[Preventive medicine: biomonitoring and chemoprevention].
The aim of chemoprevention is to delay or prevent the development of pathological conditions, or to correct abnormal regulatory mechanisms and in some cases even reverse the process. For this intervention to succeed, biomarkers must be found that characterize impaired health status in a phase when impairment is still reversible. Genotoxicological parameters may function as biomarkers of this kind, such as inhibition or delay of mitosis, inhibition of apoptosis, increase in the number of chromosomal aberrations, decrease in the capacity of DNA repairing enzymes, or parameters characterizing immunological status (eg. decreased NK activity). With the help of early signs, impending negative changes or illness (which could not be prevented without effective chemoprevention) can be predicted in apparently healthy individuals. Thus, the first and most important step in chemoprevention is risk characterization. Risk characterization is a complex concept, which includes risk analysis, risk assessment and risk management. Chemoprevention is a part of the latter process. Biomarkers, which can be studied mainly by up-to-date molecular biological methods, are used in discovering risk factors and also in the assessment of caused biological effects. Besides avoiding risk factors, it is very important to strengthen the protective mechanisms, to promote the metabolism of toxic substances, and to repair damage (ward off denaturation of macromolecules caused by free oxygen radicals with antioxidants for example). Chemopreventive agents are therefore diverse in their targets. Most of them have antioxidant properties, such as plant-derived substances, like glycosides, flavonoids, various vitamins, carotinoids, and some trace elements such as selenium. Another group of chemopreventive agents inhibit cell proliferation, or induce programmed cell death (apoptosis). Another group influence terminal differentiation, or inhibit angiogenesis. Some chemopreventive agents affect the metabolism or detoxification of xenobiotics, or boost the functions of the immune system. In many cases these effects are mediated by the rate of methylation of DNA molecules.
Tompa
Anna
A
Országos Kémiai Biztonsági Intézet, Fodor József Országos Közegészségügyi Központ, Budapest, 1450, Hungary. tompa.okbi@antsz.hu
Szende
Béla
B
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000008:administration & dosage*; D017209:Apoptosis; D014408:Biomarkers, Tumor / Q000097:blood*; D004249:DNA Damage; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000517:prevention & control*; D018384:Oxidative Stress; D011322:Primary Prevention / Q000379:methods; D012306:Risk; D015398:Signal Transduction / Q000187:drug effects
D000893:Anti-Inflammatory Agents; D016588:Anticarcinogenic Agents; D000975:Antioxidants; D014408:Biomarkers, Tumor