Fine particulate matter (PM2.5) is a major air pollutant linked to lung cancer progression. In Southeast Asia, seasonal smoke-haze produces biomass-derived PM2.5, yet its acute effects on genetically diverse lung tumours remain unclear. We investigate how Chiang Mai haze-derived PM2.5 impacts oxidative stress and gene expression in three non-small-cell lung cancer (NSCLC) cell lines: A549 (KRAS-mutant), NCI-H1975 (EGFR-mutant), and NCI-H460 (KRAS/PIK3CA-mutant). Cells were exposed to PM2.5 (0–200 µg/mL) and assessed for viability (MTT), reactive oxygen species (ROS; H₂O₂, •OH) and malondialdehyde (MDA) levels, mitochondrial-associated fluorescence, and whole-transcriptome responses. Acute exposure caused dose- and time-dependent viability loss, with A549 and NCI-H1975 more sensitive than NCI-H460. ROS profiling normalized to viable cells revealed genotype-specific oxidative patterns: cumulative increases in A549, sharp reversible spikes in NCI-H1975, and modest changes in NCI-H460. MitoTracker intensity trended downward without significance, with subtle fluorescence changes and particulate uptake. RNA-seq identified robust induction of xenobiotic metabolism (CYP1A1, CYP1B1), oxidative/metabolic stress mediators (GDF15, TIPARP), and tumour-associated genes (FOSB, VGF), alongside repression of tumour suppressors (FAT1, LINC00472). Pathway enrichment analyses highlighted oxidative stress, IL-17, NF-κB, and immune checkpoint signaling. Together, biomass haze-derived PM2.5 from Northern Thailand drives genotype-dependent oxidative stress and transcriptional remodeling in NSCLC cells.

Short-wavelength ultraviolet radiation can impair biological systems by causing DNA damage, oxidative stress, and disruption of photosynthetic processes. Although ultraviolet C (UVC) at 254 nm is widely used as a controlled laboratory stressor, the extent to which trophic condition influences repeated UVC tolerance in phototrophic protists remains unclear. Here, we examined the response of Euglena gracilis grown under photoautotrophic or ethanol-supported mixotrophic conditions and exposed to daily UVC pulses for five days. Cell growth, photosynthetic pigments, intracellular oxidative stress measured by 2′,7′ dichlorodihydrofluorescein diacetate fluorescence, and lipid peroxidation estimated as thiobarbituric acid reactive substances equivalent malondialdehyde were assessed, together with qualitative fluorescence microscopy. Repeated UVC exposure reduced cell density in both trophic conditions, with stronger inhibition under photoautotrophy. Photoautotrophic UVC-treated cultures showed the highest oxidative stress signal, whereas malondialdehyde displayed only a non-significant directional increase. Mixotrophic cultures maintained higher cell density under UVC and showed lower oxidative stress signals than photoautotrophic UVC-treated cultures. Pigment responses also differed between trophic conditions, with increased chlorophyll a and carotenoids per cell under photoautotrophic UVC treatment, while mixotrophic pigment levels remained comparatively stable. These findings show that trophic condition shapes repeated UVC stress responses in E. gracilis and that ethanol-supported mixotrophy is associated with improved physiological robustness under the present experimental conditions.