Akademik Veri Yönetim Sistemi
Molecular Biology and Biotechnology Congress, Konya, Türkiye, 25 - 27 Nisan 2018, ss.228
Iron is an essential nutrient for all living organisms. Although it is required for many
vital biological processes such as energy production, oxygen transport, synthesis
of DNA, RNA and protein, the accumulation of iron in the body produces reactive
oxygen species which causes oxidative stress. Thus, preventing oxidative damage
via antioxidant system is indispensable for cell survival. Since the misregulation of
iron metabolism may cause cardiovascular diseases, cancer, neurodegenerative diseases,
and thalassemia, iron homeostasis is firmly regulated to organize a complex
biochemical network in the body. In the present study, effects of iron overload on
thioredoxin reductase (TrxR), which is one of the enzymatic antioxidant system, was
investigated in mouse heart at the gene and protein levels. For this purpose, 10 male
BALB/c mice were divided into 2 groups. Control group was intraperitoneally injected
with 0.5 mg of dextran 5 solution. In the treatment group, 5 mg iron dextran solution
was intraperitoneally injected twice weekly for 3 weeks to form systemic iron
loading. The expression of hepcidin (Hamp), ferroportin (Fpn), ferritin (Fth) genes
was examined by qPCR in mouse heart. Quantitative iron content, GSH level, and
TrxR enzyme activities were examined. According to our results, quantitative iron
content was significantly increased. However, no changes were seen in GSH level.
While the gene expressions of Hamp and Fpn was increased, no changes were seen in
Fth expression. TrxR enzyme activity was significantly increased. It may be said that
TrxR protects the cell against iron-overload induced oxidative stress in mouse heart.
Keywords: Iron, Hepcidin, Oxidative stress, Thioredoxin reductase