Mutagenic activation and detoxification of benzo[a]pyrene in vitro by hepatic cytochrome P450 1A1 and phase II enzymes in three meat-producing animals

Darwish, Wageh Sobhy; Ikenaka, Yoshinori; Eldaly, Elsaid A.; Ishizuka, Mayumi

doi:10.1016/j.fct.2010.06.026

Cited by 16 publications

(11 citation statements)

References 31 publications

(37 reference statements)

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“…This indicated that folic acid played an important role of antagonism to the BaPinduced mutagenicity. BaP acted as the indirect mutagen in the experiment and was activated by microsome oxidase into benzopyrene dihydrodiol epoxide (BPDE) that resulted in DNA damage (23). While folic acid, the necessary micro vitamin for DNA metabolic activity, was involved in the repair of DNA and was benefi cial for the synthesis of DNA at certain doses (24), which might explain the antimutagenicity of folic acid.…”

Section: Discussionmentioning

confidence: 99%

Folic Acid Supplementation Reduces the Mutagenicity and Genotoxicity Caused by Benzo(a)pyrene

Zhang

Zhan

et al. 2016

J Nutr Sci Vitaminol

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Summary Folate is a vital vitamin for the human being and its defi ciency can lead to a variety of clinical abnormalities ranging from neural tube defects to cancers. Benzo(a)pyrene (BaP), a strong mutagen and carcinogen, is considered one of the common contaminants in food. The aim of this study was to investigate the positive effect of folate on cancer prevention at a fundamental level. In the present study, we investigated the impact of folic acid on BaP-induced mutagenicity and genotoxicity by means of in vitro and in vivo experiments. The reformed Ames test was applied to study the antimutagenicity of folic acid against BaP. The protective effect of folic acid on cytotoxicity caused by BaP in human liver cell line L02 was evaluated by MTT assay. In addition, the effect of folic acid on the BaP-induced genotoxicity in vivo was assessed by mouse bone marrow micronucleus assay. The results indicated that folic acid signifi cantly inhibited the reverse mutation of Salmonella typhimurium strains TA98 and TA100, and protected the viability of human liver cells against BaP (pϽ0.01). The micronucleus test showed that all doses of folic acid had a remarkable protective effect for the female mice (pϽ0.01). In conclusion, folic acid was found to reduce the mutagenicity and genotoxicity induced by BaP.

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Section: Discussionmentioning

confidence: 99%

Folic Acid Supplementation Reduces the Mutagenicity and Genotoxicity Caused by Benzo(a)pyrene

Zhang

Zhan

et al. 2016

J Nutr Sci Vitaminol

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“…Benzo(a)pyrene induces the expression of bioactivation enzymes in liver to a greater extent than detoxifying enzymes (90). Our earlier observations in F-344 rat model revealed that dietary exposure to B(a)P resulted in higher induction of aryl hydrocarbon hydroxylase activities in liver (66).…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Polycyclic Aromatic Hydrocarbons and Digestive Tract Cancers: A Perspective

Diggs

Huderson

Harris

et al. 2011

Journal of Environmental Science and Health, Part C

233

107

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Cancers of the colon are most common in the Western world. In majority of these cases, there is no familial history and sporadic gene damage seems to play an important role in the development of tumors in the colon. Studies have shown that environmental factors, especially diet, play an important role in susceptibility to GI tract cancers. Consequently, environmental chemicals that contaminate food or diet during its preparation becomes important in the development of GI cancers. Polycyclic aromatic hydrocarbons (PAHs) are one such family of ubiquitous environmental toxicants. These pollutants enter the human body through consumption of contaminated food, drinking water, inhalation of cigarette smoke, automobile exhausts, and contaminated air from occupational settings. Among these pathways, dietary intake of PAHs constitutes a major source of exposure in humans. Although many reviews and books on PAHs and their ability to cause toxicity and breast or lung cancer have been published, aspects on contribution of diet, smoking and other factors towards development of digestive tract cancers and strategies to assess risk from exposure to PAHs have received much less attention. This review, therefore, focuses on dietary intake of PAHs in humans, animal models, and cell cultures used for GI cancer studies along with epidemiological findings. Bioavailability and biotransformation processes, which influence the disposition of PAHs in body and the underlying causative mechanisms of GI cancers, are also discussed. The existing data gaps and scope for future studies is also emphasized. This information is expected to stimulate research on mechanisms of sporadic GI cancers caused by exposure to environmental carcinogens.

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“…The Ames test was performed using the S. typhimurium strain TA98 and the S9 fractions (4 mg protein/mL) according to our previous modifications (Darwish and others ) of the preincubation method of Ames and others (). In brief, 500 μL of the S9 fraction containing the complete NADPH‐generating system and NADH, as well as 100 μL of an overnight culture of TA98 and coenzymes (30 mM GSH and 15 mM UDPGA, or 0.1 M KPB as a control) were added to the test tubes.…”

Section: Methodsmentioning

confidence: 99%

“…Heterocyclic amines’ (HCAs) mutagens are formed during cooking of food, particularly meat, at high temperatures. Ingestion of contaminated foods is considered the major route of exposure to xenobiotics such as polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines (Darwish and others ; Maté and others ; Ho and others ). Xenobiotic metabolism takes place predominantly in the liver, although extra‐hepatic tissues, including the gastrointestinal tract (GIT), have capacity for numerous phase I and II metabolic reactions.…”

Section: Introductionmentioning

confidence: 99%

Metabolic Activation of Heterocyclic Amines and Expression of Xenobiotic‐Metabolizing Enzymes in the Gastrointestinal Tract of Rats

Darwish

Nakayama

Itotani

et al. 2015

Journal of Food Science

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ABSTRACT:28 Heterocyclic amines (HCAs) get entry into human body mainly through ingestion of 29 pan-fried meats cooked at high temperatures. Exposure of the gastrointestinal tract (GIT) to 30 ingested xenobiotics prior to delivery to the liver may lead to metabolic activation, which may 31 explain the high incidence of GIT carcinogenesis. Therefore, the current study investigated the 32 mutagenic activation of two heterocyclic amines, 2-aminoanthracene (2-AA) and 3-amino-1- and rectum, and it was detected at high levels in the ileum and cecum. Furthermore, we 37 revealed high metabolic activation of 2-AA and Trp-P-2 in the jejunum. The mRNA expression 38 of phase I and II enzymes in rat GIT corresponded with their mutagenic activation ability. In 39 conclusion, our results suggest that different expression levels of XME among GIT tissues may 40 contribute to the tissue-specific differences in metabolic activation of xenobiotics such as 41 heterocyclic amines in rats.

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Mutagenic activation and detoxification of benzo[a]pyrene in vitro by hepatic cytochrome P450 1A1 and phase II enzymes in three meat-producing animals

Cited by 16 publications

References 31 publications

Folic Acid Supplementation Reduces the Mutagenicity and Genotoxicity Caused by Benzo(a)pyrene

Folic Acid Supplementation Reduces the Mutagenicity and Genotoxicity Caused by Benzo(a)pyrene

Polycyclic Aromatic Hydrocarbons and Digestive Tract Cancers: A Perspective

Metabolic Activation of Heterocyclic Amines and Expression of Xenobiotic‐Metabolizing Enzymes in the Gastrointestinal Tract of Rats

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