Induction of the metabolic activation system in rat liver by a combined treatment with 5,6-benzoflavone and phenobarbital; comparison with Aroclor 1254, using the Ames test

Author(s):  
Ina E. Mattern
2008 ◽  
Vol 6 (4) ◽  
pp. 29-33 ◽  
Author(s):  
Nazira S Karamova ◽  
Alexandra P Denisova ◽  
Zenon Stasevski

The mutagenic activity of five pesticides actara, sencor, mospilan, pencozeb, fastac widely used for treatment of potato plant lands in Tatarstan was tested in the Ames test. The non toxic concentrations of the pesticides determined in preliminary cytotoxicty test were used in the Ames assay. Pesticides actara, mospilan, pencozeb, fastac did not show mutagenic effect in Salmonella typhimurium TA 100 without rat liver S9 fraction. The weak mutagenic effect of herbicide sencor was established at concentration 1 ug/plate. Metabolic activation in vitro using rat liver S9 fraction decreased the mutagenic activity of sencor and did not alter the mutagenicity rate of the pesticides actara, mospilan, pencozeb and fastac.


2019 ◽  
Vol 19 (1) ◽  
pp. 159-162
Author(s):  
Ahmad Mukifza Harun ◽  
Noor Baizura Ab Ghani ◽  
Nor Farid Mohd Noor ◽  
Razif Abas ◽  
Mohammad Khursheed Alam

Backgrounds: The mutagenic properties of modified hydrothermal nanotitania extract were carried out using the Ames test (genotoxicity). Materials and methods: The Ames test was performed on Salmonella strains (TA98, TA100, TA1535, TA1537 and TA 102) which contain mutations in several genes with and without S9 metabolic activation from rat liver using the standard assay. The materials were extracted in distilled water and the serial dilutions of concentration ranging from 313 to 5000 μg/mLwere used after the incubation period of 24 h at 37° C. Results: These results suggested that all tested concentrations of the material extracts did not produce mutagenic effect in all the strains tested. Conclusions: Findings from this study showed that the modified hydrothermal nanotitania extract was non-mutagenic under present conditions. Bangladesh Journal of Medical Science Vol.19(1) 2020 p.159-162


Toxins ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 458
Author(s):  
Caroline Lanier ◽  
David Garon ◽  
Natacha Heutte ◽  
Valérie Kientz ◽  
Véronique André

The mutagenic patterns of A. flavus, A. parasiticus and A. fumigatus extracts were evaluated. These strains of toxigenic Aspergillus were collected from the agricultural environment. The Ames test was performed on Salmonella typhimurium strains TA98, TA100 and TA102, without and with S9mix (exogenous metabolic activation system). These data were compared with the mutagenicity of the corresponding pure mycotoxins tested alone or in reconstituted mixtures with equivalent concentrations, in order to investigate the potential interactions between these molecules and/or other natural metabolites. At least 3 mechanisms are involved in the mutagenic response of these aflatoxins: firstly, the formation of AFB1-8,9-epoxide upon addition of S9mix, secondly the likely formation of oxidative damage as indicated by significant responses in TA102, and thirdly, a direct mutagenicity observed for higher doses of some extracts or associated mycotoxins, which does not therefore involve exogenously activated intermediates. Besides the identified mycotoxins (AFB1, AFB2 and AFM1), additional “natural” compounds contribute to the global mutagenicity of the extracts. On the other hand, AFB2 and AFM1 modulate negatively the mutagenicity of AFB1 when mixed in binary or tertiary mixtures. Thus, the evaluation of the mutagenicity of “natural” mixtures is an integrated parameter that better reflects the potential impact of exposure to toxigenic Aspergilli.


1991 ◽  
Vol 14 (1-2) ◽  
pp. 143-160 ◽  
Author(s):  
Douglas J. Fort ◽  
James R. Rayburn ◽  
Donna J. Deyoung ◽  
John A. Bantle

2021 ◽  
Vol 22 (16) ◽  
pp. 8447
Author(s):  
Przemysław J. Danek ◽  
Wojciech Kuban ◽  
Władysława A. Daniel

In order to achieve a desired therapeutic effect in schizophrenia patients and to maintain their mental wellbeing, pharmacological therapy needs to be continued for a long time, usually from the onset of symptoms and for the rest of the patients’ lives. The aim of our present research is to find out the in vivo effect of chronic treatment with atypical neuroleptic iloperidone on the expression and activity of cytochrome P450 (CYP) in rat liver. Male Wistar rats received a once-daily intraperitoneal injection of iloperidone (1 mg/kg) for a period of two weeks. Twenty-four hours after the last dose, livers were excised to study cytochrome P450 expression (mRNA and protein) and activity, pituitaries were isolated to determine growth hormone-releasing hormone (GHRH), and blood was collected for measuring serum concentrations of hormones and interleukin. The results showed a broad spectrum of changes in the expression and activity of liver CYP enzymes, which are important for drug metabolism (CYP1A, CYP2B, CYP2C, and CYP3A) and xenobiotic toxicity (CYP2E1). Iloperidone decreased the expression and activity of CYP1A2, CP2B1/2, CYP2C11, and CYP3A1/2 enzymes but increased that of CYP2E1. The CYP2C6 enzyme remained unchanged. At the same time, the level of GHRH, GH, and corticosterone decreased while that of T3 increased, with no changes in IL-2 and IL-6. The presented results indicate neuroendocrine regulation of the investigated CYP enzymes during chronic iloperidone treatment and suggest a possibility of pharmacokinetic/metabolic interactions produced by the neuroleptic during prolonged combined treatment with drugs that are substrates of iloperidone-affected CYP enzymes.


1982 ◽  
Vol 206 (1) ◽  
pp. 139-146 ◽  
Author(s):  
Dietrich O. R. Keppler ◽  
Christa Schulz-Holstege ◽  
Joachim Fauler ◽  
Karl A. Reiffen ◽  
Friedhelm Schneider

d-Galactosone (d-lyxo-2-hexosulose) is phosphorylated and metabolized to the uridine diphosphate derivative in AS-30D hepatoma cells and rat liver. These reactions were catalysed in vitro by galactokinase and hexose-1-phosphate uridylyltransferase. Nucleotide analyses by high-performance liquid chromatography and enzymic assays revealed that this galactose analogue interferes with cellular pyrimidine nucleotide metabolism leading to a deficiency of UTP. [14C]Uridine labelling of hepatoma cells indicated a division of [14C]uridylate from UTP into UDP-galactosone; the latter was formed at a rate of more than 1.7mmol×h−1×(kg AS-30D or liver wet wt.)−1. As a consequence of UTP deficiency, d-galactosone (1mmol/1 or 1mmol/kg body wt.) strongly enhanced the rate of pyrimidine synthesis de novo as evidenced by incorporation of 14CO2 into uridylate and by an expansion of the uridylate pool. This resulted in a doubling of the total acid-soluble uridylate pool within 70min in the hepatoma cells and within 110min in rat liver. Combined treatment of hepatoma cells with d-galactosone and N-(phosphonoacetyl)-l-aspartate, an inhibitor of aspartate carbamoyltransferase, prevented the expansion of the uridylate pool and led to a synergistic reduction of UTP to 10% of the content in control cells. Hepatic UTP deficiency was selective with respect to other nucleotide 5′-triphosphates but was associated with reduced contents of UDP-glucose, UDP-glucuronate, and UDP-N-acetylhexosamines. Isolation of the UDP derivative of d-galactosone revealed an extremely alkali-labile UDP-sugar, probably an isomerization product of UDP-galactosone, that was degraded by elimination of UDP with a half-life of 45min at pH7.5 and 37°C. The instability of UDP-galactosone may contribute in vivo to limit the time period of severe uridine phosphate deficiency in addition to the compensatory role of pyrimidine synthesis de novo. During the initial time period, however, d-galactosone is effective as a powerful uridylate-trapping sugar analogue.


1988 ◽  
Vol 62 (2-3) ◽  
pp. 103-109 ◽  
Author(s):  
W. K. Lutz ◽  
R. Deuber ◽  
M. Caviezel ◽  
P. Sagelsdorff ◽  
U. Friederich ◽  
...  
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