Effect of acidosis and anoxia on iron delocalization from brain homogenates

Bralet, J; Schreiber, Lisbeth; Bouvier, Christine

doi:10.1016/0006-2952(92)90602-f

Cited by 88 publications

(35 citation statements)

References 41 publications

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“…Ferritin acts as an iron donor when exposed to metabolic conditions associated with ischemia that causes low oxygen tension, high levels of the superoxide anion, and acidosis (Bralet et al, 1992;Paul, 2000). Iron that is overloaded in CECs after TFI is likely released from ferritin.…”

Section: Levels Of [mentioning

confidence: 99%

Iron mediates endothelial cell damage and blood-brain barrier opening in the hippocampus after transient forebrain ischemia in rats

et al. 2011

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Blood cells are transported into the brain and are thought to participate in neurodegenerative processes following hypoxic ischemic injury. We examined the possibility that transient forebrain ischemia (TFI) causes the blood-brain barrier (BBB) to become permeable to blood cells, possibly via dysfunction and degeneration of endothelial cells in rats. Extravasation of Evans blue and immunoglobulin G (IgG) was observed in the hippocampal CA1-2 areas within 8 h after TFI, and peaked at 48 h. This extravasation was accompanied by loss of tight junction proteins, occludin, and zonula occludens-1, and degeneration of endothelial cells in the CA1-2 areas. Iron overload and mitochondrial free radical production were evident in the microvessel endothelium of the hippocampus before endothelial cell damage occurred. Administration of deferoxamine (DFO), an iron chelator, or Neu2000, an antioxidant, blocked free radical production and endothelial cell degeneration. Our findings suggest that iron overload and iron-mediated free radical production cause loss of tight junction proteins and degeneration of endothelial cells, opening of the BBB after TFI.

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Section: Levels Of [mentioning

confidence: 99%

Iron mediates endothelial cell damage and blood-brain barrier opening in the hippocampus after transient forebrain ischemia in rats

et al. 2011

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“…Total Fe content was analyzed by two independent techniques: (a) according to Bralet et al (1992) with modifications: approximately 40 mg of DG was homogenized in 1 mL of 150 mM KCl in 0.1 N HCl, pH 2.5, prepared with IFW. The samples were incubated for 24 h at 37°C in the presence of 9 mg/mL pepsin, 4.5 mM 2,2′ dipyridyl and 103 mM ascorbic acid, pH 7 prepared in IFW.…”

Section: Total Fe Contentmentioning

confidence: 99%

Exposure to excess dissolved iron in vivo affects oxidative status in the bivalve Mya arenaria

González

Abele

Puntarulo

2010

Comparative Biochemistry and Physiology Part C: Toxicology &

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The effect of in vivo Fe exposure on the oxidative metabolism of the bivalve Mya arenaria was studied. Fe was supplemented in natural seawater and resulted in a significant increase in the total Fe content in the bivalve digestive gland (DG) between 9 to 17 days of exposure. Mortality of treated animals increased drastically after day 18. Oxidative stress conditions were characterized in DG through assessment of the generation of reactive oxygen species (ROS) and ascorbyl radical (A•) content. Both parameters were affected following a biphasic profile showing significant increases by days 2 and 9 of Fe exposure. The content of 2-thiobarbituric acid reactive substances (TBARS) was significantly increased over control values by days 2, 9 and 17 of treatment. The labile Fe pool (LIP) in isolated DG was elevated over control values by day 7, and maintained this increase until day 17 of Fe exposure. The content of NO, assessed by EPR spin trapping, was 60% lower in DG of animals exposed for 2 days to Fe than in control values, with no further changes. The biphasic profile of oxidative stress response to Fe exposure in DG suggests that at early stages of Fe supplementation the cellular control mechanisms, such as CAT activity, were operative to limit oxidative damage, but further Fe exposure overwhelmed these abilities. Moreover, the second phase could be understood as the consequence of the exhaustion of cellular protective systems that could also involve NO.

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“…This iron level resulted in intensifying of the EDs on AMPA and NMDA EPSPs of neurons in piriform cortex. Such acute iron exposure may be a result of brain tissue hypoxia and acidosis that might accompany ICH (Bralet et al 1992;Lee et al 1999). On the contrary, in the hippocampal slices ferrous chloride (50 μM and 100 μM) depressed the field EPSP (Yip and Sastry 2000).…”

Section: How Ferric Ions Influence On Synaptic Activity In Piriform Cmentioning

confidence: 96%

Effects of the blood components on the AMPA and NMDA synaptic responses in brain slices in the onset of hemorrhagic stroke

Mokrushin¹,

Pavlinova²

2013

gpb

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Abstract. Blood-borne events play a major role in post bleeding disturbances of the neuronal network. However, very little is known about the early effects of blood plasma, leucocytes, and the red blood cells on the AMPA and NMDA-mediated synaptic responses in the onset of experimental intracranial hemorrhage (ICH). In this study, we used the technique of on-line monitoring of electrophysiological parameters referred to synaptic activity in piriform cortex of SHR rat slice. We exposed the olfactory cortex slices to diluted autologous blood or its components and compared with effects of ferric chloride. Whole blood exerted a total inhibition of synaptic activity in piriform cortex within first 5 min. Dilution of blood induced prolonged epileptic synaptic activation of NMDA receptors. Blood plasma and fraction of leucocytes induced hyperactivation of neurons transforming to epileptiform discharges. Fraction of red blood cells acted biphasic, an initial sharp activity of AMPA-and NMDAmediated receptors replaced by a following total depression. Our slice-based models of experimental stroke revealed the mechanism of the earliest pathophysiologic events occur in brain tissue during bleeding that may be relevant to the human ICH.

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Effect of acidosis and anoxia on iron delocalization from brain homogenates

Cited by 88 publications

References 41 publications

Iron mediates endothelial cell damage and blood-brain barrier opening in the hippocampus after transient forebrain ischemia in rats

Iron mediates endothelial cell damage and blood-brain barrier opening in the hippocampus after transient forebrain ischemia in rats

Exposure to excess dissolved iron in vivo affects oxidative status in the bivalve Mya arenaria

Effects of the blood components on the AMPA and NMDA synaptic responses in brain slices in the onset of hemorrhagic stroke

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