R. Di, et al., “Pectic Oligosaccharide Structure-Function Relationships: Prebiotics, Inhibitors of Escherichia coli O157:H7 Adhesion and Reduction of Shiga Toxin Cytotoxicity in HT29 Cells,” Food Chem. 227, 245–254 (2017). P.P. Ruvolo, “Galectin-3 as a Guardian of the Tumor Microenvironment,” Biochim. Biophys. Acta. 1863(3), 427–437 (2016). Androgen-dependent and -independent human prostate cancer cell lines (LNCaP and PC3, respectively), androgen-dependent and -independent murine prostate cancer cell lines (CASP2.1 and CASP1.1, respectively), as well as noncancerous human benign prostate hyperplasia BPH-1 cell line, were used in the study. MTT assay revealed that 1.0% PectaSol exerted cytotoxicity on LNCaP, PC3, CASP2.1, CASP1.1, and BPH-1 cells for 4-day treatment by 48.0% +/- 2.1%, 54.4% +/- 0.3%, 15.4% +/- 0.8%, 46.1% +/- 1.7%, and 27.4% +/- 1.6%, respectively; whereas 1.0% PectaSol-C showed cytotoxity by 52.2% +/- 1.8%, 48.2% +/- 2.9%, 23.0% +/- 2.6%, 49.0% +/- 1.3%, and 26.8% +/- 2.6%, respectively. Western blotting further confirmed that both MCPs inhibit MAP kinase activation, increase the expression level of its downstream target Bim, a pro-apoptotic protein, and induce the cleavage of Caspase-3 in PC3 and CASP1.1 prostate cancer cells.

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Glucose concentration in medium supernatant of cells was detected according to the protocol of Glucose Assay Kit (NJJCBIO, Wuhan, China). The amount of glucose uptake is equal to the amount of glucose in fresh medium minus the amount of glucose in the medium supernatant of treatment group. Cells were collected and the number of cells was counted by cell counter. The values of glucose level were normalized to the number of cells. Lactate acid assay On the other hand, colonocyte apoptosis activation in animals fed with pectin is also largely due to butyrate, a molecule coming from pectin fermentation by colon bacteria flora ( Avivi-Green et al., 2000a, b). Indeed, intracolonic instillation of butyrate recapitulates the effect of orally administered pectin ( Avivi-Green et al., 2000b). Butyrate is also able to induce apoptosis in colonocytes in vitro in a p53-independent manner ( Kolar et al., 2007) and by inducing mitochondrial Ca 2+ overload ( Kolar et al., 2011). In parallel, both in vitro in rat intestinal epithelial cells exposed to butyrate and in mice fed with a diet supplemented with 20% pectin, TGF-ß signaling has been demonstrated to be enhanced, leading to colonocyte growth inhibition and apoptosis. Apoptosis seems to be induced via an increased expression of Id2 (inhibitor of differentiation 2), probably via inhibition of selective isoforms of HDACs ( Cao et al., 2011). Anti-Tumor Activity of pH-Modified Pectin For example, although other chelating agents can effectively remove toxic metals (such as lead) from the body, they can also lower zinc levels, causing a deficiency, particularly in small children [ 2]. This natural product is derived from the pith of citrus fruit peels, including lemons, limes, oranges and grapefruits, and is modified using a proprietary enzymatic and pH process. This unique modification process ensures that PectaSol-C MCP has the correct molecular weight necessary to promote optimal cellular wellness of the chest, male organ, lungs and more. PectaSol-C Professional is manufactured in facilities that meet or exceed current Good Manufacturing Practices (cGMP). Quality control tests are performed at every stage of the process from rigorous raw material testing to finished product testing. The product is tested by a third-party analytical laboratory to confirm it meets our strict quality standards.MCP may also help with the activation of natural killer cells, as well as T-cytotoxic cells, helping the immune system to fight leukemia [ 11].

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Studies on the effect of pectin in myeloma therapy are ongoing. Alkali-soluble pectin reduces immunoglobulin E (IgE) production in human myeloma cell line U266 in a study examining the effects of water- (WP), hexametaphosphate- (HXP), acid- (HP), and alkali-soluble (OHP) pectin solutions. However, whereas OP altered cell viability, WP, HXP, and HP did not. Moreover, pectin increased the proportion of IL-2 receptor (IL-2R)-positive cells in mesenteric lymph node (MLN) lymphocytes, indicating that its immunoglobulin modifying effect was mediated by activated Th1 cells [ 58]. Similar results were obtained by Cheng et al. (2011) who tested the anti-tumor activity of different polysaccharide fractions isolated from ginseng on colon cancer HT-29 cells. While fractions rich in HG stopped cell cycle in G2/M phase, fractions rich in HG and modified by heat treatment exerted a much higher anti-proliferative activity, which was accompanied by caspase-3 activation and apoptosis induction ( Cheng et al., 2011). Similarly, potato pectin, rich in HG, inhibited in vitro HT-29 cell proliferation and provoked a cell cycle arrest in G2/M phase. This inhibition was due to a decrease in cyclin B1 expression and in CDK-1 activity ( Cheng et al., 2013). It is important to note that Kang et al. (2006) also produced a citrus pectin-derived oligosaccharide, which was biologically active, by irradiation, i.e., without chemical treatment. Pectin irradiated with 20 kGy and then dialyzed (WT <10,000) inhibited cancer cell growth. Immunopotentiating Activity of Pectin J.R. Sádaba, et al., “Role for Galectin-3 in Calcific Aortic Valve Stenosis,” J. Am. Heart Assoc. 5(11), pii: e004360 (2016). In the US, the researched form of MCP is patented for structure-function health claims related to cellular, cardiovascular and immune health, as well as inflammation, fibrosis and toxic metal body burden. I. Eliaz, et al., “The Effect of Modified Citrus Pectin on Urinary Excretion of Toxic Elements,” Phytother. Res. 20(10), 859–864 (2006).A further study used Wistar DMH-treated rats to explore how AP formulations affect neoplastic damage and proliferative marker dysregulation, finding a substantial beneficial effect on colon carcinogenesis through the regulation of physiological indicators, oxidative stress, inflammatory markers, and hemodynamic alterations [ 26]. The anti-cancer activities of phenolics from apple trash have also been studied in HT29, HT115, and CaCo-2 cell lines as in vitro models of colon carcinogenesis. They found a significant decrease in HT115 cell invasion when apple phenolics were used to prevent DNA damage, a process associated with tumor initiation. In addition, hydrogen peroxide (H 2O 2)-induced damage was significantly reduced in HT29 cells, and CaCo-2 cell barrier function was increased, a process associated with reduced tumor promotion and metastatic potential [ 27]. G. Hossein, et al., “Synergistic Effects of PectaSol-C Modified Citrus Pectin an Inhibitor of Galectin-3 and Paclitaxel on Apoptosis of Human SKOV-3 Ovarian Cancer Cells,” Asian Pac. J. Cancer Prev. 14(12), 7561–7568 (2013). Gal-3, cleavage of the precursor of caspase-3, ↑ expression of the pro-apoptotic protein Bax, ↓ DNA repair pathways, poly-ADP-ribose polymerase PectaSol-C is the most advanced and effective Modified Citrus Pectin (MCP) supplement available. Gentle and highly effective formula, extensive scientific research has shown that PectaSol-C MCP can: Induced mitochondrial depolarization, reactive oxygen species generation, caspase-3 and Poly (ADP-ribose) polymerase 1 (PARP1) activation resulting in DNA fragmentation

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This was actually a large dose, so the fact that it was tolerated well by children is encouraging. The dose of MCP used in this study was equivalent to one scoop of Pectasol-C modified citrus pectin three-times daily for three months. (In our practice, we treat adults with one scoop twice daily for between 45 and 90 days, which we have found effective at lowering serum lead levels.) Slowing Heart Disease The original and only proven effective form of MCP is prepared with a proprietary, non-GMO enzymatic process controlled by pH and heat, which breaks the long chain molecules of the native pectin to produce the correct molecular size and structure of <13 kilodaltons and <5% esterification. As the research on this form of MCP continues, it’s critical to note that, in the nutraceutical world, MCP is not a carefully defined term. Experts emphasise that other “modified” citrus pectins do not offer the same benefits as the only researched, clinically studied and substantiated MCP.GI health: This MCP is also shown to offer functional prebiotic benefits as an oligosaccharide-rich fibre. One study with the USDA and Rutgers showed that as a prebiotic fibre, MCP reduced Shiga toxin cytotoxicity from the aggressive strain of E. coli 0157:H7, which has been implicated in recent food contamination outbreaks. 22 Formulating with MCP J. Ibarrola, et al., “Galectin-3 Down-Regulates Antioxidant Peroxiredoxin-4 in Human Cardiac Fibroblasts: A New Pathway to Induce Cardiac Damage,” Clin. Sci. (Lond). 132(13), 1471–1485 (2018). In my clinical experience, those with mycotoxicity (mold toxicity) often have trouble tolerating modified citrus pectin. This may be because MCP has the ability to bind to mycotoxins (like it binds to and removes metals), which could then lead to increased symptoms as the toxins are being released. C. Ramachandran, et al., “Activation of Human T-Helper/Inducer Cell, T-Cytotoxic Cell, B-Cell, and Natural Killer (NK)-Cells and Induction of Natural Killer Cell Activity Against K562 Chronic Myeloid Leukemia Cells with Modified Citrus Pectin,” BMC Complement Altern. Med. 11, 59 (2011).