Kevin C. Chan1, 2, Shu-juan Fan1, 3, Iris Y. Zhou1, 3, Ed X. Wu1, 3
1Laboratory of Biomedical Imaging and Signal Processing, The University of Hong Kong, Pokfulam, Hong Kong, China; 2Department of Ophthalmology, University of Pittsburgh, Pittsburgh, PA, United States; 3Department of Electrical and Electronic Engineering, The University of Hong Kong, Pokfulam, Hong Kong, China
Chromium (Cr) has been used histologically to stabilize lipid fractions in the retina, and is suggested to enhance oxidizable lipids in brain MRI. This study explored the feasibility, sensitivity and specificity of in vivo chromium-enhanced MRI (CrMRI) of retinal lipids, by determining its spatiotemporal profiles and toxic effect after intravitreal Cr(VI) injection to normal and injured adult rats. One day after 3gL Cr(VI) administration at 1mM to 100mM, the normal retina exhibited a dose-dependent increase in T1-weighted hyperintensity until 50mM. Time-dependently, significant T1-weighted hyperintensity persisted up to 2 weeks after 10mM Cr(VI) administration. While CrMRI demonstrated reduced Cr enhancement in hypoxic-ischemic-injured retina, 3D-CrMRI of ex vivo normal eyes at isotropic 50gm resolution showed at least 5 alternating bands across retinal layers, with the outermost layer being the brightest. This agreed with histology indicating alternating lipid contents with the highest level in the photoreceptor layer of the outer retina. While Cr(VI) reduction may induce oxidative stress and depolymerize microtubules, manganese-enhanced MRI after CrMRI showed a dose-dependent effect of Cr toxicity on Mn uptake and axonal transport along the visual pathway. These results potentiated longitudinal CrMRI studies on retinal lipid metabolism upon further optimization of Cr doses with visual cell viability.
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