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Metabolic conversion of IQ and MeIQ to bacterial mutagens
Authors:A J Alldrick  B G Lake  J Flynn  I R Rowland
Institution:1. Key Laboratory of Integrated Regulation and Resource Development on Shallow Lakes, Ministry of Education, Hohai University, Nanjing 210098, China;2. College of Environment, Hohai University, Nanjing 210098, China;3. State Key Laboratory of Pollution Control and Resource Reuse, School of Environmental Science and Engineering, Tongji University, Shanghai 200092, China;4. College of Environmental Science and Engineering, Hunan University, Changsha 410082, China;5. Shaanxi Key Laboratory of Energy Chemical Process Intensification, School of Chemical Engineering and Technology, Xi''an Jiaotong University, Xi''an, China;1. FishWise, Santa Cruz, CA, United States;2. University of California Santa Cruz, Santa Cruz, CA, United States;1. FarmHannong Co., Ltd., Yeoui-daero 24, Yeongdeungpo-gu, Seoul 07320, Republic of Korea;2. Korean Agency for Technology and Standards, Isu-ro 93, Maengdong-myeon, Eumseong-gun, Chungcheongbuk-do 27737, Republic of Korea
Abstract:The metabolic conversion of 2-amino-3-methyl- and 2-amino-3,4-dimethyl-imidazo4,5-f]quinoline (IQ and MeIQ respectively) to bacterial mutagens was studied using a bacterial mutation assay. Studies were performed using S9 fractions derived from either corn oil (uninduced) or Aroclor-1254-treated Sprague-Dawley rats. Aroclor 1254 treatment lowered the S9 protein concentration required for optimum levels of mutagenesis, enhanced the numbers of mutants observed and altered the effects of metabolic inhibitors and cofactors added to the assay. Studies with uninduced preparations revealed that IQ and MeIQ exhibited similar responses to the effects of metabolic inhibitors and cofactors involved in detoxication reactions. Both IQ and MeIQ activation appeared to be inhibited by the biogenic amines tryptamine and tyramine and inactivated by conjugation with either acetyl coenzyme A or glutathione.
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