The Malmö biomarker programme

Publisher Website
Google Scholar
Abstract
Evaluation of pro‐oxidant/antioxidant dietary factors in relation to individual susceptibility to cancer and cardiovascular disease is justified based on a review of the literature. This working hypothesis is amendable to further scientific validation from biomarkers with end‐point sensitivity to oxygen radicals. So far, the biomarker programme developed around this theme may be divided into three distinct classes:(1) Markers of genotoxic exposure estimate DNA damage either directly as a bilogically effective dose, or indirectly by estimating aberrant cellular functions that lead to accumulation of DNA damage. The examples included are ADP‐ribosylation in mononuclear leucocytes (R. Pero, A. Olsson), oxidative DNA damage (K. Frenkel), gene expression in lymphocytes (S. Garte. G. Cosma), serum alpha macroglobulin (W. Troll) and oxidized DNA damage and repair (N. Christie).(2) Markers of genetic predisoposition have been shown to have genetic inheritance patterns that relate to individual susceptibility to cancer or cardiovascular disease. The examples included are glutathione transferase mu phenotyping (R. Pero. J. Seidegård) and poly (ADP‐ribose) polymerase pseudogene polymorphism (M. Smulson).(3) Markers of dietary status have been validated to estimate the amount of a particular nutrient or xenobiotic in the diet that has been taken up and metabolized or distributed to body fluids or tissues. The example included here is niacin nutriture (E. Jacobson. M. Jacobson). This biomarker is presented in Section 5 (pp. 59–62) of the Malmö Diet and Cancer Programme Minisymposium reported in this issue of the journal.

This publication has 24 references indexed in Scilit: