Kidney and liver distribution of ochratoxin A in male and female F344 rats

Vettorazzi, Ariane; Trocóniz, Iñaki F.; González-Peñas, Elena; Arbillaga, Leire; Corcuera, L.A.; Gil, Ana Gloria; Ceráin, Adela López de

doi:10.1016/j.fct.2011.04.021

Cited by 33 publications

(31 citation statements)

References 24 publications

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“…After 3h, AFB1 could be detected in plasma and kidney but only quantified in liver, due to its high metabolization rate. On the contrary, the OTA levels remained very high in plasma and also in tissues after 24h, being very similar to those found by Vettorazzi et al (2009Vettorazzi et al ( , 2010Vettorazzi et al ( and 2011. Apparently, the co-administration decreased the levels of AFB1 and increased the levels of OTA found in plasma and tissues.…”

Section: Discussionsupporting

confidence: 59%

“…The single dose of AFB1 (0.25 mg/kg bw) was similar to the one used to characterize expression profiles of genotoxic carcinogens (0.24 mg/kg bw/day) (Ellinger-Ziegelbauer et al, 2006). The single OTA dose selected (0.5 mg/kg 12 bw) was approximately the carcinogenic dose described by the NTP studies during 24 months (0.7 mg/kg bw) (NTP, 1989) and has been previously used in other studies (Vettorazzi et al, 2009;Vettorazzi et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

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Genotoxicity of Aflatoxin B1 and Ochratoxin A after simultaneous application of the in vivo micronucleus and comet assay

Corcuera

Vettorazzi

Arbillaga

et al. 2015

Food and Chemical Toxicology

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(max. 200 words)Aflatoxin B1 (AFB1) and Ochratoxin A (OTA) are genotoxic mycotoxins that can contaminate a variety of foodstuffs, the liver and the kidney being their target organ, respectively. The micronucleus (MN) assay (bone marrow) and the comet assay (liver and kidney) were performed simultaneously in F344 rats, treated with AFB1 (0.25 mg/kg b.w.), OTA (0.5 mg/kg b.w.) or both mycotoxins. After AFB1 treatment, histopathology and biochemistry analysis showed liver necrosis, focal inflammation and an increase in Alanine Aminotransferase and Aspartate Aminotransferase. OTA alone did not cause any alteration. The acute hepatotoxic effects caused by AFB1 were less pronounced in animals treated with both mycotoxins. With regard to the MN assay, after 24h, positive results were obtained for AFB1 and negative results were obtained for OTA, although both toxins caused bone marrow toxicity. In the combined treatment, OTA reduced the toxicity and the number of MN produced by AFB1. In the comet assay, after 3h, positive results were obtained for AFB1 in the liver and for OTA in the 1 kidney. The combined treatment reduced DNA damage in the liver and had no influence in the kidney. Altogether, these results may be indicative of an antagonistic relationship regarding the genotoxicity of both mycotoxins.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Genotoxicity of Aflatoxin B1 and Ochratoxin A after simultaneous application of the in vivo micronucleus and comet assay

Corcuera

Vettorazzi

Arbillaga

et al. 2015

Food and Chemical Toxicology

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“…Some possible consequences of this higher amount of food in the stomach of males, such as delayed gastric emptying or the trapping effect of the food contents towards the mycotoxin have been commented in Vettorazzi et al (2010Vettorazzi et al ( , 2011. The fact that food in the stomach may lead to less OTA absorption coincides with the fact that OTA appears to be less toxic when acquired as a dietary component Miljkovic et al, 2003).…”

Section: Absorptionmentioning

confidence: 99%

“…In the main rat kinetic studies performed to date with HPLC-FLD or HPLC-MS, complete data from the validation for each matrix is not given or the extraction and/or detection methods were developed for other species (Li et al, 1997;Mantle et al, 2008;. In some kinetic studies in which a specifically validated method was used, only plasma, kidney and liver levels were measured (Vettorazzi et al, 2009(Vettorazzi et al, , 2010(Vettorazzi et al, , 2011. Recently a new validated HPLC-MS method has been developed for uncovering in vivo kinetics of OTA in rats in plasma, heart, liver, spleen, lung, kidney and brain .…”

Section: Analytical Techniques For Ochratoxin a Toxicokinetic Studiesmentioning

confidence: 99%

“…In all of the kinetic analyses performed to date with OTA, only Kane et al (1986), Suzuki et al (1977) Vettorazzi et al (2009Vettorazzi et al ( , 2011 and Han et al (2013), included control animals. As stated by the EMEA/CPMP/SWP/1094/04 Guideline, control sampling and analytical procedures should be integrated into the toxicokinetic evaluations in order to check for possible contamination between samples during the in vivo experiment or during sample preparation.…”

Section: Analytical Techniques For Ochratoxin a Toxicokinetic Studiesmentioning

confidence: 99%

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Ochratoxin A kinetics: A review of analytical methods and studies in rat model

Vettorazzi

González-Peñas

Ceráin

2014

Food and Chemical Toxicology

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Ochratoxin A (OTA) is a thermostable mycotoxin that contaminates a great variety of foodstuffs. It is nephrotoxic in all of the mammalian species tested, being the pig the most sensitive one; among rodents, rats are the most susceptible to OTA carcinogenicity. Kinetics, by studying the absorption, distribution, metabolism and excretion of xenobiotics, is an important tool for the extrapolation of animal toxicity data. The most important kinetic studies performed with OTA in rats have been reviewed, together with the different methods used for OTA quantification in biological matrices. Thirteen studies in Wistar, Sprague-Dawley or F344 rats, using radiolabeled OTA or TLC, HPLC-FLD or HPLC-MS have been summarized. Very often methods validated for food have been directly applied to tissues. Strain, sex and age differences have been detected but the interpretation is difficult due to the different experimental conditions, and the connection of the several factors that may account for these differences.

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The influence of ochratoxin A on DNA adduct formation by the carcinogen aristolochic acid in rats

et al. 2014

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quinone oxidoreductase (NQO1) activating AA to DNA adducts, their combined treatment did not lead to either higher NQO1 enzyme activity or higher AA-DNA adduct levels in ex vivo incubations. Oxidation of AA I (8-methoxy-6-nitrophenanthro[3,4-d]-1,3-dioxole-5-carboxylic acid) to its detoxification metabolite, 8-hydroxyaristolochic acid, was lower in microsomes from rats treated with AA and OTA, and this was paralleled by lower activities of cytochromes P450 1A1/2 and/or 2C11 in these microsomes. Our results indicate that a decrease in AA detoxification after combined exposure to AA and OTA leads to an increase in AA-DNA adduct formation in liver and kidney of rats.

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Kidney and liver distribution of ochratoxin A in male and female F344 rats

Cited by 33 publications

References 24 publications

Genotoxicity of Aflatoxin B1 and Ochratoxin A after simultaneous application of the in vivo micronucleus and comet assay

Genotoxicity of Aflatoxin B1 and Ochratoxin A after simultaneous application of the in vivo micronucleus and comet assay

Ochratoxin A kinetics: A review of analytical methods and studies in rat model

The influence of ochratoxin A on DNA adduct formation by the carcinogen aristolochic acid in rats

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