Accumulation of promutagenic DNA adducts in the mouse distal colon after consumption of heme does not induce colonic neoplasms in the western diet model of spontaneous colorectal cancer. Issue 3 (1st October 2013)
- Record Type:
- Journal Article
- Title:
- Accumulation of promutagenic DNA adducts in the mouse distal colon after consumption of heme does not induce colonic neoplasms in the western diet model of spontaneous colorectal cancer. Issue 3 (1st October 2013)
- Main Title:
- Accumulation of promutagenic DNA adducts in the mouse distal colon after consumption of heme does not induce colonic neoplasms in the western diet model of spontaneous colorectal cancer
- Authors:
- Winter, Jean
Young, Graeme P.
Hu, Ying
Gratz, Silvia W.
Conlon, Michael A.
Le Leu, Richard K. - Abstract:
- <abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2091-sec-0010" sec-type="section"> <title>Scope</title> <p>Red meat is considered a risk factor for colorectal cancer (CRC). Heme is considered to promote colonic hyperproliferation and cell damage. Resistant starch (RS) is a food that ferments in the colon with studies demonstrating protective effects against CRC. By utilizing the western diet model of spontaneous CRC, we determined if feeding heme (as hemin chloride) equivalent to a high red meat diet would increase colonic DNA adducts and CRC and whether RS could abrogate such effects.</p> </sec> <sec id="mnfr2091-sec-0020" sec-type="section"> <title>Methods and results</title> <p>Four groups of mice: control, heme, RS and heme + RS were fed diets for 1 or 18 months. Colons were analyzed for apoptosis, proliferation, DNA adducts "8‐hydroxy‐2‐deoxyguanosine" and "O<sup>6</sup>‐methyl‐2‐deoxyguanosine" (O<sup>6</sup>MeG), and neoplasms. In the short term, heme increased cell proliferation (<italic>p</italic> &lt; 0.05). Changes from 1 to 18 months showed increased cell proliferation (<italic>p</italic> &lt; 0.01) and 8‐hydroxy‐2‐deoxyguanosine adducts (<italic>p</italic> &lt; 0.05) in all groups, but only heme‐fed mice showed reduced apoptosis (<italic>p</italic> &lt; 0.01) and increased O<sup>6</sup>MeG adducts (<italic>p</italic> &lt; 0.01). The incidence of colon neoplasms was not different between any interventions.</p><abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2091-sec-0010" sec-type="section"> <title>Scope</title> <p>Red meat is considered a risk factor for colorectal cancer (CRC). Heme is considered to promote colonic hyperproliferation and cell damage. Resistant starch (RS) is a food that ferments in the colon with studies demonstrating protective effects against CRC. By utilizing the western diet model of spontaneous CRC, we determined if feeding heme (as hemin chloride) equivalent to a high red meat diet would increase colonic DNA adducts and CRC and whether RS could abrogate such effects.</p> </sec> <sec id="mnfr2091-sec-0020" sec-type="section"> <title>Methods and results</title> <p>Four groups of mice: control, heme, RS and heme + RS were fed diets for 1 or 18 months. Colons were analyzed for apoptosis, proliferation, DNA adducts "8‐hydroxy‐2‐deoxyguanosine" and "O<sup>6</sup>‐methyl‐2‐deoxyguanosine" (O<sup>6</sup>MeG), and neoplasms. In the short term, heme increased cell proliferation (<italic>p</italic> &lt; 0.05). Changes from 1 to 18 months showed increased cell proliferation (<italic>p</italic> &lt; 0.01) and 8‐hydroxy‐2‐deoxyguanosine adducts (<italic>p</italic> &lt; 0.05) in all groups, but only heme‐fed mice showed reduced apoptosis (<italic>p</italic> &lt; 0.01) and increased O<sup>6</sup>MeG adducts (<italic>p</italic> &lt; 0.01). The incidence of colon neoplasms was not different between any interventions.</p> </sec> <sec id="mnfr2091-sec-0030" sec-type="section"> <title>Conclusion</title> <p>We identified heme to increase proliferation in the short term, inhibit apoptosis over the long term, and increase O<sup>6</sup>MeG adducts in the colon over time although these changes did not affect colonic neoplasms within this mouse model.</p> </sec> </abstract> … (more)
- Is Part Of:
- Molecular nutrition & food research. Volume 58:Issue 3(2014:Mar.)
- Journal:
- Molecular nutrition & food research
- Issue:
- Volume 58:Issue 3(2014:Mar.)
- Issue Display:
- Volume 58, Issue 3 (2014)
- Year:
- 2014
- Volume:
- 58
- Issue:
- 3
- Issue Sort Value:
- 2014-0058-0003-0000
- Page Start:
- 550
- Page End:
- 558
- Publication Date:
- 2013-10-01
- Subjects:
- Food -- Biotechnology -- Periodicals
Food -- Microbiology -- Periodicals
Nutrition -- Periodicals
Food -- Toxicology -- Periodicals
Nutrition -- Periodicals
Food Microbiology -- Periodicals
Food Technology -- Periodicals
Molecular Biology -- Periodicals
664.0705 - Journal URLs:
- http://onlinelibrary.wiley.com/ ↗
- DOI:
- 10.1002/mnfr.201300430 ↗
- Languages:
- English
- ISSNs:
- 1613-4125
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 5900.817992
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 3214.xml