Chemistry Reference
In-Depth Information
18.3.2.5 Carcinogenesis
Colorectal cancer is the fourth most common cause of cancer morbidity and
mortality worldwide (8.9 percent of all new cancers, with about 400,000 deaths/
year). High incidence rates are found in Western Europe, North America, and
Australia.
128
Colon cancer occurs due to somatic mutations in colon cells occurring
during the lifetime of an individual. Genotoxic carcinogens including heterocyclic
aromatic amines, which are formed during cooking of meat, are a potential risk
factor of colon cancer in high meat consumers. These enzymes include glycosidase,
β-glucuronidase, azoreductase, and nitroreductase. The protective role of probiot-
ics and prebiotics in colon cancer has been reviewed in the past decade. At pres-
ent, direct experimental evidence is lacking for suppression of cancer in humans by
probiotic bacteria, but a good deal of indirect evidence has been described. Some
suggested mechanisms (Figure 18.5) are (1) inhibition of carcinogens and/or procar-
cinogens, (2) inhibition of bacteria that convert procarcinogens to carcinogens, (3)
activation of host's immune system, (4) reduction of intestinal pH to reduce micro-
bial activity, and (5) alteration of colonic motility and transit time.
In vitro
studies
have demonstrated that the cell wall of lactic acid bacteria can bind with heterocy-
clic amines.
27
There has been evidence that some probiotics produce butyric acid
and this molecule can influence the rate of apoptosis in enterocytes. Probiotics also
neutralize the activity of mutagens, such as 4-nitroquinoline-
N
-oxide, 2-nitrofluo-
rene, and benzopyrene.
128
Some probiotics may decrease the fecal concentration of
enzymes, mutagens, and secondary bile salts that may be involved in colon carcino-
genesis. Kim et al.
129
assessed the anticancer activity and bacterial enzyme inhibition
of
B. adolescentis
SPM0212.
Bifidobacterium adolescentis
SPM0212 inhibited the
proliferation of three human colon cancer cell lines: HT-29, SW 480, and Caco-2.
SPM0212 also dose-dependently inhibited TNF-α production and changes in cellular
morphology.
B. adolescentis
SPM0212 inhibited harmful fecal enzymes, including
α-glucuronidase, α-glucosidase, tryptophanase, and urease. Thus,
B. adolescentis
SPM0212 exerts an anticancer effect and inhibits harmful fecal enzymes.
Modulate
immune system
Producion of
antitumorigenic
and antimutagenic
compounds
Degrade potential
carcinogens
Probiotics in
Colon Cancer
Improve intestinal
microbiology
Alter physiochemical
condition of colon
Bind to
carcinogens
Figure 18.5
Modulatory effect of probiotics on colon cancer.
