What is Citrus Pectine
High molecular weight polysaccharides that are present in the cell walls of plants.
From where it is extracted
Citrus pectin can be obtained from the peel and citrus pomace, which is an industrial by-product of citrus fruits.
What is it for?
Anti-tumour activity and membrane permeability of 1 kDa oligogalacturonide (PET-pectin), prepared from citrus pectin after 24 h hydrolysis, by commercial pectic enzyme produced by Aspergillus niger, on four human cell lines (HepG2, A549, Colo 205, and HEK293) and the uptake of oligogalacturonide by HEK293 cell and BALB/c mouse were investigated. PET-pectin causes a higher value of growth inhibition, lactate dehydrogenase release, and galactin-3 release in human cancer cells, as compared to the human normal HEK293 cell. There was a good correlation between growth inhibition of human cells and the uptake of rhodamine B-PET-pectin content by these cells. Additionally, almost no difference between growth inhibitions of human normal HEK293 cells cultivated with PET-pectin and pectin was found. Total pectin content in the blood of PET-pectin administrated mice increased to a maximum at 2 h after oral administration, while it did not increase and change in pectin administrated mice. These findings suggested that citrus PET-pectin can be developed as a potential dietary supplement in plant origin for cancer prevention (1).
Modified citrus pectin
The present study aimed to investigate the physical, structural and rheological modifications caused by the chemical modification process of citrus pectin. Therefore, three commercial citrus pectins with different degree of esterification were chemically modified by sequential alkali and acidic hydrolytic process to produce modified citrus pectins (MCP) with special properties. The molar mass (Mw), degree of esterification (DE), monosaccharide composition, 13C NMR spectra, homogeneity, morphology (SEM) and rheological behavior of both native and modified citrus pectins (MCP) were investigated. The chemical modification reduced the acid uronic content (up to 28.3%) and molar mass (up to 29.98%), however, showed little influence on the degree of esterification of native pectins. Modified citrus pectins presented higher amounts of neutral monosaccharides, mainly galactose, arabinose and rhamnose, typical of the Ramnogalacturonana-I (RG-I) region. Rheological tests indicated that the native and modified citrus pectins presented pseudoplastic behavior, however, the MCP samples were less viscous, compared to the native ones. Modified samples presented better dissolution in water and less strong gels, with good stability during oscillatory shearing at 25°C. This study aims to better understand the implications that chemical modifications may impose on the structure of citrus pectins (2).
Galectin-3 is a carbohydrate-binding lectin, which has been implicated in the modulation of atherosclerotic pathophysiology, and is highly expressed in monocytes, macrophages and endothelial cells within atherosclerotic plaques. Modified citrus pectin (MCP) is produced from citrus pectin via pH and temperature modifications, which break it into shorter, non‑branched, galactose‑rich carbohydrate chains. MCP is able to tightly bind with galectin‑3, via recognition of its carbohydrate recognition domain, and facilitates the modulation of galectin‑3‑induced bioactivity. The present study explored the effects of MCP on the initiation of atherosclerosis. Eight‑week‑old apolipoprotein E‑deficient mice were treated with 1% MCP and fed an atherogenic diet for 4 weeks. The effects of MCP on atherosclerotic initiation were determined by pathological analysis and scanning electron microscope (SEM) imaging. MCP treatment reduced the size of atherosclerotic lesion areas, which was accompanied by decreased numbers of macrophages and smooth muscle cells (SMCs). Furthermore, SEM examination of the surface of the atheroma‑prone vessel wall indicated that MCP treatment reduced endothelial injury. To analyze the effects of MCP on monocyte adhesion, firstly, oxidized‑low density lipoprotein and various concentrations of MCP (0.025, 0.05, 0.1 and 0.25%) were incubated with the human umbilical vein endothelial cells (HUVECs) for stimulation and following this, the U937 cells were plated onto the HUVECs. The results revealed that MCP reduced the adhesion of U937 monocytes to HUVECs, indicating the adhesion-inhibiting effects of MCP. In conclusion, the present study revealed that MCP, a galectin‑3 inhibitor, reduced the size of atherosclerotic lesions by inhibiting the adhesion of leucocytes to endothelial cells. Inhibition of galectin‑3 function may be a therapeutic strategy for the treatment of atherosclerosis (3).
Molecular Formula : C5H10O5
Molecular Weight : 150.13 g/mol
CAS : 9000-69-5 20235-19-2 41247-05-6 609-06-3 58-86-6 5328-37-0 1114-34-7 147-81-9
Synonyms :
- Methoxyl Pectin
- Pectinose
- Lyxose, D-
- DL-Arabinose
- DL-Xylose
- NSC1941
Bibliografia______________________________
(1) The uptake of oligogalacturonide and its effect on growth inhibition, lactate dehydrogenase activity and galactin-3 release of human cancer cells. Huang, P.H., Fu, L.C., Huang, C.S., Wang, Y.T., and Wu, M.C. Food Chem. 2012; 132: 1987–1995
(2) Chemical modification of citrus pectin: Structural, physical and rheologial implications.
Fracasso AF, Perussello CA, Carpiné D, Petkowicz CLO, Haminiuk CWI.
Int J Biol Macromol. 2018 Apr 1;109:784-792. doi: 10.1016/j.ijbiomac.2017.11.060. Epub 2017 Nov 11.
(3) Modified citrus pectin inhibits galectin-3 function to reduce atherosclerotic lesions in apoE-deficient mice.
Lu Y, Zhang M, Zhao P, Jia M, Liu B, Jia Q, Guo J, Dou L, Li J.
Mol Med Rep. 2017 Jul;16(1):647-653. doi: 10.3892/mmr.2017.6646. Epub 2017 May 29
Citrus Pectin 
Acid uronic
