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Effects of 16O Charged-Particle Irradiation on Cognition, Hippocampal Morphology and Mutagenesis in Female Mice

ABSTRACT: Six-month old female C57BL/6 mice were irradiated with 16O at dosages of 0, 0.1 or 0.25 Gy (600 MeV/n) at NASA?s space radiation laboratory in Upton, NY. Three months following irradiation, animals were tested for hippocampus-dependent cognitive performance in the Y-Maze and Novel Object Recognition (NOR) paradigms. Upon sacrifice, brains were fixated and morphological assessments were conducted on hippocampal tissues.

INSTRUMENT(S): -

ORGANISM(S): Mus Musculus

SUBMITTER: University of Arkansas for Medical Sciences

PROVIDER: PRJEB39892 | EVA | 2020-08-17

REPOSITORIES: EVA

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			Action	DRS
	872-951_merged.accessioned.vcf.gz	Vcf
	872-951_merged.vcf.gz	Vcf
	872-951_merged.vcf.gz.tbi	Vcf

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Project description:In the present work endothelial function in the aorta and femoral artery assessed in vivo by magnetic resonance imaging (MRI) was characterized in male and female 8-, 14-, 22-, 28-, and 40-week-old E3L.CETP and C57BL/6J mice. Vascular nitric oxide (NO), eicosanoids and hydrogen peroxide (H2O2) production in the aorta, were measured by electron paramagnetic resonance spectroscopy (EPR), mass spectrometry (LC/MS) and fluoresence assay, respectively. Endothelial-specific protein plasma biomarkers and global alterations in plasma proteome were asssesed by targeted and non-targeted preotomics, respectively. In C57BL/6J endothelial dysfunction was observed in 40-week-old female and male mice as evidenced by impaired endothelium-dependent vasodilation induced by acetylcholine (Ach) in the aorta or by flow in the femoral artery (flow-mediated vasodilation, FMD). In E3L.CETP mice age-dependent endothelial dysfunction was accelerated and appeared in 14-22-week-old male and 22-28-week-old female mice. In 40 week-old E3L.CETP mice endothelial dysfunction was severe in both male and female mice and was more pronounced as compared with age-matched C57BL/6J mice. Despite severe endothelial dysfunction in 40 week-old mice E3L.CETP mice neither in the aortic roots nor in brachiocephalic artery atherosclerotic plaques were not detected. Interestingly, in the presence of NOS-inhibitor (L-NAME), FMD was inhibited in all experimental groups. However, effect of L-NAME on Ach–induced vasodilation in E3L.CETP mice, was blunted as compared with C57BL/6J mice, in particular in young E3L.CETP female mice. Furthermore, Ach–induced vasodilation in the aorta was inhibited by catalase, while H2O2 production was increased, in young female but not in male E3L.CETP mice. A switch from NO to H2O2-dependent vasodilation in young female E3L.CETP mice was associated with a blunted systemic inflammation and lower number of differentially expressed proteins (DEPs) in plasma than in young E3L.CETP male mice as compared with age-and sex-matched C57BL/6J mice. However, female and male 40-week-old E3L.CETP mice displayed similar number of DEPs in plasma vs respective sex-matched younger E3L.CETP mice. In the present work endothelial function in the aorta and femoral artery assessed in vivo by magnetic resonance imaging (MRI) was characterized in male and female 8-, 14-, 22-, 28-, and 40-week-old E3L.CETP and C57BL/6J mice. Vascular nitric oxide (NO), eicosanoids and hydrogen peroxide (H2O2) production in the aorta, were measured by electron paramagnetic resonance spectroscopy (EPR), mass spectrometry (LC/MS) and fluoresence assay, respectively. Endothelial-specific protein plasma biomarkers and global alterations in plasma proteome were asssesed by targeted and non-targeted preotomics, respectively. In C57BL/6J endothelial dysfunction was observed in 40-week-old female and male mice as evidenced by impaired endothelium-dependent vasodilation induced by acetylcholine (Ach) in the aorta or by flow in the femoral artery (flow-mediated vasodilation, FMD). In E3L.CETP mice age-dependent endothelial dysfunction was accelerated and appeared in 14-22-week-old male and 22-28-week-old female mice. In 40 week-old E3L.CETP mice endothelial dysfunction was severe in both male and female mice and was more pronounced as compared with age-matched C57BL/6J mice. Despite severe endothelial dysfunction in 40 week-old mice E3L.CETP mice neither in the aortic roots nor in brachiocephalic artery atherosclerotic plaques were not detected. Interestingly, in the presence of NOS-inhibitor (L-NAME), FMD was inhibited in all experimental groups. However, effect of L-NAME on Ach–induced vasodilation in E3L.CETP mice, was blunted as compared with C57BL/6J mice, in particular in young E3L.CETP female mice. Furthermore, Ach–induced vasodilation in the aorta was inhibited by catalase, while H2O2 production was increased, in young female but not in male E3L.CETP mice. A switch from NO to H2O2-dependent vasodilation in young female E3L.CETP mice was associated with a blunted systemic inflammation and lower number of differentially expressed proteins (DEPs) in plasma than in young E3L.CETP male mice as compared with age-and sex-matched C57BL/6J mice. However, female and male 40-week-old E3L.CETP mice displayed similar number of DEPs in plasma vs respective sex-matched younger E3L.CETP mice.

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Effects of 16O Charged-Particle Irradiation on Cognition, Hippocampal Morphology and Mutagenesis in Female Mice

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