Modified citrus pectin confers a preventative effect on cancer-related pathways in CdCl2-treated C. elegans

Authors: CAI SHI, DENIA - Rutgers University; Hotchkiss, Arland; LAWTON, MICHAEL - Rutgers University; DI, RONG - Rutgers University

Submitted to: Food Hydrocolloid for Health
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/2/2023
Publication Date: 10/4/2023
Citation: Cai Shi, D., Hotchkiss, A.T., Lawton, M.A., Di, R. 2023. Modified citrus pectin confers a preventative effect on cancer-related pathways in CdCl2-treated C. elegans. Food Hydrocolloid for Health. 4:100161. https://doi.org/10.1016/j.fhfh.2023.100161.
DOI: https://doi.org/10.1016/j.fhfh.2023.100161

Interpretive Summary: Modified citrus pectin has many bioactive properties but more information is needed to determine its mode of action. Changes in gene expression in a worm model system in response to a carcinogenic metal compound was investigated by Rutgers University scientists in collaboration with ARS (Wyndmoor, PA). Modified citrus pectin protected worms from metal-induced cell death by modifying gene expression in cancer-related and inflammation-related pathways. This research provides a better understanding of modified citrus pectin bioactivity in worms and provides insights for more complex organisms.

Technical Abstract: Cadmium chloride (CdCl2) is a toxic compound found as a pollutant in the environment due to agricultural and industrial sources. Exposure to Cd2+ is known to promote malignant tumors such as lung cancer and leukemia. While the current medications for cadmium toxicity focus on treatments to promote the excretion from the body, treatments to improve health after cadmium exposure are less well studied. Modified citrus pectin (MCP) is a polysaccharide derived from citrus peels that has been shown to induce natural killer cell activity in myeloid leukemia cells and also act as a natural chelation agent to help excrete toxic metals from healthy human subjects. We hypothesized that MCP might have a counteracting effect against CdCl2 toxicity through cancer-related pathways. This study investigates the effects of MCP on CdCl2 toxicity in C. elegans, which shares a number of cancer-related pathways with mammals. The results indicated that MCP was able to significantly counter the toxic effects of CdCl2 on C. elegans lifespan and development. Our studies suggest that the beneficial effects of MCP may result from its ability to mitigate the effects of CdCl2 on gene expression, particularly in conserved pathways associated with apoptosis, tumor induction and suppression and inflammation-related pathways.