Oxidative Stress and Iron Homeostasis: Mechanistic and Health Aspects

Galaris, Dimitrios; Pantopoulos, Kostas

doi:10.1080/10408360701713104

Cited by 302 publications

(211 citation statements)

References 143 publications

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“…In other words, excess iron promoted the activity of osteoclasts, and then elevated bone resorption process, with resultant loss of bone strength. In terms of the molecular mechanisms, previous studies have demonstrated that intracellular iron retention would cause massive production of reactive oxygen species (ROS) through Fenton reaction (Fridovich, 1978;Galaris and Pantopoulos, 2008;Halliwell and Gutteridge, 1990), and ROS is postulated to be an instigator of bone resorption (Jia et al, 2012). Jia and colleagues demonstrated that iron overload could promote osteoclast differentiation and bone resorption through stimulation of ROS (Ishii et al, 2009;Yamasaki and Hagiwara, 2009).…”

Section: Discussionmentioning

confidence: 99%

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Sun

Guo

Yin

et al. 2014

Gene

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Osteoporosis is one of the leading disorders among aged people. Bone loss results from a number of physiological alterations, such as estrogen decline and aging. Meanwhile, iron overload has been recognized as a risk factor for bone loss. Systemic iron homeostasis is fundamentally governed by the hepcidin-ferroportin regulatory axis, where hepcidin is the key regulator. Hepcidin deficiency could induce a few disorders, of which iron overload is the most representative phenotype. However, there was little investigation of the effects of hepcidin deficiency on bone metabolism. To this end, hepcidin-deficient (Hamp1 −/− ) mice were employed to address this issue. Our results revealed that significant iron overload was induced in Hamp1 −/− mice. Importantly, significant decreases of maximal loading and maximal bending stress were found in Hamp1 −/− mice relative to wildtype (WT) mice.Moreover, the levels of the C-telopeptide of type I collagen (CTX-1) increased in Hamp1 −/− mice. Therefore, hepcidin deficiency resulted in a marked reduction of bone load-bearing capacity likely through enhancing bone resorption, suggesting a direct correlation between hepcidin deficiency and bone loss. Targeting hepcidin or the pathway it modulates may thus represent a therapeutic for osteopenia or osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Sun

Guo

Yin

et al. 2014

Gene

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“…Studies have shown that iron deficiency and excess can cause damage to the body. Iron deficiency can cause iron deficiency anemia, while excessive iron intake can lead to excessive production of oxygen free radicals [1] , which can cause the damage of the tissue and organs [2,3] . Studies have found that iron deficiency can cause liver fibrosis and hepatocellular carcinoma [4] ,while the increasing risk of hemochromatosis patients who suffering from liver cancer is related to abnormal high iron levels in the liver of chronic liver injury [5] .…”

Section: Introductionmentioning

confidence: 99%

Effects of Iron Overload on Growth and Intestinal Mucosa in Rats

Jiang¹,

Sun²,

Gong³

et al. 2017

ijSciences

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Objective: To detect the mechanism of excess iron intake on growth and intestinal mucosa in rats. Methods: Forty-eight male Wistar rats were randomly divided into four groups: Low Iron Group, Normal Iron Group, Medium Iron Group and High Iron Group upon daily iron intake of 7mg/kg, 16.8mg/kg, 35mg/kg, 70mg/kg respectively via fodder for eight weeks. The general condition, body weight and food intake were documented simultaneously. Serum level of Ferritin, IL-6 and IL-10 were detected using ELISA. The observation of morphology of intestine was also included concurrently. Results: The weight obtained was significantly lower in the High Iron Group compared with the other three groups while the average weight of the rats in the High Iron Group was lower than the Normal Iron Group. Meanwhile, the average amount food uptake of the High Iron Group had slightly decreased in the eighth week. In addition, the level of IL-6 in small intestine of the High Iron Group is higher than that of the Normal Iron Group (P<0.05), while the level of IL-10 in small intestine of the High Iron Group is lower than that of the Normal Iron Group (P<0.05). The histopathology results showed that normal morphology was found in Low Iron Group and Normal Iron Group, but the mucosa showed a slight injury in the Medium Iron Group with apical microvilli slightly off. Irregular shape of microvilli and necrosis were found in some epithelial cells of intestinal mucosa in the High Iron Group. Conclusion: Excessive dietary iron intake plays a negative effect on the normal growth and development, and resulted in intestinal inflammatory injury in rats.

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“…Nevertheless, it is required in a relatively narrow range, otherwise iron becomes a high potential generator of ROS [121]. Iron catalyses the Fenton reaction by generating the 8-hydroxy-guanine adduct, one of the most common DNA oxidative damages [13], found also in telomeres [17].…”

Section: What Can Be Done To Help Maintain Telomere Length?mentioning

confidence: 99%

Telomere Length and Its Relation to Human Health

Kahl¹,

Silva²

2016

Telomere - A Complex End of a Chromosome

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Telomeres are complex nucleotide sequences that cap the end of chromosomes from degradation, unwanted recombination-fusion, inappropriate activation of DNA damage response and play a critical role in cell division and chromosome stability. There is growing evidence that telomere stability can be affected by occupational and environmental exposure, as some of these factors have been correlated with increase in inflammation, oxidative stress, DNA damage, chromosome aberration, and epigenetic alterations. Both extremely short and long telomeres have been associated with neurodegenerative, cardiovascular diseases (CVD) and cancer risk. Occupational and environmental exposure to several synthetic and natural chemicals has been found to be associated with changes in telomere length, although the molecular mechanism is not fully understood. Telomeric DNA is relatively less capable of repair, resulting in accelerated shortening during the cell cycle and replicative senescence. It is recognized that diet plays an important role in telomere maintenance. Prevention of exposure to environmental and occupational hazards as well as psychological stressors can reduce the risk of telomere instability. This review provides a broad evaluation of the associated mechanism between human health and environmental and occupational exposure with telomere length, including recent findings and future perspectives.

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Oxidative Stress and Iron Homeostasis: Mechanistic and Health Aspects

Cited by 302 publications

References 143 publications

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Effects of Iron Overload on Growth and Intestinal Mucosa in Rats

Telomere Length and Its Relation to Human Health

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