Abstract
Whether disruption of iron metabolism is implicated in human muscle aging is presently unclear. We explored the relationship among iron metabolism, muscle mitochondrial homeostasis, inflammation, and physical function in older adults and young controls. Eleven young and 23 older men and women were included. Older adults were classified into high–functioning (HF) and low–functioning (LF) groups according to their Short Physical Performance Battery score. Vastus lateralis muscle biopsies were assayed for total iron content, expression of 8-oxoguanine and DNA glycosylase (OGG1), 3-nitrotyrosine (3-NT) levels, and mitochondrial DNA (mtDNA) content and damage. Circulating ferritin and hepcidin levels were also quantified. Muscle iron levels were greater in the old group. Protein expression of transferrin receptor 1, Zrt-Irt-like protein (ZIP) 8, and ZIP14 were lower in old participants. Circulating levels of ferritin, hepcidin, interleukin 6 (IL6), and C-reactive protein were higher in the old group. Old participants showed lower mtDNA content and greater mtDNA damage. OGG1 protein expression declined with age, whereas 3-NT levels were greater in old participants. Finally, a negative correlation was determined between ZIP14 expression and circulating IL6 levels in LF older adults. None of assayed parameters differed between HF and LF participants. Our findings suggest that muscle iron homeostasis is altered in old age, which might contribute to loss of mtDNA stability. Muscle iron metabolism may therefore represent a target for interventions against muscle aging.
Highlights
Iron is the most abundant transition metal in living organisms and is involved in multiple biochemical processes including oxygen binding and transport, energy production, regulation of cellCells 2019, 8, 1525; doi:10.3390/cells8121525 www.mdpi.com/journal/cellsCells 2019, 8, 1525 growth and differentiation, and a variety of enzyme reactions
In the attempt to shed light on this relevant research question, we determined the relative content of mitochondrial DNA (mtDNA) and mtDNA damage load in muscle samples of young and old enrollees
Iron homeostasis is altered in muscle of old rodents, possibly contributing to muscle fibre atrophy
Summary
Iron is the most abundant transition metal in living organisms and is involved in multiple biochemical processes including oxygen binding and transport, energy production, regulation of cell. 5% of cellular iron exists as chelatable non-haem iron, referred to as labile iron pool This iron fraction consists of both ferrous (Fe2+ ) and ferric (Fe3+ ) ions associated with a variety of small molecules, including organic anions, polypeptides, and phospholipids. Studies have shown that non-haem iron accumulates in muscle during ageing possibly causing oxidative damage to biomolecules and organelles, including mitochondria [14,15,16,17,18]. To provide an initial appraisal of the subject, the present study was undertaken to assess total iron content, the expression of selected iron transporters, and indexes of mitochondrial damage in muscle biopsies obtained from healthy young adults and older people with varying levels of physical performance. The relationship between muscle iron content and systemic inflammation was explored
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