Iron and Advanced Glycation End Products: Emerging Role of Iron in Androgen Deficiency in Obesity

Chen, Seu Hwa; Yuan, Kuo Ching; Lee, Yu Chieh; Shih, Chun Kuang; Tseng, Sung Hui; Tinkov, Alexey A.; Skalny, Anatoly V.; Chang, Jung Su

doi:10.3390/antiox9030261

Cited by 10 publications

(9 citation statements)

References 56 publications

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“…In patients with β-thalassemia major, serum iron and especially non-transferrin-bound iron are typically elevated, and a positive correlation has been reported between this elevation and AGE (carboxymethyl-lysine and pentosidine) concentrations [97]. Correspondingly, in our recent experimental study Fe supplementation in obese rats induced a significant accumulation of AGEs and especially of CML in the liver [98]. Iron (Fe 3+ ) is capable of inducing formation of DNA-AGE adducts, especially when combined with glyoxal and arginine [99].…”

Section: Glycation and Age Toxicity In Ad As Influenced By Fesupporting

confidence: 60%

Copper, Iron, Selenium and Lipo-Glycemic Dysmetabolism in Alzheimer’s Disease

Aaseth

Skalny

Roos

et al. 2021

IJMS

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The aim of the present review is to discuss traditional hypotheses on the etiopathogenesis of Alzheimer’s disease (AD), as well as the role of metabolic-syndrome-related mechanisms in AD development with a special focus on advanced glycation end-products (AGEs) and their role in metal-induced neurodegeneration in AD. Persistent hyperglycemia along with oxidative stress results in increased protein glycation and formation of AGEs. The latter were shown to possess a wide spectrum of neurotoxic effects including increased Aβ generation and aggregation. In addition, AGE binding to receptor for AGE (RAGE) induces a variety of pathways contributing to neuroinflammation. The existing data also demonstrate that AGE toxicity seems to mediate the involvement of copper (Cu) and potentially other metals in AD pathogenesis. Specifically, Cu promotes AGE formation, AGE-Aβ cross-linking and up-regulation of RAGE expression. Moreover, Aβ glycation was shown to increase prooxidant effects of Cu through Fenton chemistry. Given the role of AGE and RAGE, as well as metal toxicity in AD pathogenesis, it is proposed that metal chelation and/or incretins may slow down oxidative damage. In addition, selenium (Se) compounds seem to attenuate the intracellular toxicity of the deranged tau and Aβ, as well as inhibiting AGE accumulation and metal-induced neurotoxicity.

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Section: Glycation and Age Toxicity In Ad As Influenced By Fesupporting

confidence: 60%

Copper, Iron, Selenium and Lipo-Glycemic Dysmetabolism in Alzheimer’s Disease

Aaseth

Skalny

Roos

et al. 2021

IJMS

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“…ncoa4 is an autophagy cargo receptor, TFr1 is a transferrin receptor and dMT1 transports metal ions across membranes in mammals; all are necessary for iron release into the cytoplasm (34). The potential association between aGes level and iron overload has been suggested in previous studies (35,36). aGes were also reported to enhance heme oxygenase-1 (Ho-1) mrna expression in endothelial cells (37) and inhibited nrf2 activation in H9c2 cells (38).…”

Section: Discussionmentioning

confidence: 83%

Advanced glycation end products promote osteoporosis by inducing ferroptosis in osteoblasts

Ge¹,

Jian²,

Yao³

et al. 2022

Mol Med Rep

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advanced glycation end products (aGes) have been widely reported to play an important role in osteoporosis (oP), particularly in diabetes-related oP. The aim of the present study was to investigate the effect of aGes on osteoblast function and the underlying mechanisms. The level of bone mineral density (BMd), serum aGes and fasting blood glucose (FBG) was measured in patients with oP and healthy individuals, and the correlation between aGe levels and BMd or FBG was then analyzed. For the in vitro experiments, the hFoB1.19 osteoblast cell line was cultured in medium containing aGes and serum from healthy individuals or patients with oP, and with or without type-2 diabetes mellitus (T2dM). cell proliferation, differentiation, mineralization, apoptosis and ferroptosis were evaluated using cell counting Kit-8 and alkaline phosphatase (alP) assays, alizarin red and Tunel staining, iron indicator, lipid peroxidation tests and western blot analysis, respectively. in a separate set of experiments, the ferroptosis inhibitor, deferoxamine (dFo), was also added to the culture medium of cells treated with aGes and serum from patients with oP and T2dM. The results demonstrated that patients with oP had a higher level of serum aGes and FBG compared with that in healthy individuals. The level of serum aGes in patients with oP was negatively correlated with BMd, but was positively correlated with FBG. in addition, aGes and serum from patients with oP markedly inhibited hFoB1.19 cell proliferation, alP production and mineralized nodule formation. Apoptosis and ferroptosis were significantly promoted by aGes and serum from patients with oP. Moreover, serum from oP patients with T2dM caused stronger effect than that from oP patients with normal FBG. However, dFo reversed the effects induced by aGes and serum from patients with oP and T2dM on hFoB1.19 cells. collectively, aGes could disrupt the functions of osteoblasts by inducing cell ferroptosis, thus contributing to oP.

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“…This can lead to cell death, cell differentiation or reduced cell adhesion and migration. Previous studies have shown a potential association between AGEs levels and iron overload (Mirlohi et al, 2018;Chen et al, 2020). In patients with ß-Thalassemia major, iron overload and oxidative stress can increase the formation of AGEs and lead to different complications (Mirlohi et al, 2018).…”

Section: Agesmentioning

confidence: 99%

Oxidative Stress and Lipid Peroxidation: Prospective Associations Between Ferroptosis and Delayed Wound Healing in Diabetic Ulcers

Feng

Wang

et al. 2022

Front. Cell Dev. Biol.

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Diabetic ulcers are one of the major complications of diabetes, and patients usually suffer from amputation and death due to delayed ulcer wound healing. Persistent inflammation and oxidative stress at the wound site are the main manifestations of delayed wound healing in diabetic ulcers. In addition, chronic hyperglycemia in patients can lead to circulatory accumulation of lipid peroxidation products and impaired iron metabolism pathways leading to the presence of multiple free irons in plasma. Ferroptosis, a newly discovered form of cell death, is characterized by intracellular iron overload and accumulation of iron-dependent lipid peroxides. These indicate that ferroptosis is one of the potential mechanisms of delayed wound healing in diabetic ulcers and will hopefully be a novel therapeutic target for delayed wound healing in diabetic patients. This review explored the pathogenesis of diabetic ulcer wound healing, reveals that oxidative stress and lipid peroxidation are common pathological mechanisms of ferroptosis and delayed wound healing in diabetic ulcers. Based on strong evidence, it is speculated that ferroptosis and diabetic ulcers are closely related, and have value of in-depth research. We attempted to clarify prospective associations between ferroptosis and diabetic ulcers in terms of GPX4, iron overload, ferroptosis inhibitors, AGEs, and HO-1, to provide new ideas for exploring the clinical treatment of diabetic ulcers.

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Iron and Advanced Glycation End Products: Emerging Role of Iron in Androgen Deficiency in Obesity

Cited by 10 publications

References 56 publications

Copper, Iron, Selenium and Lipo-Glycemic Dysmetabolism in Alzheimer’s Disease

Copper, Iron, Selenium and Lipo-Glycemic Dysmetabolism in Alzheimer’s Disease

Advanced glycation end products promote osteoporosis by inducing ferroptosis in osteoblasts

Oxidative Stress and Lipid Peroxidation: Prospective Associations Between Ferroptosis and Delayed Wound Healing in Diabetic Ulcers

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