Induction of increased phosphatidylcholine hydroperoxide by an iron-deficient diet in rats

Uehara, Mariko; Chiba, Hiroshige; Mogi, Hideki; Suzuki, Kazuharu; Goto, Susumu

doi:10.1016/s0955-2863(97)00045-4

Cited by 26 publications

(14 citation statements)

References 31 publications

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“…Longer periods of iron deficiency result in a smaller iron storage pool, suppressing hemoglobin biosynthesis and giving rise to anemia. As a result, lipid metabolism in serum and liver is jeopardized and dyslipidemia may ensue, which is characterized by enhanced levels of serum triacylglycerol (TG), phospholipids, and low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol in the serum, as well as enhanced levels of TG and phospholipids in the liver (27,29). Since lipid profiles may vary depending on experimental conditions, it is difficult to define the mechanism of lipid metabolic regulation during iron deficiency-associated anemia.…”

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confidence: 99%

Dietary iron-deficient anemia induces a variety of metabolic changes and even apoptosis in rat liver: a DNA microarray study

Kamei

Watanabe

Ishijima

et al. 2010

Physiological Genomics

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confidence: 99%

Dietary iron-deficient anemia induces a variety of metabolic changes and even apoptosis in rat liver: a DNA microarray study

Kamei

Watanabe

Ishijima

et al. 2010

Physiological Genomics

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“…Uehara et al (9), however, reported that iron deficiency increased lipid hydroperoxide formation in both liver and serum, probably due to the substitution of copper to iron, which compensated the process of the Fenton reaction. In the present study, irondeficient rats increased their serum antioxidation level as expected.…”

Section: Discussionmentioning

confidence: 97%

“…It was reported that an iron deficiency yielded lipid hydroper-oxides in rats (9), so the antioxidant effects of isoflavonoids appeared to be more easily confermed by this system. The purpose of this study was to find proof of the suppression of hydroperoxide production by soya-hypocotyl tea (SHT) drinking and its effect on DNA adduct formation using a biomarker of 8-hydroxy-2'-deoxyguanosine (oh 8 dG) in the liver, kidney and urine.…”

Section: Introductionmentioning

confidence: 98%

Suppression of lipid-hydroperoxide and DNA-adduct formation by isoflavone-containing soy hypocotyl tea in rats

Haba

Watanabe

Arai

et al. 2002

Environ Health Prev Med

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Objective: Phytoestrogen isoflavones (IFs) are considered to suppress estrogen-related cancers through their antiestrogenic activity. The antioxidant effect of IFs, however, has not been confirmed in an in vivo system, so suppression of hydroperoxide formation and resultant DNA adduct formation were studied.Metheds: The antioxidant effects of the soya-hypocotyl tea (SHT), which contained daidzein (14+/ 1.5 mg/l) and genistein (3+/ 0.5 mg/l), were examined in Wistar rats fed the AIN-76 control diet or iron deficient diet (FeD) for 4 weeks. The intake amount of the diet and IFs were measured daily. Urinary excretion of IFs was measured for 3 days before sacrifice. In addition to the serum lipid analyses, phosphatidylcholine hydroperoxide (PCOOH), and phosphatidylethanolamine hydroperoxide (PEOOH) production in red blood cells and the liver were measured as a biomarker of oxidants. Production of DNA adducts by oxidative stress was measured by the amount of 8-hydroxy-2'-deoxyguanosine (oh 8 dG) in the liver and kidney, and urine. Histological changes were checked by H&E staining and immunohistochemistry for oh 8 dG.Results: FeD rats showed anemia, growth retardation, hyperlipidemia. IFs only lowered the triacylglycerol level and did not change the cholesterol level. Rats fed the normal diet did not show suppression of PCOOH and PEOOH production in either red blood cells or the liver, while groups administered SHT showed suppressed production of PCOOH and PEOOH in the liver. The cumulative intake of daidzein, genistein and the total amount of IFs showed significant inverse associations with urinary excretion of oh 8 dG. oh 8 dG in the kidney showed an inverse association with the amount of oh 8 dG in the urine. Enzymehistochemically, a strong localization of oh 8 dG was found in the epithelial cells of the bile canaliculi and proximal tubules of the kidney.Conclusion: IFs and SHT showed antioxidant effects at physiological concentrations in an in vivo system. The antioxidant effects of IFs decreased oxidation stress to the nuclear DNA, which was shown by the decreased oh 8 dG production. It is suggested that to prevent various cancers, in addition to the known antiestrogenic, antityrosin kinase, and other effects. IFs appeared to promote excretion of oh 8 dG.

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“…Iron is an essential element for cellular responses, including immune response and oxidative metabolism (7,25). Previously, we reported that iron deficiency induced oxidative stress in the liver and heart (10,34). However, limited information is available on the molecular mechanisms underlying the association between oxidative stress and autophagy during iron deficiency.…”

Section: Discussionmentioning

confidence: 99%

“…Iron deficiency leads to health problems such as cardiovascular diseases, blood loss, and anemia (8,13,18). We previously reported that iron deficiency increased the levels of phosphatidylcholine hydroperoxide (a primary peroxide in biological membranes) and copper in the liver of rats and increased the carboxylation of proteins in the heart of rats (10,34). Iron deficiency induces oxidative stress in many tissues.…”

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confidence: 99%

<b>Iron deficiency induces autophagy and activates Nrf2 signal through modulating </b><b>p62/SQSTM </b>

et al. 2017

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Iron is an essential trace metal in almost all organisms and plays an important role in the redox system. We previously reported that iron deficiency activated autophagy and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling for oxidative stress. However, regulatory mechanisms underlying the association between autophagy and Nrf2 signaling are unclear. In this study, we found that treatment of cells with an iron-specific chelator deferoxamine (DFO) increased reactive oxidative species (ROS) production by elevating the expression of p47 phox and p67 phox compared with that in untreated cells. The DFO treatment also induced protein aggregation and formed aggresome, which is a cellular response to misfolded protein. In addition, DFO treatment upregulated the expression of the autophagic gene p62/SQSTM1, which in turn activated intracellular proteolysis during autophagy. DFO treatment phosphorylated p62/SQSTM1 (Thr351) to activate Nrf2. However, silencing of p62/SQSTM1 followed by DFO treatment attenuated Nrf2 activation and resulted in the accumulation of carboxyl proteins compared with DFO treatment alone. These results indicated that iron deficiency activates Nrf2 signaling by modulating p62/SQSTM1 during autophagy.

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Induction of increased phosphatidylcholine hydroperoxide by an iron-deficient diet in rats

Cited by 26 publications

References 31 publications

Dietary iron-deficient anemia induces a variety of metabolic changes and even apoptosis in rat liver: a DNA microarray study

Dietary iron-deficient anemia induces a variety of metabolic changes and even apoptosis in rat liver: a DNA microarray study

Suppression of lipid-hydroperoxide and DNA-adduct formation by isoflavone-containing soy hypocotyl tea in rats

<b>Iron deficiency induces autophagy and activates Nrf2 signal through modulating </b><b>p62/SQSTM </b>

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