Inflammation subsequent to mild iron excess differentially alters regional brain iron metabolism, oxidation and neuroinflammation status in mice

Iron dyshomeostasis and neuroinflammation, characteristic features of the aged brain, and exacerbated in neurodegenerative disease, may induce oxidative stress-mediated neurodegeneration. In this study, the effects of potential priming with mild systemic iron injections on subsequent lipopolysaccharide (LPS)-induced inflammation in adult C57Bl/6J mice were examined. After cognitive testing, regional brain tissues were dissected for iron (metal) measurements by total reflection X-ray fluorescence and synchrotron radiation X-Ray fluorescence-based elemental mapping; and iron regulatory, ferroptosis-related, and glia-specific protein analysis, and lipid peroxidation by western blotting. Microglial morphology and astrogliosis were assessed by immunohistochemistry. Iron only treatment enhanced cognitive performance on the novel object location task compared with iron priming and subsequent LPS-induced inflammation. LPS-induced inflammation, with or without iron treatment, attenuated hippocampal heme oxygenase-1 and augmented 4-hydroxynonenal levels. Conversely, in the cortex, elevated ferritin light chain and xCT (light chain of System Xc−) were observed in response to LPS-induced inflammation, without and with iron-priming. Increased microglial branch/process lengths and astrocyte immunoreactivity were also increased by combined iron and LPS in both the hippocampus and cortex. Here, we demonstrate iron priming and subsequent LPS-induced inflammation led to iron dyshomeostasis, compromised antioxidant function, increased lipid peroxidation and altered neuroinflammatory state in a brain region-dependent manner

Use of gadolinium chloride as a contrast agent for imaging spruce knots by magnetic resonance

Treatments of knot-containing spruce wood blocks with a paramagnetic salt, gadolinium (III) chloride, in combination with solvent pretreatments, were evaluated as strategies to enhance the visualization of wood features by magnetic resonance imaging (MRI). Initial experiments with clear wood and excised knot samples showed differences in moisture uptake after pretreatments with selected solvents. For knot-containing spruce wood blocks, increased detail in the images with an ethanol pretreatment was attributed to the removal of extractives thereby resulting in higher moisture contents for the knot wood. Incorporation of the gadolinium-based contrast agent resulted in an abrupt loss in signal for a zone around each knot. Accordingly, the retention of gadolinium ions appears to be selective, thereby allowing the demarcation of what is likely to be compression wood known to surround softwood knots. Applications include studies on wood anatomy by MRI and the modeling of wood defects. The treatment of wood with contrast agents as such also shows promise as a technique to improve our understanding of the localization of different cell-wall chemistries, especially as they relate to ion exchange capacity

Diagram of MR imaging with inversion recovery magnetization-prepared fast low angle shot (MP-FLASH) pulse sequence

<p><b>Copyright information:</b></p><p>Taken from "Assessment of myocardial infarction in mice by Late Gadolinium Enhancement MR imaging using an inversion recovery pulse sequence at 9.4T"</p><p>http://www.jcmr-online.com/content/10/1/6</p><p>Journal of Cardiovascular Magnetic Resonance 2008;10(1):6-6.</p><p>Published online 24 Jan 2008</p><p>PMCID:PMC2244610.</p><p></p> IR = inversion recovery pulse; ECG = electrocardiogram; AW = acquisition window; TI = inversion time (optimal inversion is TI= TI to null uninfarcted myocardium); TR= effective repetition time (depending on TI and heart beat)

Dissociation between iron accumulation and ferritin upregulation in the aged substantia nigra:Attenuation by dietary restriction

Despite regulation, brain iron increases with aging and may enhance aging processes including neuroinflammation. Increases in magnetic resonance imaging transverse relaxation rates, R2 and R2*, in the brain have been observed during aging. We show R2 and R2* correlate well with iron content via direct correlation to semi-quantitative synchrotron-based X-ray fluorescence iron mapping, with age-associated R2 and R2* increases reflecting iron accumulation. Iron accumulation was concomitant with increased ferritin immunoreactivity in basal ganglia regions except in the substantia nigra (SN). The unexpected dissociation of iron accumulation from ferritin-upregulation in the SN suggests iron dyshomeostasis in the SN. Occurring alongside microgliosis and astrogliosis, iron dyshomeotasis may contribute to the particular vulnerability of the SN. Dietary restriction (DR) has long been touted to ameliorate brain aging and we show DR attenuated age-related in vivo R2 increases in the SN over ages 7 – 19 months, concomitant with normal iron-induction of ferritin expression and decreased microgliosis. Iron is known to induce microgliosis and conversely, microgliosis can induce iron accumulation, which of these may be the initial pathological aging event warrants further investigation. We suggest iron chelation therapies and anti-inflammatory treatments may be putative ‘anti-brain aging’ therapies and combining these strategies may be synergistic