Assessment of the protective effects of selected dietary anticarcinogens against DNA damage and cytogenetic effects induced by benzo[a]pyrene in C57BL/6J mice

Gradecka-Meesters, Dobrosława; Palus, Jadwiga; Prochazka, Gabriela; Segerbäck, Dan; Dziubałtowska, Elżbieta; Kotova, Natalia; Jenssen, Dag; Arkusz, Joanna; Lundin, Cecilia; Vikström, Elisabet; Rydzyński, K; Nilsson, Robert; Stępnik, Maciej

doi:10.1016/j.fct.2011.02.021

Cited by 16 publications

(5 citation statements)

References 70 publications

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“…Our findings with CHL are supported by a study in which mice were given a single oral dose of BP with or without CHL (45). These investigators found no alteration of BP-DNA adduct levels in the liver or leukocyte DNA, determined by 32 P-post labeling, when CHL was fed for a week prior to the administration of a single dose of BP.…”

Section: Dna Adducts In Organs Of Mice Fed Bpsupporting

confidence: 83%

Benzo[a]pyrene (BP) DNA adduct formation in DNA repair-deficient p53 haploinsufficient [Xpa(-/-)p53(+/-)] and wild-type mice fed BP and BP plus chlorophyllin for 28 days

et al. 2012

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We have evaluated DNA damage (DNA adduct formation) after feeding benzo[a]pyrene (BP) to wild-type (WT) and cancer-susceptible Xpa(-/-)p53(+/-) mice deficient in nucleotide excision repair and haploinsufficient for the tumor suppressor p53. DNA damage was evaluated by high-performance liquid chromatography/electrospray ionization tandem mass spectrometry (HPLC/ES-MS/MS), which measures r7,t8,t9-trihydroxy-c-10-(N (2)-deoxyguanosyl)-7,8,9,10-tetrahydrobenzo[a]pyrene (BPdG), and a chemiluminescence immunoassay (CIA), using anti-r7,t8-dihydroxy-t-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE)-DNA antiserum, which measures both BPdG and the other stable BP-DNA adducts. When mice were fed 100 ppm BP for 28 days, BP-induced DNA damage measured in esophagus, liver and lung was typically higher in Xpa(-/-)p53(+/-) mice, compared with WT mice. This result is consistent with the previously observed tumor susceptibility of Xpa(-/-)p53(+/-) mice. BPdG, the major DNA adduct associated with tumorigenicity, was the primary DNA adduct formed in esophagus (a target tissue in the mouse), whereas total BP-DNA adducts predominated in higher levels in the liver (a non-target tissue in the mouse). In an attempt to lower BP-induced DNA damage, we fed the WT and Xpa(-/-)p53(+/-) mice 0.3% chlorophyllin (CHL) in the BP-containing diet for 28 days. The addition of CHL resulted in an increase of BP-DNA adducts in esophagus, liver and lung of WT mice, a lowering of BPdG in esophagi of WT mice and livers of Xpa(-/-)p53(+/-) mice and an increase of BPdG in livers of WT mice. Therefore, the addition of CHL to a BP-containing diet showed a lack of consistent chemoprotective effect, indicating that oral CHL administration may not reduce PAH-DNA adduct levels consistently in human organs.

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Section: Dna Adducts In Organs Of Mice Fed Bpsupporting

confidence: 83%

Benzo[a]pyrene (BP) DNA adduct formation in DNA repair-deficient p53 haploinsufficient [Xpa(-/-)p53(+/-)] and wild-type mice fed BP and BP plus chlorophyllin for 28 days

et al. 2012

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“…CHL was found to reduce chromosomal aberrations induced by ethyl methane sulfonate in cultured mammalian cells during S and G2/S phase of the cell cycle as well as the formation of micronuclei (MN) and bone marrow toxicity in sodium nitrite treated mice (17,18). Oral administration of CHL was shown to protect against induction of DNA single strand breaks and MN in B[a] P treated C57BL/6J mice (19).…”

Section: Antigenotoxic Effectsmentioning

confidence: 98%

Chemopreventive Potential of Chlorophyllin: A Review of the Mechanisms of Action and Molecular Targets

Nagini

Palitti

Natarajan

2015

Nutrition and Cancer

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“…The protective action from orally administered ellagic acid (EA), benzyl isothiocyanate (BITC), an extract of epigallocatechins (Tegreen ® ) as well as chlorophyllin (CHL) against benzo[a]pyrene (B[a]P)-induced DNA damage and cytogenetic effects was investigated. In Comet assay, CHL or EA caused a 3-fold decrease of SSB, and a 2-fold decrease of FPG sites in comparison to animals treated with B[a]P [69]. Pre-incubation with low micromolar level polyphenols, quercetin or rutin can significantly attenuate DNA damage in cell lines, indicating that the polyphenols did not work through an enzymatic mechanism.…”

Section: Chemoprevention Of Oxidative Dna Damages For Workers' Healthmentioning

confidence: 99%

Oxidative DNA damages by chemical exposures at work

Rim¹

2012

ABB

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ABSTRACTdiseases. These include cancer, Parkinson's disease, Alzheimer's disease, atherosclerosis, heart failure, myocardial infarction, Schizophrenia, bipolar disorder, fragile X syndrome, sickle cell disease and chronic fatigue syndrome. Oxidative stress is likely to be involved in agerelated development of cancer. The reactive species produced in oxidative stress can cause direct damage to the DNA and are therefore mutagenic, and it may also suppress apoptosis and promote proliferation, invasiveness and metastasis [1].Oxidative DNA damage is an inevitable consequence of cellular metabolism, with a propensity for increased levels following toxic insult. Of the molecules subject to oxidative modification, DNA has received the greatest attention, with biomarkers of exposure and effect closest to validation. There are many chemicals in workplaces that could cause oxidative DNA damages such as carcinogens. This review concentrated on studies published between the years 2000 and 2012 that used to detect 8-oxodG in humans (workers), laboratory animals and in cell lines. Given the recent toxicological results from oxidative stress, it is important to review these studies to improve the current understanding of the oxidative DNA damages by chemical exposures at work. It also suggests that biomarkers may be responsible for understanding the role of oxidative DNA damage in disease, highlighting the need for further studies.

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Assessment of the protective effects of selected dietary anticarcinogens against DNA damage and cytogenetic effects induced by benzo[a]pyrene in C57BL/6J mice

Cited by 16 publications

References 70 publications

Benzo[a]pyrene (BP) DNA adduct formation in DNA repair-deficient p53 haploinsufficient [Xpa(-/-)p53(+/-)] and wild-type mice fed BP and BP plus chlorophyllin for 28 days

Benzo[a]pyrene (BP) DNA adduct formation in DNA repair-deficient p53 haploinsufficient [Xpa(-/-)p53(+/-)] and wild-type mice fed BP and BP plus chlorophyllin for 28 days

Chemopreventive Potential of Chlorophyllin: A Review of the Mechanisms of Action and Molecular Targets

Oxidative DNA damages by chemical exposures at work

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