Abstract
Epidemiology and experimental studies provide an
overwhelming support of the notion that diets high in red
or processed meat accompany an elevated risk of
developing pre-neoplastic colorectal adenoma and frank
colorectal carcinoma (CRC). The underlying mechanisms are
disputed; thus several hypotheses have been proposed. A
large body of reports converges, however, on haem and
nitrosyl haem as major contributors to the CRC
development, presumably acting through various
mechanisms. Apart from a potentially higher intestinal
mutagenic load among consumers on a diet rich in
red/processed meat, other mechanisms involving subtle
interference with colorectal stem/progenitor cell
survival or maturation are likewise at play. From an
overarching perspective, suggested candidate mechanisms
for red/processed meat-induced CRC appear as three partly
overlapping tenets: (i) increased N-nitrosation/oxidative
load leading to DNA adducts and lipid peroxidation in the
intestinal epithelium, (ii) proliferative stimulation of
the epithelium through haem or food-derived metabolites
that either act directly or subsequent to conversion, and
(iii) higher inflammatory response, which may trigger a
wide cascade of pro-malignant processes. In this review,
we summarize and discuss major findings of the area in
the context of potentially pertinent mechanisms
underlying the above-mentioned association between
consumption of red/processed meat and increased risk of
developing CRC.
Original language | English |
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Pages (from-to) | 614-634 |
Journal | Critical Reviews in Food Science and Nutrition |
Volume | 56 |
Issue number | 4 |
DOIs | |
Publication status | Published - 2016 |
MoE publication type | A1 Journal article-refereed |
Keywords
- Dietary patterns
- fat peroxidation
- haem
- morphogenetic pathways
- N-nitroso compounds
- nitrosyl-haem
- red/processed meat
- intestinal carcinogenesis