Chemical carcinogens and overnutrition in diet-related cancer

Lutz, Werner; Schlatter, Josef Rudolf

doi:10.1093/carcin/13.12.2211

Cited by 72 publications

(28 citation statements)

References 26 publications

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“…The major source of human exposure to environmental PAH contaminants on a daily weight basis is from the diet (64). This exposure pathway is consistent with a large pool of epidemiological data linking the incidence of human cancer (20-50%) and disease with dietary factors (4,10,37,38,56,63,65). Other general and speci c studies have supported this view (38,47,70).…”

Section: Introductionsupporting

confidence: 76%

Suppression of Arylamine Toxicity in the Fischer-344 Rat Following Ingestion of a Complex Mixture

et al. 2001

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The toxic effects of a mixture of 2-aminoanthracen e (2-AA), benzanthracen e (BA), and dinitropyrene isomers (DNP), and the toxic effects of these compound s individually, were investigated in the Fischer-344 rat following dietary exposure via a powdered basal diet. Animals were sacri ced at 14-, 30-, and 80-days of dietary exposure. Exposure to dietary 2-AA alone induced anorexia, cachexia, variable mortality, and altered serum chemistry pro les in the F-344 rat. Reduced lymphocyte counts were also shown in rats exposed to 2-AA. A temporal pattern of effect of 2-AA dietary exposure was observed in the progression of hepatic lesions in exposed animals. Dietary exposure to either DNP isomers or BA at a 10-fold higher concentration in the diet, relative to 2-AA, did not induce detectable toxic responses.However, exposure of rats to a mixture of 2-AA, BA, and DNP isomers (100 mg/kg, 1.0 g/kg, and 1.0 g/kg of diet, respectively) resulted in the attenuation of toxic effects when compared to exposure of F-344 rats to 2-AA alone. These results indicate that the toxic effects of 2-AA are suppressed by co-administration of DNP and BA and suggest that compoun d interactions need to be considered when predicting the toxic potential of speci c environmenta l pollutants.

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Section: Introductionsupporting

confidence: 76%

Suppression of Arylamine Toxicity in the Fischer-344 Rat Following Ingestion of a Complex Mixture

et al. 2001

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“…Evolutionary biologists have argued that aging is inevitable because of several tradeoffs (67)(68)(69)(70) (73)(74)(75)(76). It has been suggested that Darwinian fitness in animals is increased by the delay of reproductive function during periods of low food availability (77) and that the saved resources are invested in maintenance of the body until food resources are available for successful reproduction (78).…”

Section: Aging and Dietary Restrictionmentioning

confidence: 99%

Oxidants, antioxidants, and the degenerative diseases of aging.

Ames

Shigenaga

Hagen

1993

Proc. Natl. Acad. Sci. U.S.A.

5,393

2,987

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Metabolism, like other aspects of life, involves tradeoffs. Oxidant by-products of normal metabolism cause extensive damage to DNA, protein, and lipid. We argue that this damage (the same as that produced by radiation) is a major contributor to aging and to degenerative diseases of aging such as cancer, cardiovascular disease, immune-system decline, brain dysfunction, and cataracts. Antioxidant defenses against this damage include ascorbate, tocopherol, and carotenoids. Dietary fruits and vegetables are the principal source of ascorbate and carotenoids and are one source of tocopherol. Low dietary intake offruits and vegetables doubles the risk of most types of cancer as compared to high intake and also markedly increases the risk of heart dise and cataracts. Since only 9% of Americans eat the recommended five servings of fruits and vegetables per day, the opportunity for improving health by improving diet is great.The degenerative diseases associated with aging include cancer, cardiovascular disease, immune-system decline, brain dysfunction, and cataracts. The functional degeneration of somatic cells during aging appears, in good part, to contribute to these diseases. The relationship between cancer and age in various mammalian species illustrates this point. Cancer increases with about the fifth power of age in both short-lived species, such as rats, and long-lived species, such as humans. Thus a marked decrease in age-specific cancer rates has accompanied the marked increase in lifespan that has occurred in 60 million years of mammalian evolution; i.e., cancer rates are high in a 2-year-old rat, but low in a 2-year-old human. One important factor in longevity appears to be basal metabolic rate, which is about 7 times higher in a rat than in a human and which could markedly affect the level of endogenous oxidants and other mutagens produced as by-products of metabolism. The level of oxidative DNA damage appears to be roughly related to metabolic rate in a number of mammalian species (1-3).

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“…It is now well established that genetic factors play a significant role in determining risk for both cancer and coronary heart disease (198,199) and behavioral factors such as cigarette smoking and heavy consumption of alcohol also influence susceptibility to these diseases (199)(200)(201). Nevertheless, when these factors are taken into consideration, dietary caloric consumption may be one of the most important risk factors for a spectrum of human degenerative diseases (4,202), and human epidemiology studies have established that increased body weight-or body mass index (BMI)-is positively correlated to a number of morbidity/mortality indices. These include overall mortality in both men and women (13,203); cardiovascular disease (10,13,204); breast, renal, and endometrial cancer in women (205)(206)(207); and colon cancer in men (208).…”

Section: Influence Of Caloric Intake On Human Morbidity and Mortalitymentioning

confidence: 99%

Caloric restriction as a mechanism mediating resistance to environmental disease.

Frame

Hart

Leakey

1998

Environ Health Perspect

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It has been observed that susceptibility to many degenerative diseases increases concurrently with industrialization and rising living standards. Although epidemiologic studies suggest that specific environmental and dietary factors may be important, caloric intake alone (as reflected in body size) may account for much of the differential risk observed among diverse human populations. It has been suggested from animal studies that caloric intake may be the primary effector for many hormonal, metabolic, physiologic, and behavioral responses that coordinate reproductive strategy to apparent availability of food. When caloric intake is excessive, particularly at critical developmental stages, physiologic priorities are set for body growth and fecundity rather than for endurance and longevity. The converse occurs during periods of famine, thus increasing the probability that sufficient individuals survive to restore the population when conditions improve. Calorically restricted rodents have significantly longer reproductive and total life spans than their ad libitum-fed controls and exhibit a spectrum of biochemical and physiologic alterations that characterize their adaptation to reduced caloric intake. These include reduced stature, hypercorticism in the absence of elevated adrenocorticotropic hormone levels, increased metabolic efficiency, decreased mitogenic response coupled with increased rates of apoptosis, reduced inflammatory response, induction of stress proteins and DNA repair enzymes, altered drug-metabolizing enzyme expression, and modified cell-mediated immune function. The overall profile of these changes is one of improved defense against environmental stress. This has been suggested as the mechanistic basis for the protective effects of low body weight on radiationand chemically induced cancers in experimental animals. It may also explain the significantly higher thresholds of acute toxicity observed when calorically restricted rodents are exposed to certain test compounds.

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Chemical carcinogens and overnutrition in diet-related cancer

Cited by 72 publications

References 26 publications

Suppression of Arylamine Toxicity in the Fischer-344 Rat Following Ingestion of a Complex Mixture

Suppression of Arylamine Toxicity in the Fischer-344 Rat Following Ingestion of a Complex Mixture

Oxidants, antioxidants, and the degenerative diseases of aging.

Caloric restriction as a mechanism mediating resistance to environmental disease.

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