Abstract
Physical training and antioxidant supplementation may influence iron metabolism through reduced oxidative stress and subsequent lowering of mRNA levels of genes that are easily induced by this stress, including those responsible for iron homeostasis. Fifteen elderly women participated in our 12-week experiment, involving six weeks of training without supplementation and six weeks of training supported by oral supplementation of 1000 mg of vitamin C daily. The participants were divided into two groups (n = 7 in group 1 and n = 8 in group 2). In group 1, we applied vitamin C supplementation in the first six weeks of training, while in group 2 during the remaining six weeks of training. In both phases, the health-related training occurred three times per week. Training accompanied by vitamin C supplementation did not affect prooxidative/antioxidative balance but significantly decreased ferritin heavy chain (FTH) and ferritin light chain (FTL) mRNA in leukocytes (for FTH mRNA from 2^64.24 to 2^11.06, p = 0.03 in group 1 and from 2^60.54 to 2^16.03, p = 0.01 in group 2, for FTL mRNA from 2^20.22 to 2^4.53, p = 0.01 in group 2). We concluded that vitamin C supplementation might have caused a decrease in gene expression of two important antioxidative genes (FTH, FTL) and had no effect on plasma prooxidative/antioxidative balance.
Highlights
Oxidative stress can influence iron metabolism and iron-regulatory protein status [1]
The aim of this study was to evaluate the effects of sessions of six-week endurance training with and without six-week oral vitamin C supplementation (1000 mg daily) on plasma oxidative stress and antioxidant capacity, as well as on genes associated with cellular stress response and iron metabolism
Our findings indicated that six weeks of training supported by daily supplementation of 1000 mg of vitamin C did not influence prooxidative/antioxidative balance but did cause a significant decrease in ferritin heavy chain (FTH) and ferritin light chain (FTL) mRNA levels in elderly women
Summary
Oxidative stress can influence iron metabolism and iron-regulatory protein status [1]. Genes associated with cellular stress response and iron metabolism, such as FTH1 (ferritin heavy chain 1), FTL (ferritin light chain), PCBP1 (poly(rC)-binding protein 1), PCBP2 (poly(rC)-binding protein 2), FOXO3a (forkhead box O3A), or CAT (catalase) are induced by oxidative stress. Oxidants can directly induce ferritin gene expression by targeting conserved regions of these genes [2] as well as by regulating the activity of mRNA at transcriptional levels, and proteins at post-transcriptional levels [3]. Inactivation of iron-regulating protein 1 (IPR1) by oxidative stress can be associated with not blocking ferritin mRNA [4]. Expression of these genes is directly regulated by cellular iron status. It is well known that these genes represent the level of the labile iron pool (LIP), and their upregulation or downregulation is associated with free iron levels [5,6]
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