Ayman Hawash

Mesenchymal stromal cells (MSCs) are essential for connective tissue repair, and impaired healing is well documented in tobacco users. MSCs are one plausible target for these adverse effects, but the underlying cellular mechanisms of high localized nicotine exposure remain poorly understood. This study investigated how short-term nicotine and cigarette smoke extract (CSE) exposure affect human MSC function, viability, and inflammatory signaling in vitro. MSCs isolated from bone marrow were exposed to CSE containing 4–40 µM nicotine or to 100 µM–10 mM pure nicotine. CSE produced markedly stronger cytotoxicity than nicotine, reducing proliferation and rapidly inducing necrotic cell death at 20–40 µM nicotine equivalents. Pure nicotine elicited a biphasic response: concentrations below 5 mM slightly increased proliferation, while 5 mM caused apoptotic cell death with prominent lysosomal vacuolization, and 10 mM shifted cell death toward necrosis. Sublethal exposures that generated pre-apoptotic cells were associated with significant IL8 induction and MMP2 activation, whereas IL6 remained largely unchanged. Nicotine induced lysosomal disruption suggests broader impacts on MSC homeostasis beyond viability, potentially influencing lineage commitment. These findings elucidate short-term effects of nicotine and CSE; high-dose nicotine and CSE are toxic to MSCs, while the lower doses perturb the inflammatory signaling and lysosomal function. Such alterations may compromise tissue regeneration, wound healing, and periodontal stability in users of potent localized nicotine delivery products.

Selenium (Se), an important micronutrient with several biological effects, exhibits improved stability, biocompatibility, and safety through nanoparticle (NP) formulation. We present here a novel approach for producing smaller and structurally stable biogenic selenium nanoparticles (SeNPs) with bioactive coating. Poly(allylamine hydrochloride)-coated SeNPs were synthesized biogenically using Trachyspermum ammi (TA) seed extract, in parallel to chemically synthesized SeNPs. NPs were characterized and assessed for their in vitro antioxidant/radical scavenging potential through multiple complementary chemical assays along with the intracellular reactive oxygen species (ROS) scavenging and biocompatibility assay using human dermal fibroblasts. Both NPs were spherical and positively charged, with TA-SeNPs having a smaller size and a more amorphous nature. X-ray photoelectron spectroscopy confirmed the presence of elemental Se. Fourier transform infrared spectroscopy (FTIR) indicated the functional groups common to both NPs, with unique aliphatic, aromatic and glycosidic linkages, and phenolic compounds in TA-SeNPs, attributed to the TA extract. Both NPs showed dose-dependent antioxidative properties, with TA-SeNPs exhibiting significantly increased antioxidant activity among all the tested samples and showing similar to relatively higher activity relative to L-ascorbic acid (AA) and TA extract in several assays. Viability assays revealed that both NPs were nontoxic at low concentrations; however, cell viability is decreased at high concentrations, indicating dose-dependent cytotoxicity. TA-SeNPs suppressed reactive oxygen species more effectively at low concentrations, whereas SeNPs showed stronger activity at high concentrations. Our findings showed that the TA extract-mediated biosynthesis offers a cost-effective and biologically favorable route to produce SeNPs, with potential for safer antioxidant nanomedicine applications.