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Elevated caspase-3 and Fas mRNA expression in jejunum of adult rats during subclinical zinc deficiency

Authors :
Andrea Didier
Michael W. Pfaffl
Wilhelm Windisch
Source :
Journal of Trace Elements in Medicine and Biology. 18:41-45
Publication Year :
2004
Publisher :
Elsevier BV, 2004.

Abstract

The programmed cell death-so-called apoptosis-is a physiological process occurring in all multicellular organisms to control cell-number homeostasis. Nevertheless, increase of apoptotic cell death in different organs can lead to pathological alterations. As zinc is a potent inhibitor of apoptosis, we investigated the influence of zinc deficiency on mRNA expression levels of caspase-3 and Fas in adult rats. For this purpose, 24 adult rats fed a Zn-deficient diet for up to 29 days were compared to seven animals in the control group. After 1, 2, 4, 7, 11, 16, 22 and 29 days of treatment three animals were sacrificed (n = 24). Total RNA extraction from thymus, liver, jejunum and colon was carried out. Samples were reverse transcribed and subjected to real-time PCR. Relative quantification of caspase-3 and Fas mRNA expression was achieved on the basis of normalisation by glycerolaldehyd-3-phosphate-dehydrogenase mRNA expression levels in all samples. In jejunum, up to day 11 the relative mRNA expression of the respective genes decreased. A significant increase in caspase-3 and Fas expression was found from day 11 of zinc deficiency onward. In contrast, mRNA expression in liver and colon remained unaffected, whereas thymus showed a slight but not significant increase in the expression of these genes. This study provides the first evidence that even moderate zinc deficiency in an adult, non-growing rat model is able to elevate mRNA expression levels of factors involved in early stages of apoptosis.

Details

ISSN :
0946672X
Volume :
18
Database :
OpenAIRE
Journal :
Journal of Trace Elements in Medicine and Biology
Accession number :
edsair.doi.dedup.....45e960b5b30fc5fb6e98db5ec06be034
Full Text :
https://doi.org/10.1016/j.jtemb.2004.04.006