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Natural Biopolymeric Nanoformulations for Brain Drug Delivery
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nanocarriers for Brain Targeting, 2019
Josef Jampílek, Katarina Král’ová
Fluorescent-tagged NPs were observed in the cerebral cortex parenchyma after i.v. administration of PLGA NPs functionalized with an apolipopro-tein E modified peptide (pep-apoE) responsible for low-density lipoprotein receptor (LDLR) binding or with lipocalin-type prostaglandin-D-synthase (l-PGDS) to mice, whereby the NPs were mostly internalized by neurons and microglia; glial cells showed a weak activation. Because this observation was not obtained with non-functionalized NPs, it could be stated that the peptidic moieties enable BBB traversal of the NPs and could be considered as potential brain drug carriers (Portioli et al., 2017).
Development of Ophthalmic Formulations
Published in Sandeep Nema, John D. Ludwig, Parenteral Medications, 2019
Paramita Sarkar, Martin Coffey, Mohannad Shawer
Tear fluid contains proteins in high concentration, about 13.04 ± 3.46 μg/μL in adults [8]. Major components include lysozyme (an antibacterial enzyme), lactoferrin (which sequesters iron), secretory immunoglobulin A (an antibody important for mucosal immunity), serum albumin, lipocalin, and lipophilin [9]. In addition, more than 400 other proteins have been identified that serve various roles in the tear fluid [9]. The intercalation of proteins like lipocalin with the TFLL and ionic interactions among the proteins themselves can affect the structure and properties of the tear film such as the rheological behavior of the tear film [10].
Iron-Siderophore and Tumorigenesis
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Sayantan Maitra, Dibyendu Dutta
Overexpression of TFR1 and STEAP reductase in cancer cells gets accompanied by lipocalin 2 (LCN2), an overexpressed protein that is involved in alternative pathway of iron uptake. LCN2 binds with siderophores which were previously chelated with iron molecules. Thus, iron gets circulated in blood in the form of LCN2-siderophore complex and gets bind to cell surface receptor 24p3R and can serve as an alternative mechanism of iron delivery (Figure 17.2) [16].
Effects of cross-fostering and developmental exposure to mixtures of environmental contaminants on hepatic gene expression in prepubertal 21 days old and adult male Sprague-Dawley rats
Published in Journal of Toxicology and Environmental Health, Part A, 2019
D. Desaulniers, N. Khan, C. Cummings-Lorbetskie, K. Leingartner, G-H. Xiao, A. Williams, C.L. Yauk
The down-regulation of Cyp2c7, Retsat, Lcn2, and Tff3, and up-regulation of Akr1c1 in the MM group relative to M suggests that cross-fostering modulated the influence of M on mechanisms involving retinoid and lipid metabolism. As discussed previously, CYP2C7 is a retinoic acid and steroid hydroxylase enzyme (Fan et al. 2004), whereas AKR1C1 (AKR1C4 in human) is a member of the aldo-keto reductase family that catalyzes the reduction of retinaldehyde to retinol (Ruiz et al. 2011). Retinol saturase (Retsat) is an oxidoreductase that is also involved in retinoid metabolism, catalyzing conversion of retinol to 13,14-dihydroretinol (Moise et al. 2004). Lipocalin-2 (LCN2) is a transport protein for lipids, steroid hormones, and retinoids. Recently Guo et al. (2016) reported that Lcn2 deficient mice displayed diminished levels of retinol, retinyl ester, and all-trans retinoic acid in adipose tissue. As previously discussed, a different preparation of the same mixture produced a reduction in hepatic retinol (Elabbas et al. 2014). Taken together, these results suggest that cross-fostering modulated the effect of M on retinoid metabolism; however, retinoid biochemistry analyses would be required to determine if cross-fostering amplified or lowered the M-induced retinoid deficiency. Implication of Retsat and Tff3 on lipid and glucose metabolism is presented in Suppl. S5.3.