Deferoxamine induces prolonged cardiac preconditioning via accumulation of oxygen radicals

Dendorfer, Andreas; Heidbreder, Marc; Hellwig-Bürgel, Thomas; Jöhren, Olaf; Qadri, Fatimunnisa; Dominiak, Peter

doi:10.1016/j.freeradbiomed.2004.10.015

Cited by 63 publications

(42 citation statements)

References 43 publications

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“…In addition, some preconditioning strategies that induce HIF-1 have been applied for myocardial infarction and for ischemic rescue in the brain (Rodríguez-Jiménez and MorenoManzano, 2012). The iron chelator, deferoxamine, is the first natural product shown to activate HIF-1 (Wang and Semenza, 1993a); chelation of iron by deferoxamine stabilizes HIF-1a by disrupting the hydroxylation of HIF-1a by inhibition of PHD (Dendorfer et al, 2005). The b-diketone dibenzoylmethane found in licorice (Glycyrrhiza glabra) stabilizes HIF-1a protein and increases expression of vascular endothelial growth factor (Mabjeesh et al, 2003b).…”

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confidence: 99%

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

et al. 2014

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confidence: 99%

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

et al. 2014

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“…The critical evidence that assigns a causal role to iron are studies that have reported diminished tissue injury after stressors with pretreatment of the iron chelator, deferoxamine (DFO) (1,10,30,35,42,49). DFO is protective in animal models of tissue injury (19,35) and in human cases of iron overload (49) and cardiovascular disease (1).…”

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confidence: 99%

Dysregulation of hepatic iron with aging: implications for heat stress-induced oxidative liver injury

Bloomer

Brown

Buettner

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Bloomer SA, Brown KE, Buettner GR, Kregel KC. Dysregulation of hepatic iron with aging: implications for heat stressinduced oxidative liver injury. Am J Physiol Regul Integr Comp Physiol 294: R1165-R1174, 2008. First published February 13, 2008 doi:10.1152/ajpregu.00719.2007.-Environmental heat stress is associated with an age-related increase in hepatic oxidative damage and an exaggerated state of oxidative stress. The purpose of this investigation was to evaluate the regulation of hepatic iron after heat stress. A secondary aim was to determine a potential role for iron in heat stress-induced liver injury. Hyperthermia-induced alterations in hepatic iron were evaluated in young (6 mo) and old (24 mo) Fischer 344 rats by exposing them to a two-heat stress protocol. Livers were harvested at several time points after the second heating and assayed for labile and nonheme iron. In the control condition, there was no difference in labile iron between age groups. Both labile iron and storage iron were not altered by hyperthermia in young rats, but both were increased immediately after heating in old rats. To evaluate a role for iron in liver injury, hepatic iron content was manipulated in young and old rats, and then both groups were exposed to heat stress. Iron administration to young rats significantly increased hepatic iron content and ferritin but did not affect markers of lipid peroxidation under control conditions or after heat stress. In old rats, iron chelation with deferoxamine prevented the increase in nonheme iron, labile iron, ferritin, and lipid peroxidation after heat stress. These results suggest that iron may play a role in hepatic injury after hyperthermia. Thus, dysregulation of iron may contribute to the gradual decline in cellular and physiological function that occurs with aging.

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“…Protection and PKC activation can be mimicked by extracellular generation or application of ROS [25] . Limited oxidative stress can actually induce preconditioning [26] . Recently, it was reported that when TLR4 is activated, ROS are produced and inflammatory cytokines and nitric oxide are released [27] .…”

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confidence: 99%

Toll-like receptor 7/8 agonist resiquimod induces late preconditioning in neonatal cardiac myocytes

et al. 2011

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Aim: To investigate whether R-848 (resiquimod, toll-like receptor 7/8 agonist) can induce late preconditioning in neonatal cardiac myocytes. Methods:The protective effects of R-848 on neonatal myocytes against anoxia-reoxygenation-induced injury were tested, and intracellular reactive oxygen species (ROS) were determined. The protein synthesis inhibitor cyclohexamide (CH) and the ROS scavenger N-acetylcysteine (NAC) were used in this model to test if new protein synthesis and oxidative stress were necessary for their cardioprotective effects. The activation of nuclear factor kappa B (NFκB) and hypoxia inducible factor 1 (HIF1) was investigated by electrophoretic mobility shift assays (EMSA), and inducible nitric oxide synthase (iNOS) was assessed by immunoblotting. After iNOS was downregulated by small interfering RNA (siRNA) transfection, the cardioprotective effect was reassessed. Results: ROS were triggered soon after R-848 (0.01-1.0 μg/L) administration, however, the cardioprotective effect of which was induced 24 h later. This protection was abolished by CH or NAC pretreatment. NFκB and HIF1 activation and iNOS up-regulation were involved in this protective mechanism. The cardioprotective effect was also attenuated after iNOS was knocked down. Conclusion: R-848 provided a cardioprotective effect through a late preconditioning mechanism via a ROS/NFκB-HIF1/iNOS-dependent pathway.

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Deferoxamine induces prolonged cardiac preconditioning via accumulation of oxygen radicals

Cited by 63 publications

References 43 publications

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

Dysregulation of hepatic iron with aging: implications for heat stress-induced oxidative liver injury

Toll-like receptor 7/8 agonist resiquimod induces late preconditioning in neonatal cardiac myocytes

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