Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.freeradbiomed.2006.03.017
DC FieldValue
dc.titleZinc supplementation decreases the development of atherosclerosis in rabbits
dc.contributor.authorRen, M.
dc.contributor.authorRajendran, R.
dc.contributor.authorWatt, F.
dc.contributor.authorNing, P.
dc.contributor.authorJenner, A.
dc.contributor.authorHalliwell, B.
dc.contributor.authorTan, Kwong Huat B.
dc.contributor.authorChoon, Nam O.
dc.date.accessioned2011-11-29T06:11:24Z
dc.date.available2011-11-29T06:11:24Z
dc.date.issued2006
dc.identifier.citationRen, M., Rajendran, R., Watt, F., Ning, P., Jenner, A., Halliwell, B., Tan, Kwong Huat B., Choon, Nam O. (2006). Zinc supplementation decreases the development of atherosclerosis in rabbits. Free Radical Biology and Medicine 41 (2) : 222-225. ScholarBank@NUS Repository. https://doi.org/10.1016/j.freeradbiomed.2006.03.017
dc.identifier.issn08915849
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/28952
dc.description.abstractDeveloping atherosclerotic plaques in cholesterol-fed rabbits are enriched in iron but depleted in zinc. In order to examine further the role of zinc, New Zealand White rabbits were fed a high-cholesterol 1% (w/w) diet with zinc (1 g/kg) supplementation for 8 weeks. After the 8-week period, the average atherosclerotic lesion cross-sectional areas in the aortas of the animals fed with the zinc supplement were significantly decreased (1.0 mm2) compared with lesion areas of the animals fed only on the high-cholesterol diet (3.1 mm2). Using nuclear microscopy, a technique for mapping and measuring trace elements in tissue sections, lesion zinc levels (24 ppm) were observed to be unchanged in the zinc-fed rabbits compared to controls. However, average lesion Fe levels in the zinc-fed group were measured at 32 ppm, whereas in the control group the average Fe levels were significantly higher at 43 ppm (P = 0.03). Our data support the concept that zinc may have an antiatherogenic effect by decreasing iron levels in the lesion, possibly leading to inhibition of iron-catalyzed free radical reactions. © 2006 Elsevier Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.freeradbiomed.2006.03.017
dc.sourceScopus
dc.subjectAtherosclerosis
dc.subjectFree radicals
dc.subjectIron
dc.subjectLesion area
dc.subjectNuclear microscopy
dc.subjectZinc
dc.subjectZinc supplement
dc.typeArticle
dc.contributor.departmentBIOCHEMISTRY
dc.contributor.departmentPHYSICS
dc.contributor.departmentPHARMACOLOGY
dc.contributor.departmentCOMMUNITY,OCCUPATIONAL & FAMILY MEDICINE
dc.description.doi10.1016/j.freeradbiomed.2006.03.017
dc.description.sourcetitleFree Radical Biology and Medicine
dc.description.volume41
dc.description.issue2
dc.description.page222-225
dc.description.codenFRBME
dc.identifier.isiut000239039900008
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