Chelatable Fe (II) is generated in the rat kidneys exposed to ischemia and reperfusion, and a divalent metal chelator, 2, 2'-dipyridyl, attenuates the acute ischemia/reperfusion-injury of the kidneys: a histochemical study by the perfusion-Perls and -Turnbull methods

Iwatsuki, Hiroyasu; Meguro, Reiko; Asano, Yoshiya; Odagiri, S; Li, Chengtai; Shoumura, Kazuhiko

doi:10.1679/aohc.71.101

Cited by 7 publications

(10 citation statements)

References 31 publications

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“…One of the characteristic reactions of I/R is the reduction of non-heme Fe 3+ and release of Fe 2+ ions [55], which are able to react with H 2 O 2 to generate highly reactive hydroxyl radicals and result in cellular injury [56,57]. Owing to its high sensitivity, the Perls/DAB method was used to provide information about non-heme iron deposition regardless of oxidation states in normal and ischemic conditions by revealing cell population susceptible to free radical damage [58,59]. The results obtained here indicates a response to ROS generation, linked to the reperfusion period and to the non-heme ferrous iron production, which is considered to be critically involved in free radical generation.…”

Section: Discussionmentioning

confidence: 99%

Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion

et al. 2019

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(1) Background: Reperfusion injury refers to the cell and tissue damage induced, when blood flow is restored after an ischemic period. While reperfusion reestablishes oxygen supply, it generates a high concentration of radicals, resulting in tissue dysfunction and damage. Here, we aimed to challenge and achieve the potential of a delivery system based on astaxanthin, a natural antioxidant, in attenuating the muscle damage in an animal model of femoral hind-limb ischemia and reperfusion. (2) Methods: The antioxidant capacity and non-toxicity of astaxanthin was validated before and after loading into a polysaccharide scaffold. The capacity of astaxanthin to compensate stress damages was also studied after ischemia induced by femoral artery clamping and followed by varied periods of reperfusion. (3) Results: Histological evaluation showed a positive labeling for CD68 and CD163 macrophage markers, indicating a remodeling process. In addition, higher levels of Nrf2 and NQO1 expression in the sham group compared to the antioxidant group could reflect a reduction of the oxidative damage after 15 days of reperfusion. Furthermore, non-significant differences were observed in non-heme iron deposition in both groups, reflecting a cell population susceptible to free radical damage. (4) Conclusions: Our results suggest that the in situ release of an antioxidant molecule could be effective in improving the antioxidant defenses of ischemia/reperfusion (I/R)-damaged muscles.

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Section: Discussionmentioning

confidence: 99%

Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion

et al. 2019

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“…We are not aware of earlier studies using the Meguro method to visualize iron in human brain tissue, but it has been described for the detection of iron in paraffin-embedded tissue of rats, mice, monkeys, and guinea pigs (Meguro et al 2005;Freret et al 2008;Iwatsuki et al 2008;Meguro et al 2008;Butt et al 2010;Winter et al 2010;Butt et al 2011;Shpyleva et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Comparison of Histological Techniques to Visualize Iron in Paraffin-embedded Brain Tissue of Patients with Alzheimer’s Disease

Duijn

Nabuurs

Duinen

et al. 2013

J Histochem Cytochem.

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SummaryBetter knowledge of the distribution of iron in the brains of Alzheimer's disease (AD) patients may facilitate the development of an in vivo magnetic resonance (MR) marker for AD and may cast light on the role of this potentially toxic molecule in the pathogenesis of AD. Several histological iron staining techniques have been used in the past but they have not been systematically tested for sensitivity and specificity. This article compares three histochemical techniques and ferritin immunohistochemistry to visualize iron in paraffin-embedded human AD brain tissue. The specificity of the histochemical techniques was tested by staining sections after iron extraction. Iron was demonstrated in the white matter, in layers IV/V of the frontal neocortex, in iron containing plaques, and in microglia. In our hands, these structures were best visualized using the Meguro iron stain, a method that has not been described for iron staining in human brain or AD in particular. Ferritin immunohistochemistry stained microglia and iron containing plaques similar to the Meguro method but was less intense in myelin-associated iron. The Meguro method is most suitable for identifying iron-positive structures in paraffinembedded human AD brain tissue. (J Histochem Cytochem 61:785-792, 2013)

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“…Modified Perl's and Lillie's methods were applied as previously described 36,37 to localize ferric and ferrous ions in renal tissues, respectively. The protocols involve extra steps to intensify the Prussian blue and Turnbull blue stains by incubating the sections with 3,3′-Diaminobenzidine (DAB) substrate to produce a permanent brown stain.…”

Section: Tissue Localization Of Iron Ionsmentioning

confidence: 99%

“…The protocols involve extra steps to intensify the Prussian blue and Turnbull blue stains by incubating the sections with 3,3′-Diaminobenzidine (DAB) substrate to produce a permanent brown stain. 36,37 All slides were treated with 3% (vol/vol) H 2 O 2 in methanol for 60 min before staining with Prussian blue (Santa-Cruz Biotechnology Inc.) and Turnbull blue (Sigma-Aldrich Co.) to control the activities of endogenous peroxidases and catalases on the substrate. Sections were then incubated with DAB (Vector Laboratories, Inc.; Burlingame, CA) for 30 min and later counterstained with hematoxylin.…”

Section: Tissue Localization Of Iron Ionsmentioning

confidence: 99%

Acute and Chronic Iron Overloading Differentially Modulates the Expression of Cellular Iron-homeostatic Molecules in Normal Rat Kidney

Refaat

Abdelghany

BaSalamah

et al. 2018

J Histochem Cytochem.

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Little is known about the renal responses to acute iron overloading. This study measured the renal tubular expression of transferrin receptor-1 (TfR1), cubilin/megalin receptors, hepcidin, ferroportin, and ferritin chains following subacute intoxication of 40 male Wistar rats with a single oral dose of ferrous iron (300 mg/kg). The animals were randomly subdivided into 4 equal subgroups at the time of necropsy (1, 2, 4, and 8 hr). The results were compared with the controls ( n=15) and with the chronic group ( n=15), which received iron for 4 weeks (75 mg/kg/day; 5 days/week). Although both toxicity models inhibited TfR1, they upregulated the cubilin/megalin receptors and hepcidin, and triggered iron deposition in tubular cells. The ferritin heavy-chain and ferroportin were downregulated in the 2-hr and 4-hr acute subgroups, whereas chronic toxicity promoted their expression, compared with controls. Moreover, the 4-hr and 8-hr subgroups had higher intracellular Fe and marked cell apoptosis compared with the chronic group. In conclusion, the kidney appears to sustain iron reabsorption in both intoxication models. However, the cellular iron storage and exporter proteins were differentially expressed in both models, and their inhibition post-acute toxicity might contribute toward the intracellular accumulation of Fe, oxidative stress, and ferroptosis.

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Chelatable Fe (II) is generated in the rat kidneys exposed to ischemia and reperfusion, and a divalent metal chelator, 2, 2'-dipyridyl, attenuates the acute ischemia/reperfusion-injury of the kidneys: a histochemical study by the perfusion-Perls and -Turnbull methods

Cited by 7 publications

References 31 publications

Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion

Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion

Comparison of Histological Techniques to Visualize Iron in Paraffin-embedded Brain Tissue of Patients with Alzheimer’s Disease

Acute and Chronic Iron Overloading Differentially Modulates the Expression of Cellular Iron-homeostatic Molecules in Normal Rat Kidney

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