Nutritional carcinogenesis
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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
Published on: December 19, 2019
1Department of Internal Medicine, Faculty of Medicine, University of Indonesia-Cipto Mangunkusumo Hospital-Dharmais Cancer Hospital, Letjen S. Parman Kav. 84-86 Slipi Jakarta Barat, Indonesia. levinapakasi@cbn.net.id
Abstract:
Human beings are often being exposed to carcinogenic factors during their life, some of which are the nutritional factors. From the mechanistic view, nutritional factors are classified into genotoxic and non-genotoxic agents. Genotoxic agent begins their action at the DNA level, causing DNA damage through several mechanisms, e.g. gene point mutations, deletions and insertions, recombinations, rearrangements and amplifications, as well as chromosomal aberrations. Most genotoxic agents are micro components of nutrition, i.e. polycyclic aromatic hydrocarbon (PAH) or heterocyclic amines (HCAs), aflatoxin, and N-nitrosamine. Non-genotoxic agents are less defined in their modes of action, but they are presumed to indirectly affect the cell through tumor promoters. These agents are generally macro components, e.g. high fat. Moreover, epigenetic factors, including changes in the DNA methylation pattern, and peroxidation process resulting reactive oxygen species (ROS), are also known to cause cancer. On the other hand, it is also well recognized that diet and nutrition contain components that can reduce the risk of cancer, in some cases by decreasing the effects of food mutagens, or through carcinogen detoxification, or protection of DNA from electrophilic carcinogen. Thus nutritionally related cancer ultimately develops from an imbalance of carcinogenesis and anti-carcinogenesis process.
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