Giallongo Sebastiano, Bellia Francesco, Russo Andrea, Fallico Matteo, Polosa Riccardo, Castellino Niccolò, Longo Antonio, Emma Rosalia, Partsinevelos Konstantinos, Caruso Massimo, Kartasasmita Arief S, Sferrazzo Giuseppe, Barbagallo Ignazio Alberto, Caltabiano Rosario, Broggi Giuseppe, Alanazi Amer M, Li Volti Giovanni
Department of Surgery and Medicine, University of Enna "Kore," Enna, Italy.
Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
Invest Ophthalmol Vis Sci. 2025 Apr 1;66(4):4. doi: 10.1167/iovs.66.4.4.
Tobacco smoke harbors toxic combustion by-products contributing to inflammatory diseases. Cigarette smoke's impact on ocular diseases has been poorly characterized, despite conjunctival mucosa's sensitivity to these toxicants. Of note, cigarette smoke triggers redness, tearing, and discomfort, accounting as a risk factor for glaucoma, macular degeneration, cataracts, and other eye conditions. Low quit rates of cessation highlight the need for alternatives. Heated tobacco products (HTPs), may represent a less toxic alternative for those smokers. This study evaluates cigarette smoke and HTPs effects on cornea under standard and clinically relevant conditions.
Corneal tissues collected from donors and in vitro model in two different cell lines of corneal epithelium were exposed to cigarette (1R6F) smoke and HTPs vapor. Air exposure was included as a control. Tissue pathological evaluation was carried out by hematoxylin and eosin staining. Reactive oxygen species (ROS) were measured, and quantitative PCR assessed inflammatory and antioxidant genes expression. Proteome analysis was used to evaluate differentially expressed proteins related to the oxidative stress. Scratch assay measured smoke and HTPs impact on cells.
Hematoxylin & eosin staining highlighted that cigarette smoke impairs corneal tissue integrity, leading to ROS accumulation and inflammation, as proved by qPCR analysis. Proteomic analysis showed that corneal tissue's proteins were differently oxidized by the different experimental conditions. HTP targeted structural intracellular proteins, whereas 1R6F affects different members of collagen family. Finally, cigarette smoke, but not HTPs, impairs epithelial cells wound closure.
Smoking increases oxidative stress, leading to significant corneal damage and inflammation. HTPs may offer a less toxic alternative.
烟草烟雾中含有有毒的燃烧副产物，会引发炎症性疾病。尽管结膜黏膜对这些有毒物质敏感，但香烟烟雾对眼部疾病的影响仍未得到充分描述。值得注意的是，香烟烟雾会引发眼红、流泪和不适，是青光眼、黄斑变性、白内障及其他眼部疾病的危险因素。戒烟成功率低凸显了寻找替代方法的必要性。加热烟草制品（HTPs）可能是对那些吸烟者毒性较小的替代品。本研究评估了在标准和临床相关条件下香烟烟雾和HTPs对角膜的影响。
从供体收集角膜组织，并将两种不同角膜上皮细胞系的体外模型暴露于香烟（1R6F）烟雾和HTPs蒸气中。以暴露于空气中作为对照。通过苏木精和伊红染色进行组织病理学评估。测量活性氧（ROS），并通过定量PCR评估炎症和抗氧化基因的表达。蛋白质组分析用于评估与氧化应激相关的差异表达蛋白质。划痕试验测量烟雾和HTPs对细胞的影响。
苏木精和伊红染色表明，香烟烟雾会损害角膜组织的完整性，导致ROS积累和炎症，定量PCR分析证实了这一点。蛋白质组分析表明，在不同实验条件下，角膜组织中的蛋白质被不同程度地氧化。HTP靶向细胞内结构蛋白，而1R6F影响胶原蛋白家族的不同成员。最后，香烟烟雾而非HTPs会损害上皮细胞的伤口闭合。
吸烟会增加氧化应激，导致角膜严重损伤和炎症。HTPs可能是毒性较小的替代品。
