User:Anthpulido/sandbox

Anthpulido/sandbox
	Chemical structure of carboxyethyllysine
Names
	Other names CEL
Identifiers
CAS Number	5746-04-3;
3D model (JSmol)	Interactive image;
	SMILES OC(CNCCCC[C@H](N)C(O)=O)=O;
Properties
Chemical formula	C8H16N2O4
Molar mass	204.2
	Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). Infobox references

Anthpulido/sandbox
Names
	Other names IUPAC: (2S)-2-Amino-6-(carboxymethylamino)hexanoic acid
Identifiers
CAS Number	5746-04-3 S ;
3D model (JSmol)	Interactive image; Interactive image;
Beilstein Reference	4989963 S
ChEBI	CHEBI:53014 ;
ChemSpider	11217184 ; 110350 S ; 21467765 R ;
MeSH	N(6)-carboxymethyllysine
PubChem CID	15691192; 26175690 R; 123800 S;
	InChI InChI=1S/C8H16N2O4/c9-6(8(13)14)3-1-2-4-10-5-7(11)12/h6,10H,1-5,9H2,(H,11,12)(H,13,14) Key: NUXSIDPKKIEIMI-UHFFFAOYSA-N ;
	SMILES NC(CCCCNCc(:[o]):[oH])c(:[o]):[oH]; NC(CCCCNCC(O)=O)C(O)=O;
Properties
Chemical formula	C8H16N2O4
Molar mass	204.226 g·mol−1
Related compounds
	Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). verify (what is ?) Infobox references

This is the user sandbox of Anthpulido. A user sandbox is a subpage of the user's user page. It serves as a testing spot and page development space for the user and is not an encyclopedia article. Create or edit your own sandbox here.

Other sandboxes: Main sandbox | Template sandbox

Finished writing a draft article? Are you ready to request review of it by an experienced editor for possible inclusion in Wikipedia? Submit your draft for review!

Please do not move until April 21st.

Typing a fake sentence for a fake reference ^[1]

^ Person, Fake. Fake Book Title. 2012. Notareal University.

N(6)-Carboxymethyllysine (CML), also known as N(epsilon)-(carboxymethyl)lysine, is an advanced glycation endproduct (AGE). CML has been the most used marker for AGEs in food analysis. ^[2]

CML is a common side product of metabolic pathways. CML forms when the products of an Amadori rearrangement react with amino acids. CML is a reversible AGE with high heat stability. Unlike many AGEs, CML lacks fluorescence or any cross-links. ^[3]

Mechanism of Action

CML is made by an interaction between amino acids and reducing sugars, called a Maillard reaction. Formation of reactive oxygen species is the major cause of the reactions forming CML. There has also been an correlation between oxidative glycation and the presence of free radicals. ^[4]

Effects

CML has oxidative properties, and like many AGEs are suspected to contribute to aging and diseases, including diabetes, obesity, [cardiovascular disease]], and dementia. ^[5] ^[6]

Food

CML is often found in foods ^[7], but the direct impact of dietary AGEs is still speculated ^[8]. Increased levels of CML and carboxyethyllysine are apparent when ground beef is heated. The increased heat accelerates the reaction process leading to AGE production, allowing for four predicted pathways depending on heating conditions. ^[9]

Multiple foods have chemicals known to inhibit glycation effects: ·garlic ·tomato paste

or CML production: ·cinnamon ·certain teas ·certain herbs

References

^ PubChem CID: 123800
^ Semba RD, Nicklett EJ, Ferrucci L (2010). "Does accumulation of advanced glycation end products contribute to the aging phenotype?". THE JOURNALS OF GERONTOLOGY. 65A (9): 963–975. doi:10.1093/gerona/glq074. PMC 2920582. PMID 20478906.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Wu, C.H., Huang, S. M., Lin, J. A., and Yen, G. C. (2011) Inhibition of advanced glycation endproduct formation by foodstuffs. Food & Function 2. 224.
^ Hunt JV1, Wolff SP. Oxidative glycation and free radical production: a causal mechanism of diabetic complications. Free Radic Res Commun.
^ J.M. Ames. Evidence against dietary advanced glycation endproducts being a risk to human health. Molecular Nutrition & Food Research, 51 (2007), pp. 1085–1090
^ Du H, Li P, Wang J., Qing X, Li W. 2012. The interaction of amyloid β and the receptor for advanced glycation end- products induces matrix metalloproteinase-2 expression in brain endothelial cells. Cell Mol Neurobiol 32:141–7.
^ Du H, Li P, Wang J., Qing X, Li W. 2012. The interaction of amyloid β and the receptor for advanced glycation end-products induces matrix metalloproteinase-2 expression in brain endothelial cells. Cell Mol Neurobiol 32:141–7.
^ J.M. Ames. Evidence against dietary advanced glycation endproducts being a risk to human health. Molecular Nutrition & Food Research, 51 (2007), pp. 1085–1090
^ http://www.sciencedirect.com.ezproxy.neu.edu/science/article/pii/S0308814614015143

Category:Amino acid derivatives

This biochemistry article is a stub. You can help Wikipedia by expanding it.

(NEW ARTICLE HERE) GLYCOTOXIN--------

Glycotoxins are sugar-based metabolic byproducts that primarily contribute to oxidative stress. Glycotoxins often refer to advanced glycation endproducts (AGEs) which are formed by formation of a sugar and a protein ^[1] ^[2]. The term may also describe reactive oxygen species that lead to the formation of AGEs. These reactive oxygen species come from the carbonyl groups of sugars and sugar byproducts, which are commonly AGE precursors. Some AGE precursors include methylglyoxal, glyoxal, and 3-deoxyglucosone. With hyperglycemia or diabetes, there is a correlation with an increase in glycotoxin concentration. ^[3]

References

^ Cai, W., Uribarri, J., Zhu, L., Chen, X., Swamy, S., Zhao, Z., Grosjean, F., Simonaro, C., Kuchel, G. A., Schnaider-Beeri, M., Woodward, M., Striker, G. E., and Vlassara, H. (2014) Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans. PNAS 111.
^ Wu, C.H., Huang, S. M., Lin, J. A., and Yen, G. C. (2011) Inhibition of advanced glycation endproduct formation by foodstuffs. Food & Function 2. 224.
^ Cai, W., Uribarri, J., Zhu, L., Chen, X., Swamy, S., Zhao, Z., Grosjean, F., Simonaro, C., Kuchel, G. A., Schnaider-Beeri, M., Woodward, M., Striker, G. E., and Vlassara, H. (2014) Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans. PNAS 111.

(NEW ARTICLE HERE) CARBOXYETHYLLYSINE----

N(6)-Carboxyethyllysine (CEL), also known as N(epsilon)-(carboxyethyl)lysine, is an advanced glycation endproduct (AGE). ^[1]

^ Semba RD, Nicklett EJ, Ferrucci L (2010). "Does accumulation of advanced glycation end products contribute to the aging phenotype?". THE JOURNALS OF GERONTOLOGY. 65A (9): 963–975. doi:10.1093/gerona/glq074. PMC 2920582. PMID 20478906.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[1] Person, Fake. Fake Book Title. 2012. Notareal University.

[2] PubChem CID: 123800

[3] Semba RD, Nicklett EJ, Ferrucci L (2010). "Does accumulation of advanced glycation end products contribute to the aging phenotype?". THE JOURNALS OF GERONTOLOGY. 65A (9): 963–975. doi:10.1093/gerona/glq074. PMC 2920582. PMID 20478906.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[4] Wu, C.H., Huang, S. M., Lin, J. A., and Yen, G. C. (2011) Inhibition of advanced glycation endproduct formation by foodstuffs. Food & Function 2. 224.

[5] Hunt JV1, Wolff SP. Oxidative glycation and free radical production: a causal mechanism of diabetic complications. Free Radic Res Commun.

[6] J.M. Ames. Evidence against dietary advanced glycation endproducts being a risk to human health. Molecular Nutrition & Food Research, 51 (2007), pp. 1085–1090

[7] Du H, Li P, Wang J., Qing X, Li W. 2012. The interaction of amyloid β and the receptor for advanced glycation end- products induces matrix metalloproteinase-2 expression in brain endothelial cells. Cell Mol Neurobiol 32:141–7.

[8] Du H, Li P, Wang J., Qing X, Li W. 2012. The interaction of amyloid β and the receptor for advanced glycation end-products induces matrix metalloproteinase-2 expression in brain endothelial cells. Cell Mol Neurobiol 32:141–7.

[9] J.M. Ames. Evidence against dietary advanced glycation endproducts being a risk to human health. Molecular Nutrition & Food Research, 51 (2007), pp. 1085–1090

[10] ttp://www.sciencedirect.com.ezproxy.neu.edu/science/article/pii/S0308814614015143

[11] Cai, W., Uribarri, J., Zhu, L., Chen, X., Swamy, S., Zhao, Z., Grosjean, F., Simonaro, C., Kuchel, G. A., Schnaider-Beeri, M., Woodward, M., Striker, G. E., and Vlassara, H. (2014) Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans. PNAS 111.

[12] Wu, C.H., Huang, S. M., Lin, J. A., and Yen, G. C. (2011) Inhibition of advanced glycation endproduct formation by foodstuffs. Food & Function 2. 224.

[13] Cai, W., Uribarri, J., Zhu, L., Chen, X., Swamy, S., Zhao, Z., Grosjean, F., Simonaro, C., Kuchel, G. A., Schnaider-Beeri, M., Woodward, M., Striker, G. E., and Vlassara, H. (2014) Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans. PNAS 111.

[14] Semba RD, Nicklett EJ, Ferrucci L (2010). "Does accumulation of advanced glycation end products contribute to the aging phenotype?". THE JOURNALS OF GERONTOLOGY. 65A (9): 963–975. doi:10.1093/gerona/glq074. PMC 2920582. PMID 20478906.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[1]

[1]

[2]

[3]

[4]

[5]

[6]

[7]

[8]

[9]

[1]

[2]

[3]

[1]