Protection from renal ischemia-reperfusion injury by the 2-methylaminochroman U83836E

doi:10.1046/J.1523-1755.1998.00072.X

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Protection from renal ischemia-reperfusion injury by the 2-methylaminochroman U83836E

Journal Article•DOI•

Protection from renal ischemia-reperfusion injury by the 2-methylaminochroman U83836E

Elena De Vecchi¹, Lorenzo Lubatti¹, Claudio Beretta¹, Stefano Ferrero¹, Paola Rinaldi¹, Marzia Galli Kienle¹, Rinaldo Trazzi¹, Rita Paroni¹ - Show less +4 more•Institutions (1)

University of Milan¹

01 Sep 1998-Kidney International (Nature Publishing Group)-Vol. 54, Iss: 3, pp 857-863

TL;DR: There is a protective effect of U83836E in ischemia-reperfusion injury, in that tissue damage due to oxidative stress is reduced, thus ameliorating renal function impairment.

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About: This article is published in Kidney International.The article was published on 1998-09-01 and is currently open access. It has received 27 citations till now. The article focuses on the topics: Kidney & Kidney disease.

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Journal Article•DOI•

Reactive oxygen species and acute renal failure

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Karl A. Nath¹, Suzanne M. Norby¹•Institutions (1)

Mayo Clinic¹

01 Dec 2000-The American Journal of Medicine

TL;DR: Evidence indicating that the inordinate or aberrant generation of reactive oxygen species (ROS) may contribute to the initiation and maintenance of ATN is reviewed, and the possibility that ROS may participate in the recovery phase of ATn is raised.

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402 citations

Journal Article•DOI•

Mitochondria-Targeted Peptide Accelerates ATP Recovery and Reduces Ischemic Kidney Injury

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Hazel H. Szeto¹, Shaoyi Liu¹, Yi Soong¹, Dunli Wu¹, Shaun Darrah¹, Feng Ying Cheng¹, Zhihong Zhao¹, Michael Ganger¹, Clara Y. Tow¹, Surya V. Seshan¹ - Show less +6 more•Institutions (1)

Cornell University¹

01 Jun 2011-Journal of The American Society of Nephrology

TL;DR: Treatment with SS-31 protected mitochondrial structure and respiration during early reperfusion, accelerated recovery of ATP, reduced apoptosis and necrosis of tubular cells, and abrogated tubular dysfunction, suggesting that it may protect against ischemic renal injury.

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Abstract: The burst of reactive oxygen species (ROS) during reperfusion of ischemic tissues can trigger the opening of the mitochondrial permeability transition (MPT) pore, resulting in mitochondrial depolarization, decreased ATP synthesis, and increased ROS production. Rapid recovery of ATP upon reperfusion is essential for survival of tubular cells, and inhibition of oxidative damage can limit inflammation. SS-31 is a mitochondria-targeted tetrapeptide that can scavenge mitochondrial ROS and inhibit MPT, suggesting that it may protect against ischemic renal injury. Here, in a rat model of ischemia-reperfusion (IR) injury, treatment with SS-31 protected mitochondrial structure and respiration during early reperfusion, accelerated recovery of ATP, reduced apoptosis and necrosis of tubular cells, and abrogated tubular dysfunction. In addition, SS-31 reduced medullary vascular congestion, decreased IR-mediated oxidative stress and the inflammatory response, and accelerated the proliferation of surviving tubular cells as early as 1 day after reperfusion. In summary, these results support MPT as an upstream target for pharmacologic intervention in IR injury and support early protection of mitochondrial function as a therapeutic maneuver to prevent tubular apoptosis and necrosis, reduce oxidative stress, and reduce inflammation. SS-31 holds promise for the prevention and treatment of acute kidney injury.

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254 citations

Journal Article•DOI•

Resveratrol, a polyphenol found in wine, reduces ischemia reperfusion injury in rat kidneys.

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Luca Giovannini¹, Massimiliano Migliori, Biancamaria Longoni, Dipak K. Das, A. A. E. Bertelli, Vincenzo Panichi, C Filippi, Aldo Bertelli - Show less +4 more•Institutions (1)

University of Pisa¹

01 Mar 2001-Journal of Cardiovascular Pharmacology

TL;DR: The results suggest that resveratrol reduced the renal ischemia reperfusion injury through a nitric oxide-dependent mechanism.

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Abstract: Reactive oxygen species have been implicated in the pathophysiology of renal ischemia reperfusion injury. Antioxidants including polyphenolics have been found to protect renal cells from the cellular injury induced by ischemia and reperfusion. Resveratrol, a stilbene polyphenol found in grapes and red wine, has recently been found to protect isolated rat heart from ischemia reperfusion injury. This study was sought to determine if resveratrol could also protect renal cells from ischemic injury. Male Wistar rats were treated with control, resveratrol (0.23 microg/kg), vehicle used to solubilize resveratrol, and resveratrol plus L-NAME (15 mg/kg body wt), a nitric oxide blocker. Our results demonstrated that resveratrol administration reduced the mortality of ischemic rats from 50% to 10% and renal damage was reduced as indicated by histologic examination and serum creatinine level. The short-term administration of resveratrol also inhibited renal lipid peroxidation induced by ischemia and reperfusion both in cortex and in medulla. Electron paramagnetic resonance detected an increased formation of nitric oxide in the resveratrol-treated kidney that was reduced to the baseline value after treating the rats with L-NAME in addition to resveratrol. The results suggest that resveratrol reduced the renal ischemia reperfusion injury through a nitric oxide-dependent mechanism.

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151 citations

Journal Article•DOI•

Oxidative stress and reactive nitrogen species generation during renal ischemia.

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Lisa M. Walker¹, J. Lyndal York, Syed Z. Imam, Syed F. Ali, Kenneth L. Muldrew, Philip R. Mayeux - Show less +2 more•Institutions (1)

University of Arkansas for Medical Sciences¹

01 Sep 2001-Toxicological Sciences

TL;DR: The data clearly demonstrate that oxidative stress and RNS generation occur in the kidney during ischemia, and indicates that reactive nitrogen species (RNS) formation during I-R injury is driven by oxidant stress.

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106 citations

Cites background from "Protection from renal ischemia-repe..."

...The ability of superoxide dismutase (SOD), allopurinol, deferoxamine, and other antioxidants to attenuate renal I-R injury suggests that reactive oxygen species contribute to the development of renal injury (De Vecchi et al., 1998; Paller and Hedlund, 1988; Palleret al., 1984)....
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Journal Article•DOI•

Oxidative stress and kidney dysfunction due to ischemia/reperfusion in rat: Attenuation by dehydroepiandrosterone

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Manuela Aragno¹, Juan Carlos Cutrin¹, Raffaella Mastrocola¹, Maria-Giulia Perrelli¹, F Restivo¹, Giuseppe Poli¹, Oliviero Danni¹, Giuseppe Boccuzzi¹ - Show less +4 more•Institutions (1)

University of Turin¹

01 Sep 2003-Kidney International

TL;DR: Rats supplemented with DHEA and subjected to I/R had reduced pro-oxidant state, oxidative damage, and improved renal functionality, indicating an attenuation of oxidative injury and dysfunctions mediated by I-R.

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102 citations

Cites background from "Protection from renal ischemia-repe..."

...This protective effect may be related to the ability of antioxidant compounds to normalize early intracellular events linked to the progression of oxidative damage [8, 9]....
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Journal Article•

Nonsteroidal lazaroid U78517F in models of focal and global ischemia.

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Edward D. Hall¹, K E Pazara, Braughler Jm, K. L. Linseman, Eric Jon Jacobsen - Show less +1 more•Institutions (1)

Upjohn¹

01 Nov 1990-Stroke

TL;DR: The results document the anti-ischemic efficacy of a novel and potent inhibitor of iron-catalyzed lipid peroxidation and further support a key role of oxygen radicals in postischemi brain damage.

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Abstract: U78517F is a novel inhibitor of iron-catalyzed lipid peroxidation that combines the tetramethylchroman antioxidant ring portion of alpha-tocopherol with the amine of the previously described 21-aminosteroids (e.g., U74006F). U78517F inhibited 200 microM FeCl2-initiated lipid peroxidation in rat brain homogenates by 50% at a concentration of 0.6 microM compared with 8 microM for U74006F, 28 microM for alpha-tocopherol, and 43 microM for the ring portion of alpha-tocopherol (i.e., trolox). U78517F is devoid of hypothermic or antiexcitotoxic actions or interactions with known neurotransmitter receptors. When administered intraperitoneally to male gerbils at 10 minutes before and again at the end of a 3-hour period of unilateral carotid artery occlusion, U78517F decreased 24-hour postischemic cortical neuronal necrosis. Neuronal density in the medial portion of the cortex was increased from 34.2% of normal in vehicle-treated animals to 86.3% in the U78517F-treated animals. In the lateral cortical area, the vehicle group showed only 3.3% neuronal survival versus 48.2% in the drug-treated group. In a separate series of experiments with the same focal ischemia model, identical dosing with U78517F enhanced the postischemic recovery of cortical extracellular calcium without any effect on ischemic or postischemic cortical blood flow. The effect on calcium recovery was observed at intraperitoneal doses as low as 0.1 mg/kg. The compound also was effective in partially attenuating 1-week postischemic hippocampal CA1 neuronal loss in a gerbil global ischemia model involving brief (15-minute) bilateral carotid occlusion, but sustained dosing was required. These results document the anti-ischemic efficacy of a novel and potent inhibitor of iron-catalyzed lipid peroxidation and further support a key role of oxygen radicals in postischemic brain damage.

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42 citations

"Protection from renal ischemia-repe..." refers background in this paper

...focal and global cerebral ischemia [13], in cerebrovascular...
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...The antioxidant capacity of the 2-methylaminochroman, U78517F, a second generation lazaroid, has been reported to be tenfold that of the 21-aminosteroid U74006F and 100-fold that of vitamin E, probably because the association of the antioxidant properties of vitamin E with the amino portion of U74006F enhances drug antioxidant potency and efficacy [13]....
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Journal Article•

Glomerular alterations in an ischemic model of acute renal failure.

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J. L. Barnes, R. W. Osgood¹, H. J. Reineck¹, J. H. Stein¹•Institutions (1)

University of Texas Health Science Center at San Antonio¹

01 Oct 1981-Laboratory Investigation

32 citations

"Protection from renal ischemia-repe..." refers background in this paper

...Ischemia-reperfusion injury sustained by kidney during surgical revascularization of the renal artery or after transplantation often results in temporary or permanent alterations of renal function [22, 23]....
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Journal Article•DOI•

An in vitro EPR study of the free-radical scavenging actions of the lazaroid antioxidants U-74500A and U-78517F

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Weiguo Zhao¹, J. Steven Richardson¹, Michael J. Mombourquette¹, John A. Weil¹•Institutions (1)

University of Saskatchewan¹

01 Jul 1995-Free Radical Biology and Medicine

TL;DR: Observations are consistent with the lazaroids being scavengers of oxygen-based and nitrogen-based free radicals and suggest that the neuroprotective actions of the lazeroids in cerebral ischemia may involve direct interactions of theLazaroids with several different species of free radicals.

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31 citations

"Protection from renal ischemia-repe..." refers background in this paper

...The 2-methylaminochromans as well as the 21-aminosteroids exert their effects via several mechanisms such as scavenging of peroxyl radicals [11], inactivation of iron-mediated toxic reactions by interaction with ferrous iron [2], and the blocking of calcium channels by inhibition of ion pump ATPase [18]....
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...The long lasting protection from lipid peroxidation and from nucleotide depletion in the kidney by U83836E even after 24 hours of reperfusion can also be ascribed to a longer metabolic half-life in comparison with the relatively short one of the old generation of 21- aminosteroids (U34389F) [11]....
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...The long lasting protection from lipid peroxidation and from nucleotide depletion in the kidney by U83836E even after 24 hours of reperfusion can also be ascribed to a longer metabolic half-life in comparison with the relatively short one of the old generation of 21aminosteroids (U34389F) [11]....
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Journal Article•DOI•

Increased susceptibility to lipid peroxidation in rabbit kidneys: A consequence of warm ischaemia and subsequent reperfusion

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Cj Green¹, G. Healing¹, S. Simpkin¹, Joseph Lunec², Bj Fuller³ - Show less +1 more•Institutions (3)

Northwick Park Hospital¹, Selly Oak Hospital², Royal Free Hospital³

01 Jan 1986-Comparative Biochemistry and Physiology B

TL;DR: An early index of lipid peroxidation (diene conjugation) suggested peroxidative damage during the warm ischaemic period itself, whilst detection of Schiff bases was only possible after in vitro incubation of the tissue.

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Abstract: 1. 1. Rabbit kidneys were clamped and rendered warm ischaemic (WI) in situ for 60 and 120 min. They were then either removed immediately after the ischaemic insult or after reperfusion with blood for 60 min or 24 hr. 2. 2. Homogenates were assayed for phospholipid-Schiff base fluorescence (Ex. 360 nm, Em. 435 nm) and for diene conjugate formation by u.v. spectrophotometry (240 nm) as indices of lipid peroxidation. 3. 3. No alteration in tissue levels of Schiff base was evident immediately after WI but when the homogenates were incubated at 37°C for 90 min, the rate of peroxidation was significantly elevated compared to controls ( P after WI of 60 min and P after 120 min of WI). 4. 4. These values were still further elevated after reperfusion with blood for 60 min and 24 hr ( P ). 5. 5. Diene conjugates were raised after WI alone and further still after reperfusion. 6. 6. Thus an early index of lipid peroxidation (diene conjugation) suggested peroxidative damage during the warm ischaemic period itself, whilst detection of Schiff bases was only possible after in vitro incubation of the tissue. 7. 7. Both indices of oxygen-derived free radical damage were increased after reperfusion in vivo with blood and may relate to the degree of tissue damage sustained during ischaemia and reflow.

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28 citations

Journal Article•DOI•

Two novel antioxidants, u74006f and u78517f, inhibit oxidant-stimulated calcium influx

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Paula L. Munns¹, Karen L. Leach¹•Institutions (1)

Upjohn¹

01 Mar 1995-Free Radical Biology and Medicine

TL;DR: Results indicate that U74006F and U78517F act to inhibit injury-induced calcium fluxes, which may contribute to their in vivo efficacy.

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24 citations

"Protection from renal ischemia-repe..." refers background in this paper

...The 2-methylaminochromans as well as the 21-aminosteroids exert their effects via several mechanisms such as scavenging of peroxyl radicals [11], inactivation of iron-mediated toxic reactions by interaction with ferrous iron [2], and the blocking of calcium channels by inhibition of ion pump ATPase [18]....
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...lated calcium influx have been reported [17, 18]....
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