Dietary Carcinogens and Anticarcinogens

Ames, Bruce N.

doi:10.1126/science.6351251

Cited by 2,749 publications

(775 citation statements)

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“…Yet, in the past several years, an increasing number of basic and clinical studies have pointed to the role of the reactive metabolites of oxygen, the free radicals, in these pathological processes, and the potential protective effect of antioxidant nutrients such as bcarotene, vitamin C, vitamin E, selenium and zinc (Ames, 1987;Halliwell & Gutteridge, 1989;Diplock, 1991;Byers & Perry, 1992;Frei, 1994;Hercberg et al, 1998a).…”

Section: Introductionmentioning

confidence: 99%

Serum concentrations of β-carotene, vitamins C and E, zinc and selenium are influenced by sex, age, diet, smoking status, alcohol consumption and corpulence in a general French adult population

Fe²,

et al. 2005

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Objective: To assess relationships between energy, nutrient and food intakes, alcohol consumption, smoking status and body mass index (BMI), and serum concentrations of b-carotene, a-tocopherol, vitamin C, selenium and zinc. Methods: Data on health status, alcohol consumption, smoking habits, anthropometric data and biochemical measurements were obtained in 1821 women aged 35-60 y and 1307 men aged 45-60 y, participant to the SU.VI.MAX Study. Data on dietary intake were available on a subsample who reported six 24-h dietary records during the first 18 months of the study. Results: Women had higher baseline serum b-carotene and vitamin C concentrations and lower concentration for serum vitamin E, zinc and selenium than men. In women, younger age was associated with lowered mean concentration of serum b-carotene, vitamin E and selenium. In men, only differences were observed for serum zinc, which was lower in older men. Current smokers of both sexes had significantly lower concentrations of serum b-carotene, vitamin C and selenium, and, only in women, of vitamin E, than nonsmokers. Alcohol consumers had lower concentrations of serum b-carotene and higher selenium concentrations. Serum b-carotene and vitamin C concentrations were lower in obese subjects. There were positive associations of dietary b-carotene, vitamin C and E with their serum concentrations. Age, nutrient and alcohol intakes, serum cholesterol, BMI and smoking status explained 15.2% of the variance of serum b-carotene in men and 13.9% in women, and 10.8 and 10.0% for serum vitamin C, and 26.3 and 28.6% for serum vitamin E, respectively. Conclusion: Serum antioxidant nutrient concentrations are primarily influenced by sex, age, obesity, tobacco smoking, alcohol consumption and especially dietary intake of those antioxidant nutrients. IntroductionCigarette smoking, obesity and some dietary patterns are well-known risk factors for both cardiovascular disease and cancer (WCRF/AIC; Kromhout, 2001). Yet, in the past several years, an increasing number of basic and clinical studies have pointed to the role of the reactive metabolites of oxygen, the free radicals, in these pathological processes, and the potential protective effect of antioxidant nutrients such as bcarotene, vitamin C, vitamin E, selenium and zinc (Ames, Halliwell & Gutteridge, 1989;Diplock, 1991;Byers & Perry, 1992;Frei, 1994;Hercberg et al, 1998a).Epidemiological data from cross-sectional, case-control, and prospective studies have shown a strong relationship between the intake of foods rich in antioxidant vitamins and minerals, or the actual intake of these nutrients, and the risk of cancer and ischaemic cardiovascular diseases (CVD) (Block et al, 1992;Stampfer & Rimm, 1993;Byers & Guerrero, 1995;Kohlmeier & Hastings, 1995;Stampfer & Rimm, 1995;Hercberg et al, 1998a). However, most of published randomized placebo-controlled primary prevention trials have not been able to demonstrate these potential beneficial effects (Blot et al, 1993; The AlphaTocopherol, Beta Carotene Cancer Preventi...

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Section: Introductionmentioning

confidence: 99%

Serum concentrations of β-carotene, vitamins C and E, zinc and selenium are influenced by sex, age, diet, smoking status, alcohol consumption and corpulence in a general French adult population

Fe²,

et al. 2005

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“…Replication errors by DNA polymerases and DNA lesions induced by mutagens cause mutations that are recognized as important steps in carcinogenesis [1][2][3][4]. The chemically modified DNA bases change the genetic information by base mismatch formation.…”

Section: Introductionmentioning

confidence: 99%

“…The chemically modified DNA bases change the genetic information by base mismatch formation. DNA is damaged by many endogenous/environmental mutagens, such as reactive oxygen species (ROS), which are byproducts of respiration, ultraviolet and ionizing irradiation [3,4]. The accumulation of DNA lesions seems to be involved in aging and neurodegeneration, in addition to mutagenesis and carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

UvrA and UvrB enhance mutations induced by oxidized deoxyribonucleotides

et al. 2007

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Oxidatively damaged DNA precursors (deoxyribonucleotides) are formed by reactive oxygen species. After the damaged DNA precursors are incorporated into DNA, they might be removed by DNA repair enzymes. In this study, to examine whether a nucleotide excision repair enzyme, Escherichia coli UvrABC, could suppress the mutations induced by oxidized deoxyribonucleotides in vivo, oxidized DNA precursors, 8-hydroxy-2´-deoxyguanosine 5´-triphosphate and 2-hydroxy-2´-deoxyadenosine 5´-triphosphate, were introduced into uvrA, uvrB, and uvrC E. coli strains, and mutations in the chromosomal rpoB gene were analyzed. Unexpectedly, these oxidized DNA precursors induced mutations only slightly in the uvrA and uvrB strains. In contrast, effect of the uvrC-deficiency was not observed. Next, mutT, mutT/uvrA, and mutT/uvrB E. coli strains were treated with H 2 O 2 , and the rpoB mutant frequencies were calculated. The frequency of the H 2 O 2 -induced mutations was increased in all of the strains tested; however, the increase was threeto four-fold lower in the mutT/uvrA and mutT/uvrB strains than in the mutT strain. Thus, UvrA and UvrB are involved in the enhancement, but not in the suppression, of the mutations induced by these oxidized deoxyribonucleotides. These results suggest a novel role for UvrA and UvrB in the processing of oxidative damage.

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“…The protumoral effects by ROS, including gene expression regulation (Allen and Tresini, 2000), increased mutagenic rates (Irani et al, 1997) and genomic instability (Woo and Poon, 2004) may occur at different levels. High levels of ROS have been detected in cancer cell lines and tumors from different tissues (Fernandez-Pol et al, 1982;Szatrowski and Nathan, 1991;Toyokuni et al, 1995), supporting the causal link between oxidative stress and cancer (Ames, 1983;Wagner and Nebreda, 2009;Cuadrado and Nebreda, 2010). ROS increases are sensed by p38a, and activation of p38 a limits the oncogenic capability of MAP17 by driving these cells to senescence or apoptosis.…”

Section: Discussionmentioning

confidence: 96%

p38α limits the contribution of MAP17 to cancer progression in breast tumors

et al. 2012

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MAP17 is a small, 17-kDa, non-glycosylated membrane protein that is overexpressed in a percentage of carcinomas. In the present work, we have analyzed the role of MAP17 expression during mammary cancer progression. We have found that MAP17 is expressed in 60% human mammary tumors while it is not expressed in normal or benign neoplasias. MAP17 levels increased with breast tumor stage and were strongly correlated with mammary tumoral progression. A significant increase in the levels of reactive oxygen species (ROS) was observed in MAP17-expressing cells, as compared with parental cells. This increase was further paralleled by an increase in the tumorigenic capacity of carcinoma cells but not in immortal non-tumoral breast epithelial cells, which provides a selective advantage once tumorigenesis has begun. Expression of specific MAP17 shRNA in proteinexpressing tumor cells reduced their tumorigenic capabilities, which suggests that this effect is dependent upon MAP17 protein expression. Our data show that ROS functions as a second messenger that enhances tumoral properties, which are inhibited in non-tumoral cells. We have found that p38a activation mediates this response. MAP17 triggers a ROS-dependent, senescence-like response that is abolished in the absence of p38a activation. Furthermore, in human breast tumors, MAP17 activation is correlated with a lack of phosphorylation of p38a. Therefore, MAP17 is overexpressed in late-stage breast tumors, in which oncogenic activity relies on p38 insensitivity to induce intracellular ROS.

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Dietary Carcinogens and Anticarcinogens

Cited by 2,749 publications

References 171 publications

Serum concentrations of β-carotene, vitamins C and E, zinc and selenium are influenced by sex, age, diet, smoking status, alcohol consumption and corpulence in a general French adult population

Serum concentrations of β-carotene, vitamins C and E, zinc and selenium are influenced by sex, age, diet, smoking status, alcohol consumption and corpulence in a general French adult population

UvrA and UvrB enhance mutations induced by oxidized deoxyribonucleotides

p38α limits the contribution of MAP17 to cancer progression in breast tumors

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