍,진화,유국종,조현선,강가미,김영철 대한수의학회 2004 Journal of Veterinary Science Vol.5 No.2
Toxic effects of ozone, 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and/or dibutyl phthalate (DBP)were examined through NF-κB, AP-1, Nrf2, and osteopontin (OPN) in lungs and livers of B6C3F1 mice. Electrophoretic mobility shift assay (EMSA) indicated that mice treated with combination of toxicants induced high NF-κB activities. Expression levels of p105, p65, and p50 proteins increased in all treated mice, whereas IκB activity was inhibited in NNK-,DBP-, and combination-treated ones. All treated mice exceptozone-treated one showed high AP-1 binding activities. Expression levels of c-fos, c-jun, junB, jun D, Nrf2, and OPNproteins increased in all treated mice. Additive interactions were frequently noted from two-toxicant combination micecompared to ozone-treated one. These results indicate treatment of mixture of toxicants increased toxicity through NF-κB, AP-1, Nrf2, and OPN. Our data could be applied to the elucidation of mechanism as well as the risk assessment of mixture-induced toxicity.