article · Cell Biochemistry and Biophysics
Hepatocellular carcinoma is a widespread liver cancer requiring improved treatment strategies. Iron oxide nanoparticles and chitosan-coated iron oxide nanoparticles were synthesised and evaluated against HepG2 liver cancer cells. The chitosan-coated variants exhibited a smaller, uniform spherical shape along with distinct surface and magnetic characteristics. In cellular assessments, the chitosan coating markedly enhanced anticancer activity, yielding a substantially lower inhibitory concentration than uncoated nanoparticles. Further examination demonstrated that the coated nanoparticles induced programmed cell death through extensive DNA fragmentation and damage. In addition, the treated cells displayed notable changes in oxidative stress markers and enzyme levels, including shifts in superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde. These combined effects suggest a dual mechanism of action driven by both DNA damage and oxidative stress, supporting the continued exploration of coated magnetic nanoparticles for cancer therapy.
Liver cancer is among the most prevalent cancers worldwide and often presents difficult clinical challenges. Formulating materials that attack cancer cells through multiple pathways, such as combining physical DNA disruption with oxidative stress, offers a valuable strategy for therapy design. Demonstrating that natural coatings like chitosan can drastically amplify the cell-killing performance of magnetic nanoparticles provides a clear direction for refining experimental cancer treatments.
This work sits at an early laboratory stage, having been evaluated exclusively on cultured cancer cell lines. If developed further, the materials could interest nanomedicine developers and oncology researchers seeking potent anticancer agents or drug delivery platforms for liver cancer. Moving towards commercialisation will require substantial translation, including animal safety and efficacy studies, formulation scale-up, and regulatory clinical trials, placing it far from immediate clinical application.
AI-generated from the published abstract. Always read the original work before citing.
Hepatocellular carcinoma (HCC), the fifth most prevalent cancer worldwide, is influenced by a myriad of clinic-pathological factors, including viral infections and genetic abnormalities. This study delineates the synthesis, characterization, and the biological efficacy of iron oxide nanoparticles (Fe<sub>3</sub>O<sub>4</sub>) and chitosan-coated iron oxide nanoparticles (Fe<sub>3</sub>O<sub>4</sub>-CS) against HCC. Analytical methods confirmed the successful synthesis of both nanoparticles, with Fe<sub>3</sub>O<sub>4</sub>-CS demonstrating a smaller, uniform spherical morphology and distinct surface and magnetic properties attributable to its chitosan coating. The prepared materials were analyzed using various techniques, and their potential cytotoxic effects on HepG2 cancer cells line for HCC were investigated. In biological evaluations against HepG2 cells, a notable distinction in cytotoxicity was observed. Fe<sub>3</sub>O<sub>4</sub> showed modest anticancer activity with an IC50 of 383.71 ± 23.9 µg/mL, whereas Fe<sub>3</sub>O<sub>4</sub> exhibited a significantly enhanced cytotoxic effect, with a much lower IC50 of 39.15 ± 39.2 µg/mL. The Comet assay further evidenced Fe<sub>3</sub>O<sub>4</sub>-CS potent DNA damaging effect, showcasing its superior ability to induce apoptosis through extensive DNA fragmentation. Biochemical analyses integrated into our results reveal that Fe<sub>3</sub>O<sub>4</sub>-CS not only induces significant DNA damage but also markedly alters oxidative stress markers. Compared to control and Fe<sub>3</sub>O<sub>4</sub>-treated cells, Fe<sub>3</sub>O<sub>4</sub>-CS exposure significantly elevated levels of oxidative stress markers: superoxide dismutase (SOD) increased to 192.07 U/ml, catalase (CAT) decreased to 0.03 U/L, glutathione peroxidase (GPx) rose dramatically to 18.76 U/gT, and malondialdehyde (MDA) levels heightened to 30.33 nmol/gT. These results underscore the potential of Fe<sub>3</sub>O<sub>4</sub>-CS nanoparticles not only in inducing significant DNA damage conducive to cancer cell apoptosis but also in altering enzymatic activities and oxidative stress markers, suggesting a dual mechanism of action that may underpin their therapeutic advantage in cancer treatment. Our findings advocate for the further exploration of Fe<sub>3</sub>O<sub>4</sub>-CS nanoparticles in the development of anticancer drugs, emphasizing their capability to trigger oxidative stress and enhance antioxidant defense mechanisms.
This page summarises published work. The authoritative version sits with the publisher.
DOI: 10.1007/s12013-024-01256-2
Is something wrong with this record? Report it or request removal.
Discussion
Have you built on this work, tried to replicate it, or seen it applied in practice? Share what you know. Verified researchers and MARATTO™ domain experts can open a discussion, and any member can reply. Contributions are reviewed before they appear.
No discussion yet. Open the first thread.
New to MARATTO™? Create a free account.
