ArticleMolecular biology reports2026
NaHS inhibits cell proliferation by enhancing oxidative stress and apoptosis in HCT116 cells.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundColorectal cancer remains a leading cause of cancer-related mortality, and current treatments are often limited by toxicity and therapeutic resistance. This study investigated the antiproliferative effects of the fast-releasing hydrogen sulfide (H₂S) donor sodium hydrosulfide (NaHS) in HCT116 colorectal cancer cells and explored the underlying mechanisms related to oxidative stress, DNA damage, apoptosis, inflammation, and key growth-related signaling pathways. MATERIALS AND
methodsHCT116 colorectal cancer cells and CCD-18Co normal colon fibroblast cells were cultured under standard conditions and treated with increasing concentrations of sodium hydrosulfide (NaHS). Cell viability was assessed using the XTT assay to determine antiproliferative activity and half-maximal inhibitory concentration (IC₅₀) values. Oxidative stress was evaluated by measuring total antioxidant status (TAS), total oxidant status (TOS), and intracellular reactive oxygen species (ROS) generation. Apoptosis and signaling-related proteins were analyzed by enzyme-linked immunosorbent assay (ELISA)-based quantification of BCL2-associated agonist of cell death (BAD), caspase-3, B-cell lymphoma 2 (BCL-2), phosphoinositide 3-kinase (PI3K), mitogen-activated protein kinase (MAPK), and nuclear factor kappa B (NF-κB), supported by Annexin V flow cytometry. Oxidative DNA damage and apoptotic activation were further evaluated using immunofluorescence staining for 8-hydroxy-2'-deoxyguanosine (8-OHdG) and cleaved caspase-3.
resultsNaHS significantly reduced HCT116 cell viability in a concentration- and time-dependent manner, with IC₅₀ values of 4.56, 2.549, and 1.688 mM after 24, 48, and 72 h of treatment, respectively. In contrast, lower concentrations of NaHS did not significantly affect the viability of CCD-18Co normal colon fibroblast cells. NaHS treatment induced oxidative stress, as evidenced by decreased TAS, increased TOS, and elevated intracellular ROS levels. Apoptotic responses were associated with increased BAD and caspase-3 levels, decreased BCL-2 expression, and increased early and late apoptotic cell populations. NaHS also increased 8-OHdG and cleaved caspase-3 immunofluorescence signals. In addition, reduced levels of PI3K-, MAPK-, and NF-κB-related proteins were observed following NaHS treatment.
conclusionNaHS exerts potent antiproliferative effects in colorectal cancer cells by inducing oxidative stress-mediated apoptosis and inhibiting key survival and inflammatory signaling pathways.
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