Genotoxicity of ochratoxin a in mice: DNA single-strand break evaluation in spleen, liver and kidney

Creppy, E. E.; Kane, Amadou; Dirheimer, G.; Lafarge‐Frayssinet, C.; Mousset, Sabine; Frayssinet, C

doi:10.1016/0378-4274(85)90006-2

Cited by 145 publications

(79 citation statements)

References 11 publications

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“…In addition, immunohistochemical analysis clearly demonstrated the site-specific localization of γ-H2AX-positive cells in the OS tubular epithelium of OM 73) . Comet assays using OMs of gpt delta rats treated with OTA yielded positive results 73) that were suggestive of DNA strand breaks, as was previously reported [85][86][87][88] . Concerning the detrimental effects of OTA on steric DNA structures, the formation of OTA-specific DNA adducts was observed in human tissues by 32 P postlabeling methods, and was confirmed by mass spectrum analysis in animal tissues [89][90][91][92] .…”

Section: Modes Of Carcinogenic Actionsupporting

confidence: 54%

Possible Carcinogenic Mechanisms Underlying Renal Carcinogens in Food

Umemura

2014

Food Safety

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Some chemicals contained in foods originating from a variety of sources including natural plants, food additives, residual pesticides, mycotoxins and by-products created during food processing and/or cooking have previously been demonstrated to be carcinogenic at various sites in rodents. This review focuses on reported renal carcinogens in natural products such as d-limonene and aristolochic acid (AA), food additives such as potassium bromate (KBrO 3 ) and madder color (MC), as well as mycotoxins such as ochratoxin A (OTA) and citrinin (CTN) and discusses data from reporter gene mutation assays. In addition to in vivo genotoxicity, recent information on several factors related to chemical carcinogenesis, such as DNA modifications and cell proliferation, gave insight into possible modes of action that underlie renal carcinogenesis. Given that neither d-limonene nor CTN induced increases in mutant frequencies (MFs) in some reporter genes, cell proliferation at target sites arising from compensatory and/or direct mitogenic action may play a key role in the carcinogenic mechanism of these compounds. Clear positive results from reporter gene mutation assays for AA, MC and OTA strongly suggest that genotoxic mechanisms are involved in carcinogenesis induced by these agents. While KBrO 3 elevated MFs in the red/gam gene (Spi − ), it did so to a lower extent than did potent genotoxic carcinogens. Accordingly, the participation of genotoxic mechanisms in KBrO 3 -induced renal carcinogenesis may be limited.

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Section: Modes Of Carcinogenic Actionsupporting

confidence: 54%

Possible Carcinogenic Mechanisms Underlying Renal Carcinogens in Food

Umemura

2014

Food Safety

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“…OTA has been reported as both nonmutagenic (IARC, 1993;Kuiper-Goodman and Scott, 1989) and mutagenic (Obrecht-Pflumio et al, 1999) in a variety of microbial genotoxicity tests. The formation of DNA adducts by a reactive metabolite (Castegarno et al, 1998;Creppy et al, 1985;Pfohl-Leszkowicz et al, 1991, 1993, sister chromatid exchange (Föllmann et al, 1995), unscheduled DNA synthesis (Doerrenhaus et al, 2000), and the generation of reactive oxygen species have been proposed as candidate mechanisms. However, neither the oxidative changes nor the DNA adducts reported could be corroborated using HPLC-MS or LC-MS/MS (Gautier et al, 2001a;Zepnik et al, 2001).…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Mycotoxins Affecting the Kidney

O'Brien¹,

Dietrich²

2004

Target Organ Toxicology Series

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“…OTA-induced damage to DNA, evidenced by formation of single-strand breaks, has been reported to occur both in vitro and in vivo (Creppy et al, 1985). The DNA damage was shown to be reversible with time suggesting that variation in capacity to repair DNA may account in part for differences in vulnerability to OTA between tissues.…”

Section: Introductionmentioning

confidence: 99%

“…In addition to nephrotoxicity, OTA disrupts blood coagulation (Galtier et al, 1979;Gupta et al, 1979) and glucose metabolism (Pitout, 1968). It is immunosuppressive (Creppy et al, 1983b;Haubeck et al, 1981;Lea et al, 1989;Stormer and Lea, 1995), teratogenic (Arora et al, 1983;Fukui et al, 1992;Szczech and Hood, 1981) and genotoxic (Creppy et al, 1985;Pfohl-Leszkowicz et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

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Brain's DNA Repair Response to Neurotoxicants

Sanchez‐Ramos¹

2005

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE (DD-MM-YYYY) 01-07-2005 REPORT TYPE Annual DATES COVERED (From -To PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERUniversity of Florida Tampa, FL 33620 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel CommandFort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTESOriginal contains color plates: All DTIC reproductions will be in black and white. ABSTRACTParkinson's Disease (PD) is associated with death of dopaminergic (DA) neurons in the substantia nigra (SN) of the brain. Military personnel abroad are at a greater risk of exposure to pesticides and toxins which may selectively damage DA neurons in the SN and increase the probability of development of Parkinson's disease (PD) later in life. The toxins of interest are mitochondrial poisons that create a bioenergetic crisis and generate toxic oxyradicals which damage macromolecules, including DNA. We hypothesize that regulation of the DNA repair response within certain neurons of the SN (the pars compacta) may be a critical determinant for their vulnerability to these neurotoxicants. We have measured regional differences in the brain's capacity to increase repair of oxidized DNA (indicated by oxyguanosine glycosylase (OGG1) activity) to three distinct chemical classes of neurotoxins (MPTP, two mycotoxins, and an organochloriine pesticide). At the end of the second year of the project, we have found that the temporal and spatial profile of OGG1 activity across brain regions elicted by each class of neurotoxicant is distinct and unique. Although all three toxicants cause DA depletion in striatum, only MPTP caused loss of DA neurons in midbrain. However, it is possible that superimposition of age-related loss of DA neurons over the moderate DS depletion caused by OTA may result in early onset parkinsonism. SUBJECT TERMSNo subject terms provided. REPAIR RESPONSES ELICITED BY MYCOTOXINS (OCHRATOXIN-A, RUBRATOXIN), ORGANOC...

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Genotoxicity of ochratoxin a in mice: DNA single-strand break evaluation in spleen, liver and kidney

Cited by 145 publications

References 11 publications

Possible Carcinogenic Mechanisms Underlying Renal Carcinogens in Food

Possible Carcinogenic Mechanisms Underlying Renal Carcinogens in Food

Mycotoxins Affecting the Kidney

Brain's DNA Repair Response to Neurotoxicants

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