Investigation of the tumorigenic response to benzo(a)pyrene in aqueous caffeine solution applied orally to Sprague-Dawley rats

Brune, H.; Deutsch‐Wenzel, R.; Habs, M.; Ivanković, S.; Schmähl, D.

doi:10.1007/bf00410666

Cited by 48 publications

(23 citation statements)

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“…Systemic administration produces mammary tumors; esophageal and forestomach tumors are produced by intragastric or oral administration (14)(15)(16)(17). Subcutaneous administration of BaP produces both site of injection fibrosarcomas and mammary tumors; intratracheal instillation and lung implantation both produced lung tumors (18)(19)(20)(21)(22) not been as widely studied in the rat.…”

Section: Discussionmentioning

confidence: 99%

“…Two solvent systems were routinely employed. System 1 was Dl = 1 M sodium phosphate, pH 6.0, with overnight chromatography onto a 5-cm Whatman grade 17 Chr wick, followed by a wash with water; D3 = 3.5 M lithium formate, 7 M urea, pH 3.5, with development 6-8 cm onto a Whatman-grade 1 wick, followed by a wash with water, a wash with 20 Mm This base, and an additional wash with water; D4 = 1:1 isopropanol:4 N ammonia, with development 6-8 cm onto a Whatmangrade 1 wick; and D5 = 1.7 M sodium phosphate, pH 6.8, with development 6 cm onto a Whatman-grade 1 wick. System 2 was Dl = 1 M sodium phosphate, pH 6.0, with overnight development onto a 10-cm Whatman-grade 3MM Chr wick followed by a wash with water; D2 = 2.75 M ammonium formate, developed 1 cm; D3 = 4.5 M lithium formate, 7 M urea, pH 3.5, followed by a wash with water; D4 prewash = 1 cm development with 0.5M Tris-HCl; D4 = 1.1 M lithium chloride, 0.5 M Tris-HCl, 7 M urea, pH 8.0, followed by a wash with water; and D5 = 1.0 M MgCl2, with development onto a 3-cm Whatman-grade 3MM Chr wick, followed by a final wash with water.…”

Section: Methodsmentioning

confidence: 99%

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Quantitative and Temporal Relationships between DNA Adduct Formation in Target and Surrogate Tissues: Implications for Biomonitoring

Nesnow¹,

Ross²,

Nelson³

et al. 1993

Environmental Health Perspectives

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DNA-carcinogen adducts offer a potential dosimeter for environmental genotoxicants reaching the exposed individual. Because the target tissues for many chemical carcinogens are not readily accessible for monitoring adducts in humans, peripheral blood lymphocytes (PBLs) have served as surrogate sources of exposed DNA. Both benzo[a]pyrene (BaP) and benzo [b]fluoranthene (BbF) are widely distributed in the environment as components of complex mixtures, such as automobile exhaust, cigarette smoke, foods, water, and urban air. Thus, human exposure to these chemicals is widespread, and they probably contribute to overall human lung cancer risk. The interpretation of the results of such studies would be enhanced by an understanding of the pharmacokinetics of specific DNA adduct formation and persistence in both target and surrogate tissues. Polycyclic aromatic hydrocarbons (PAHs) were administered to male Sprague-Dawley rats IP at 100 mg PAH/ kg body weight. Lung, liver, and PBL tissues were harvested 1,3, 7,14, 28, and 56 days after treatment. DNA was extracted from each tissue and 32P-postlabeling analysis of DNA adducts with nuclease P1 enhancement was conducted. In all three tissues, BaP-DNA adducts exhibit a similar pattern, reaching a maximum at 34 days, followed by a decrease to 56 days. For BbF, the maximum DNA adduct levels in each tissue were between 5 and 14 days after injection. By 56 days after administration, the total adducts remaining in all tissues were measurable. Correlation analyses ofthe amount of DNA adducts in lung or liver compared to those found in the PBL of the same animals suggest a range of correlations (R2 = 0.67-0.83). For BaP, DNA adducts in both liver and lung may be predicted by PBL DNA adduct levels. For BbF, adduct levels in PBLs directly reflect adduct levels in the liver and are less predictive of lung adduct levels. The collateral pharmacokinetics for DNA adduct persistence in lung, liver, and PBLs suggest that PBL adduct-based dosimetry may reflect patterns of adduction in other less accessible tissues. Thus, PBL DNA adducts may prove to be useful dosimeters for the delivered dose of DNA.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Quantitative and Temporal Relationships between DNA Adduct Formation in Target and Surrogate Tissues: Implications for Biomonitoring

Nesnow¹,

Ross²,

Nelson³

et al. 1993

Environmental Health Perspectives

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show abstract

“…In a lifespan study of Sprague-Dawley rats fed diets that contained benzo [a]pyrene at levels that resulted in total doses of 0, 6 or 39 mg/kg bw per year, a slightly higher incidence of forestomach papillomas was observed in high-dose animals (10/64 versus 3/64 controls; p <0.1) (Brune et al, 1981). The incidence and total number of mammary gland tumours (fibroadenomas, adenomas and adenocarcinomas) were markedly increased in female CD rats treated with benzo [a]pyrene (50 µmol [13.21 mg]) by gavage once a week for 8 weeks followed by an observation period of 41 weeks .…”

Section: Ratmentioning

confidence: 99%

Integrating Field Analyses with Laboratory Exposures to Assess Ecosystems Health

Hellou¹,

Beach²,

Leonard³

et al. 2012

Polycyclic Aromatic Compounds

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initiated a programme on the evaluation of the carcinogenic risk of chemicals to humans involving the production of critically evaluated monographs on individual chemicals. The programme was subsequently expanded to include evaluations of carcinogenic risks associated with exposures to complex mixtures, life-style factors and biological and physical agents, as well as those in specific occupations. The objective of the programme is to elaborate and publish in the form of monographs critical reviews of data on carcinogenicity for agents to which humans are known to be exposed and on specific exposure situations; to evaluate these data in terms of human risk with the help of international working groups of experts in chemical carcinogenesis Publications of the World Health Organization enjoy copyright protection in accordance with the provisions of Protocol 2 of the Universal Copyright Convention. All rights reserved.The International Agency for Research on Cancer welcomes requests for permission to reproduce or translate its publications, in part or in full. Requests for permission to reproduce or translate IARC publications -whether for sale or for noncommercial distribution -should be addressed to WHO Press, at the above address (fax: +41 22 791 4806; email: permissions@who.int).The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the World Health Organization concerning the legal status of any country, territory, city, or area or of its authorities, or concerning the delimitation of its frontiers or boundaries.The mention of specific companies or of certain manufacturers' products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.The IARC Monographs Working Group alone is responsible for the views expressed in this publication. IARC Library Cataloguing in Publication Data NOTE TO THE READERThe term 'carcinogenic risk' in the IARC Monographs series is taken to mean that an agent is capable of causing cancer under some circumstances. The Monographs evaluate cancer hazards, despite the historical presence of the word 'risks' in the title.Inclusion of an agent in the Monographs does not imply that it is a carcinogen, only that the published data have been examined. Equally, the fact that an agent has not yet been evaluated in a Monograph does not mean that it is not carcinogenic.The evaluations of carcinogenic risk are made by international working groups of independent scientists and are qualitative in nature. No recommendation is given for regulation or legislation.Anyone who is aware of published data that may alter the evaluation of the carcinogenic risk of an agent to humans is encouraged to make this information available to the Section of IARC Monographs, International Agency for...

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“…In two of these studies (Takayama and Kuwabara, 1982;Moh et al, 1984), no significant difference in the incidence of tumours at any site was found. The other three studies (Yamagami et al, 1983;Johansson, 1981;Brune et al, 1981) were found to be inadequate for evaluation (IARC, 1991). All studies on oral and intraperitoneal administration of caffeine to mice were found inadequate for evaluation.…”

Section: Studies In Experimental Animalsmentioning

confidence: 99%

Intake of caffeine and other methylxanthines during pregnancy and risk for adverse effects in pregnant women and their foetuses

Andersson¹,

Hallström²,

Kihlman³

2005

TemaNord

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Investigation of the tumorigenic response to benzo(a)pyrene in aqueous caffeine solution applied orally to Sprague-Dawley rats

Cited by 48 publications

References 5 publications

Quantitative and Temporal Relationships between DNA Adduct Formation in Target and Surrogate Tissues: Implications for Biomonitoring

Quantitative and Temporal Relationships between DNA Adduct Formation in Target and Surrogate Tissues: Implications for Biomonitoring

Integrating Field Analyses with Laboratory Exposures to Assess Ecosystems Health

Intake of caffeine and other methylxanthines during pregnancy and risk for adverse effects in pregnant women and their foetuses

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