Chemoprevention: increased potential to bear fruit

Auteur(s) :
Wolf CR.
Date :
Mar, 2001
Source(s) :
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. #98:6 p2941-2943
Adresse :
"WOLF CR,UNIV DUNDEE,NINEWELLS HOSP & MED SCH IMPERIAL CANC RES FUND MOL PHARMACOL UNIT,BIOMED RES CTR;DD1 9SY DUNDEE, SCOTLAND.rooney@icrf.icnet.uk"

Sommaire de l'article

The prevention of degenerative disease through dietary intervention (chemoprevention), either by the recommendation of specific diets or by the use of dietary supplements, has enormous potential for improving human health. This is particularly the case for the prevention of cancer, where current therapeutic approaches are crude or limited. It has been appreciated through history that diet can affect disease pathogenesis and progression. However, it is only in recent times that we have begun to gain an understanding of what the dietary factors are and how they act at a mechanistic level.

There is strong epidemiological evidence that a diet of fruit and vegetables can prevent a range of human cancers (1, 2). This, together with laboratory studies, led to the proposal that the major protective dietary components are antioxidants such as vitamin C, vitamin E, β-carotene, etc.; the specific hypothesis was that these antioxidant free radical scavenging agents protect against the toxic or mutagenic effects of reactive oxygen species generated either endogenously in the body or by exogenous chemicals present in food, water, or air (3).

The seminal work from the laboratories of Wattenberg, Talalay, and Conney has profoundly altered our perspectives on this theme. During the 1970s, Wattenberg's group (4) demonstrated that a wide range of nonnutrient dietary chemicals other than those described above, as well as phenolic antioxidants, can profoundly inhibit chemical carcinogenesis in laboratory animals. These effects were ascribed to the ability of these agents to influence both the metabolism and disposition of the carcinogen, and also to enhance the cellular capacity to combat oxidative stress (5–8). Essentially two mechanisms were proposed that involved either the inhibition of carcinogen activation, free radical production and sequestering of reactive oxygen species, or the induction of drug and foreign compound metabolizing enzymes that protect cells from …

Source : Pubmed
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