Mutagenic activation and carcinogenicity of aminoazo dyes ortho-aminoazotoluene and 3′-methyl-4-dimethylaminoazobenzene in experiments on suckling mice

Каледин, В. И.; Ilnitskaya, S. I.; Ovchinnikova, L.P.; Popova, N. A.; Bogdanova, L. A.; Morozkova, T. S.

doi:10.1134/s0006350914030117

Cited by 10 publications

(4 citation statements)

References 3 publications

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“…The removal of dyes from the aqueous environment is imperative because they are toxic and can cause carcinogenicity and mutagenicity [10][11][12][13]. Wastewater containing dyes are usually treated by biodegradation [14,15], coagulation-flocculation [15], the advanced oxidative process [16], and adsorption [17][18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Preparation of hybrids of wood sawdust with 3-aminopropyl-triethoxysilane. Application as an adsorbent to remove Reactive Blue 4 dye from wastewater effluents

Teixeira

Lima

Benetti

et al. 2021

Journal of the Taiwan Institute of Chemical Engineers

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Section: Introductionmentioning

confidence: 99%

Preparation of hybrids of wood sawdust with 3-aminopropyl-triethoxysilane. Application as an adsorbent to remove Reactive Blue 4 dye from wastewater effluents

Teixeira

Lima

Benetti

et al. 2021

Journal of the Taiwan Institute of Chemical Engineers

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“…Concerning OAT tumorigenicity, by 15 months after newborn (∼17-g) male and female A/Jax mice were given a single subcutaneous injection of 0, 0.4, or 0.7 mg OAT, ∼42-50% of males had one or more liver tumors, whereas females had about a third as many and unexposed mice had none; the OAT-exposed mice also showed a ∼4-fold elevation in pulmonary tumors [59]. Although OAT induces liver tumors potently in several mouse strains (CBA, SWR, DBA/2, A/He, and DD), much less or no observed hepatotumorigenic potency was observed in other strains (AKR and CC57Br) and in rats [77,78]. OAT was first shown to induce CAR and CAR-dependent liver cell proliferation in mice [65,79].…”

Section: Appendixmentioning

confidence: 99%

Biphasic hCAR Inhibition-Activation by Two Aminoazo Liver Carcinogens

Bogen¹

2018

Nuclear Receptor Research

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Detailed dose-response data recently archived by the National Center for Biotechnology Information (NCBI) identified 853 human CAR (hCAR) agonists by quantitative highthroughput screening (qHTS) assays applied to >9,000 chemicals tested at ≥14 concentrations using n = 3-48 replicates. By reexamining NCBI data on 746 agonists with replicate data sets each satisfying additional quality criteria, ∼95% had average values of agonist-specific Hill-model slopes estimated by NCBI that exceed 1 (i.e., exhibited an overall sublinear lowdose dose-response), and two unambiguously biphasic hCAR inhibitor-agonists were identified, 4-aminoazobenzene (n = 37) and ortho-aminoazotoluene (n = 3), both of which also cause rodent liver tumors. Although evidently rare among hCAR agonists, such biphasic responses add to evidence that nuclear receptors can exhibit complex patterns of low-dose response, consistent with previous observations and theoretical predictions for endpoints governed by ultrasensitive molecular switches. The pronounced biphasic hCAR response pattern observed for 4-aminoazobenzene is particularly noteworthy insofar as it was identified with statistical power that exceeds that of most if not all other receptor-mediated biphasic cellular responses to any single-chemical exposure reported to date.

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“…Другой путь увеличения активности онкогена, связанный с усилением синтеза матричных РНК и в итоге белкового продукта онкогена и его накопления в клетке, может реализоваться через регуляцию этого синтеза, т. е. эпигенетически, как это происходит в нормальном онто генезе и при репаративных процессах. В настоящее время имеются соображения относительно того, как могут дей ствовать канцерогены на уровне не структуры, а функции генома (NguenBa, Vasseur, 1999;Jones, Baylin, 2007;Kaledin et al, 2014aKaledin et al, , b, 2015. Обсудить их мы надеемся в следующем сообщении.…”

Section: результаты и обсуждениеunclassified

Inhibition of mutagenic activation of orthoaminoazotoluene increases its carcinogenicity for mouse liver

Каледин¹,

Ovchinnikova²,

Ilnitskaya³

et al. 2016

Vestn. VOGiS

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Various mutationally impaired genes are often found in malignant tumors of animals and humans. At the same time, a large number of carcinogens demon strate positive activity in different in vitro tests for mutagenicity. These findings are indicative of a geno toxic mechanism of carcinogen action. It is considered that chemically active carcinogens induce mutations (and tumors) directly interacting with DNA, while inactive substances are mutagenically activated in the processes of cellular metabolism in target tissues. The aminoazo dyes was found to be activated by Nhydroxilation and subsequent conjugation with sulfuric acid catalyzed by the enzyme sulfotransferase. Previously we found that it is activated metabolites of orthoaminoazotoluene that are responsible for its inhibitory effect on hormonal induction of tyrosin aminotransferase activity in the liver of sensitive mice. Inhibition of sulfoconjugation of 4amino azo benzene, another hepatocarcinogen for mice, by pentaclorophenol was reported to reduce its both mutagenic and carcinogenic activity. In this paper, we confirmed this observation. But we found that, when used orthoaminoazotoluene, pentaclorophe nol inhibited its mutagenic activity, but significantly sti mulated the hepatocarcinogenic potency. It seems that carcinogenic action is provoked by unmetabolys ed orthoaminoazotoluene per se or some of its non sulfated derivatives. The results of our comparative study with orthoaminoazotoluene and 3.4benzopy rene are in contradiction with the genotoxic theory В злокачественных опухолях человека и животных часто обнару живаются мутантные варианты генов, контролирующих размно жение и рост клеток. В то же время многие канцерогены про являют положительную активность в различных тестах на мута ген ность. Это свидетельствует в пользу представлений о гено токсическом механизме канцерогенеза. Считается, что если химически активные канцерогены вызывают мутации при непо средственном взаимодействии с ДНК, то химически неактив ные активируются до мутагенных продуктов в процессе метаболиче ских превращений в организме. Было установлено, что аминоазо красители активируются путем Nгидроксилирования и последу ющей конъюгации с остатком серной кислоты, катализиру емой печеночной сульфотрансферазой, ферментом второй фазы мета болизма ксенобиотиков. Ранее мы показали, что именно активи рованные метаболиты ортоаминоазотолуола ответственны за инги бирование глюкокортикоидной индукции тирозинаминотрансфе разы у чувствительных к его гепатоканцерогенному действию мышей. Подавление с помощью ингибитора сульфотрансферазы пентахлорфенола сульфатирования 4аминоазобензола, другого канцерогенного для мышей азокрасителя, приводило, по литера турным данным, к снижению его как мутагенной, так и канцеро генной активности. Мы подтвердили это наблюдение. Однако при использовании с ортоаминоазотолуолом пентахлорфенол так же, как в случае с 4аминоазобензолом, подавлял его мута генное действие, но значительно усиливал канцерогенное. Сле довательно, канцерогенное действие на печень оказывает нем...

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Mutagenic activation and carcinogenicity of aminoazo dyes ortho-aminoazotoluene and 3′-methyl-4-dimethylaminoazobenzene in experiments on suckling mice

Cited by 10 publications

References 3 publications

Preparation of hybrids of wood sawdust with 3-aminopropyl-triethoxysilane. Application as an adsorbent to remove Reactive Blue 4 dye from wastewater effluents

Preparation of hybrids of wood sawdust with 3-aminopropyl-triethoxysilane. Application as an adsorbent to remove Reactive Blue 4 dye from wastewater effluents

Biphasic hCAR Inhibition-Activation by Two Aminoazo Liver Carcinogens

Inhibition of mutagenic activation of orthoaminoazotoluene increases its carcinogenicity for mouse liver

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