The critical DNA damage by benzo(a)pyrene in lung tissues of smokers and approaches to preventing its formation

Alexandrov, K.; Rojas, Margarita; Satarug, Soisungwan

doi:10.1016/j.toxlet.2010.04.009

Cited by 106 publications

(73 citation statements)

References 38 publications

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“…Bladder cancer risk fell by 30% in the first 4 years after smoking cessation while a further 30% reduction occurred in 20 years later (Samanic et al 2006). Such decade-long carry over effects argue that the carcinogenic agents in tobacco such as benzo(a)pyrene, tobacco specific nitrosamines that undergo rapid clearance by cytochrome P450 enzymes (Alexandrov et al 2010) may not play a key role, but those like cadmium that are retained in bladder tissues over an extended period may be causative. Indeed, in a 20-yr Belgian cohort, Nawrot et al (2008) noted that blood and urinary cadmium levels fell slowly with a yearly decline rate at 1.8% and 3.4%, respectively, as environmental exposure continued.…”

Section: Metallothionein Sequestration and Cadmium's Long Half-lifementioning

confidence: 99%

“…CYP2A6 and CYP2E1 are involved in the activation of liver carcinogens. Induction of CYP2A6 and CYP2E1 by cadmium could be another mechanism underlying increased susceptibility to liver disease and liver cancer since a CYP-mediated reaction is a known source of free radicals that cause mitochondrial malfunction (Gobe and Crane 2010) and DNA damage (Alexandrov et al 2010). …”

Section: Hypothetical Liver Cell Model Showing Molecular Targets Of Cmentioning

confidence: 99%

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Emerging Roles of Cadmium and Heme Oxygenase in Type-2 Diabetes and Cancer Susceptibility

Satarug

2012

Tohoku J. Exp. Med.

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Many decades after an outbreak of severe cadmium poisoning, known as Itai-itai disease, cadmium continues to pose a significant threat to human health worldwide. This review provides an update on the effects of this environmental toxicant cadmium, observed in numerous populations despite modest exposure levels. In addition, it describes the current knowledge on the link between heme catabolism and glycolysis. It examines novel functions of heme oxygenase-2 (HO-2) that protect against type 2-diabetes and obesity, which have emerged from diabetic/obese phenotypes of the HO-2 knockout mouse model. Increased cancer susceptibility in type-2 diabetes has been noted in several large cohorts. This is a cause for concern, given the high prevalence of type-2 diabetes worldwide. A lifetime exposure to cadmium is associated with pre-diabetes, diabetes, and overall cancer mortality with sex-related differences in specific types of cancer. Liver and kidney are target organs for the toxic effects of cadmium. These two organs are central to the maintenance of blood glucose levels. Further, inhibition of gluconeogenesis is a known effect of heme, while cadmium has the propensity to alter heme catabolism. This raises the possibility that cadmium may mimic certain HO-2 deficiency conditions, resulting in diabetic symptoms. Intriguingly, evidence has emerged from a recent study to suggest the potential interaction and co-regulation of HO-2 with the key regulator of glycolysis: 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 4 (PFKFB4). HO-2 could thus be critical to a metabolic switch to cancer-prone cells because the enzyme PFKFB and glycolysis are metabolic requirements for cell proliferation and resistance to apoptosis.

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Section: Metallothionein Sequestration and Cadmium's Long Half-lifementioning

confidence: 99%

Section: Hypothetical Liver Cell Model Showing Molecular Targets Of Cmentioning

confidence: 99%

Emerging Roles of Cadmium and Heme Oxygenase in Type-2 Diabetes and Cancer Susceptibility

Satarug

2012

Tohoku J. Exp. Med.

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“…BaP is found in cigarettes, food and automobile exhausts (6). BaP causes DNA adduct formation, which is the initiating event in carcinogenesis (7).…”

Section: Introductionmentioning

confidence: 99%

“…The present study investigated the association between laricitrin and the BaP-associated lung cancer tumor microenvironment. 6 cells/100 mm dish) were treated with or without BaP (Sigma-Aldrich) at a concentration of 10 µM for 6 h. Subsequent to washing and culturing for 24 h, the CM of BaP-treated H1395, H1975, H2087 and HCC2935 cells (BaP-H1395-CM, BaP-H1975-CM, BaP-H2087-CM and BaP-HCC2935-CM, respectively) were harvested (Fig. 1A).…”

Section: Introductionmentioning

confidence: 99%

Laricitrin suppresses increased benzo(a)pyrene-induced lung tumor-associated monocyte-derived dendritic cell cancer progression

et al. 2016

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Abstract. Benzo(a)pyrene (BaP) stimulates lung cancer cells, promoting monocyte-derived dendritic cells to secrete soluble factors, including heparin binding-epidermal growth factor and C-X-C motif chemokine 5. The secretions from monocyte-derived dendritic cells stimulate the progression of lung cancer cells, including the migration and invasion of cells. To the best of our knowledge, these secretions remain unknown, and require additional study. The present study identified that treatment with BaP-H1395-tumor-associated dendritic cell-conditioned medium had the most marked effect on cell migration and invasion. This result may be associated with the female gender, stage 2 adenocarcinoma or mutation of the proto-oncogene B-Raf (BRAF), according to the cell line background. Laricitrin, a dietary flavonoid derivative present in grapes and red wine, suppresses certain factors and decreases the progression of lung cancer cells that are promoted by BaP in the lung cancer tumor microenvironment. The results of the present study suggest that prolonged exposure to BaP exacerbates lung cancer, particularly in female lung cancer patients with the BRAF mutation, but that laricitrin may ameliorate this effect.

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“…Against this background, we have focused on the relationships between DNA damage, chromosomal aberration, gene mutation and these diseases. It is considered that the starting point of these diseases is gene mutation, following DNA damage induced by endogenous and exogenous stresses, such as cigarette smoke, ultraviolet radiation, ionizing radiation and reactive oxygen species (ROS) generated in energy metabolism (Alexandrov et al, 2010;Ikehata & Ono, 2011;Lagerwerf et al, 2011;Mladenov & Iliakis, 2011;Murata et al, 2012). These stresses induce DNA damage and genomic dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of raw and cooked blackcurrant extract on DNA damage induced by hydrogen peroxide in human lymphoblastoid cells

Yamamoto

Nakashima

Kawamorita

et al. 2014

Pharmaceutical Biology

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Context: Blackcurrant (Ribes nigrum L.) is a classical fruit that has long been used to make juice, liqueur and sometimes medicines in Europe. The beneficial effects of blackcurrant, which are inhibition of lipopolysaccharide-stimulated inflammatory, anticarcinogenesis and other health effects, have been reported. Objective: Previously, we reported the antimutagenic activities of blackcurrant using a yeast gene mutation assay. In this study, we investigated whether this antimutagenicity of blackcurrant was confirmed in human cells. Materials and methods:We prepared four types of aqueous blackcurrant extracts (BCE) from mature and premature with or without heat treatment by microwave. Antioxidant activities of BCE were measured by the DPPH radical scavenger assay. In the DPPH radical scavenger assay, the maximum concentration of BCE was 1.6 mg/reaction. We investigated the antigenotoxic activities of BCE by the comet assay and micronucleus test using the human lymphoblastoid cell line TK6. In the comet assay, TK6 was treated with 300 mM H 2 O 2 without or with BCE at concentrations of 0.5, 1.0, 2.0 and 3.0 mg/mL. In the micronucleus test, TK6 was treated with 1 mg/mL BCE without or with H 2 O 2 . Results: All BCEs exhibited more than 90% of inhibition rates of DPPH radicals at the maximum concentration of BCE. DNA damage and micronuclei induced by H 2 O 2 significantly decreased in the each BCE-treated condition. Conclusion:The results suggest that BCE treatment can reduce the genomic instability induced by H 2 O 2 in human cells. We consider that these antigenotoxic effects are related to polyphenols, L-ascorbic acid and other antioxidant compounds.

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The critical DNA damage by benzo(a)pyrene in lung tissues of smokers and approaches to preventing its formation

Cited by 106 publications

References 38 publications

Emerging Roles of Cadmium and Heme Oxygenase in Type-2 Diabetes and Cancer Susceptibility

Emerging Roles of Cadmium and Heme Oxygenase in Type-2 Diabetes and Cancer Susceptibility

Laricitrin suppresses increased benzo(a)pyrene-induced lung tumor-associated monocyte-derived dendritic cell cancer progression

Protective effects of raw and cooked blackcurrant extract on DNA damage induced by hydrogen peroxide in human lymphoblastoid cells

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