Bacterial mutagenesis and hepatocyte unscheduled DNA synthesis induced by chrysoidine azo-dye components

Sandhu, Punam; Chipman, J.K.

doi:10.1016/0165-1218(90)90062-7

Cited by 25 publications

(7 citation statements)

References 31 publications

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“…The p ‐phenylene‐diamine did not have a mutagenic effect with or without metabolic activation, showing that the mutagenicity of DMPD could be ascribed to the presence of the dimethyl group [(‐CH 3 ) 2 ] located on the benzene ring in the para position to the amino group and to its absence in the PPD structure. This is in agreement with the observation of Sandhu and Chipman [37], who reported that mutagenicity of dyes because of the methyl (CH 3 ) substituents was more important than the non‐methylated counterpart.…”

Section: Discussionsupporting

confidence: 93%

In vitro study of DNA damage induced by acid orange 52 and its biodegradation derivatives

Mansour¹,

Barillier²,

Corroler³

et al. 2009

Enviro Toxic and Chemistry

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Mutagenicity of acid orange 52 (AO52) and its degradation products by Pseudomonas putida mt-2 was evaluated with the use of Salmonella Typhimurium TA102 and TA104 with and without the metabolic activation system (S9). No mutagenicity was observed in the absence of S9 and in the presence of S9 for biodegradation under shaking conditions, but it increased significantly in the presence of S9 after biodegradation under static conditions. In addition, the ability of tested compounds to induce DNA damage in vitro was evaluated with the DNA strand scission assay. The toxicity generated by the pure azo dye and the corresponding azoreduction products (4-aminobenzenesulfonic acid and N,N'-dimethyl-p-phenylenediamine) were compared. We suggest that the mutagenicity mechanism of these molecules occurs through free radical generation processes. In this study, we demonstrate that P. putida mt-2 incubated under aerobic conditions undergoes catabolism that enables it to degrade AO52 completely and, especially, to detoxify the dye mixtures.

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Section: Discussionsupporting

confidence: 93%

In vitro study of DNA damage induced by acid orange 52 and its biodegradation derivatives

Mansour¹,

Barillier²,

Corroler³

et al. 2009

Enviro Toxic and Chemistry

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“…This chemical was suggested to relate with bladder cancer in humans (Cartwright et al, 1983;Sole and Sorahan, 1985), but it is still controversial because the data of a later conducted case-control study denied its relation to the cancer (Sorahan and Sole, 1990). There are no data on the genetic and related effects of the chemical in humans, but it is mutagenic to bacteria and toxic to rat hepatocytes in vitro (Sandhu and Chipman, 1990). In the mice orally administered, it produced liver carcinoma, leukemia, and reticulum cell sarcomas (Anonymous, 1975).…”

Section: Figmentioning

confidence: 96%

Chelating Compound, Chrysoidine, Is More Effective in Both Antiprion Activity and Brain Endothelial Permeability Than Quinacrine

et al. 2007

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1. As an extension of our previous study of quinacrine and its derivatives, chelating chemicals were screened to obtain more effective, better brain-permeable antiprion compounds using either prion-infected neuroblastoma cells or brain capillary endothelial cells.2. Eleven chemicals were found to have antiprion activity. Most of them shared a common structure consisting of benzene or naphthalene at either end of an azo bond. Structure-activity data suggest that chelating activity is not necessary but might contribute to the antiprion action.3. Chrysoidine, a representative compound found here, was about 27 times more effective in the antiprion activity and five times more efficiently permeable through the brain capillary endothelial cells than quinacrine was.4. These chemicals might be useful as compounds for development of therapeutics for prion diseases.

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“…To ensure representation of each of these different categories, treatments included light, NQO, the progenotoxic aromatic amine chrysoidine, and the proximate genotoxic hydroxylated aromatic amide N ‐hydroxy‐2‐acetylaminofluorene ( N‐OH ‐2‐AAF). Since a wide range of environmentally relevant progenotoxic carcinogens require metabolic activation by CYP isozymes to reactive metabolites or reactive oxygen species, we also measured ethoxyresorufin‐ O ‐deethylase (EROD) activity as an indicator of activity similar to mammalian CYP1A, involved in the oxidative activation of many carcinogens, including chrysoidine [17] and 2‐acetylami‐nofluorene (2‐AAF), relevant to the present study [18].…”

Section: Introductionmentioning

confidence: 99%

Induction of dna strand breaks by genotoxicants in the alga Chlamydomonas reinhardtii

David¹,

Winter²,

Chipman³

2009

Enviro Toxic and Chemistry

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The use of unicellular algae in ecotoxicity testing is well established, particularly regarding whole-organism and population-level end points such as lethality and population growth. Conflicting information exists, however, on the potential for genetic toxicity to be incorporated into the safety studies in this test organism. In the present study, DNA strand breaks (Comet assay) and ethoxyresorufin-O-deethylase (EROD) activity were used as indicators of genetic toxicity and cytochrome P450 1A baseline xenobiotic metabolism, respectively, in the unicellular green alga Chlamydomonas reinhardtii. DNA strand breaks were quantified following exposure to the direct-acting genotoxic agents 4-nitroquinoline-1-oxide (NQO) and the N-hydroxy metabolite of 2-acetylaminofluorene (N-OH-2-AAF) and the indirect-acting genotoxin chrysoidine. Following compound exposure, chrysoidine and N-OH-2-AAF produced statistically significant increases in DNA strand breaks at both 0.1 and 10 microM and 0.05 and 5 microM, respectively (p < 0.05 and p < 0.01). Different light sources were also found to influence DNA strand breaks, the minimum response being observed using a source that omits the ultraviolet range. Compared to many mammalian cells, both DNA damage responses and EROD activity were relatively weak. EROD activity was 0.03 pmol/min/10(6) cells in control cells, and the maximum level of DNA strand breaks observed was 14.1% at a 5 nM concentration of NQO. The responses exhibited were not enhanced by the use of a cell wall-free mutant strain. In conclusion, C reinhardtii responded, albeit weakly, to selected direct- and indirect-acting genotoxicants and also exhibited measurable EROD activity.

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Bacterial mutagenesis and hepatocyte unscheduled DNA synthesis induced by chrysoidine azo-dye components

Cited by 25 publications

References 31 publications

In vitro study of DNA damage induced by acid orange 52 and its biodegradation derivatives

In vitro study of DNA damage induced by acid orange 52 and its biodegradation derivatives

Chelating Compound, Chrysoidine, Is More Effective in Both Antiprion Activity and Brain Endothelial Permeability Than Quinacrine

Induction of dna strand breaks by genotoxicants in the alga Chlamydomonas reinhardtii

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