ArticleToxicology reports2025
Investigating a novel solid-state oxygenating therapeutic: Influence on oxidative stress and cellular responses in human lung cells.
Article in Toxicology reports, 2025. 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
Hypoxia is a common pathological state found in a diverse array of diseases, including those associated with pulmonary dysfunctions such as ARDS, COPD, and emphysema. BaylorOx is a novel solid-state oxygenating therapeutic that aims to supplement current oxygenating therapies by supplying 8-15 times more oxygen than human hemoglobin. While increased O2 levels can alleviate cellular damage associated with hypoxia, supraphysiological oxygen levels can also produce reactive oxygen species (ROS), which can lead to oxidative stress at elevated levels. Due to BaylorOx's high oxygen capacity, it is essential to determine whether this novel drug has any indication of causing oxidative stress. The goal of this study was, firstly, to investigate the cytotoxicity of BUOx on the human bronchial epithelial (BEAS-2B) and adenocarcinoma human alveolar basal epithelial (A549) cell lines under standard and hypoxic atmospheric conditions. Cytotoxicity was measured by performing the lactate dehydrogenase (LDH) and MTT cell viability assays. The second aim of this study was to determine the effects of BUOx on oxidative stress in the BEAS-2B and A549 cell lines. ROS production was measured using the DCFH-DA assay after 24 h. exposure to BUOx and 48 h. incubation in hypoxic or normoxic conditions. From the cell viability assays, BUOx showed no signs of cytotoxicity up to doses as high as 100 ppm. Interestingly, ROS production, as determined through the DCFH-DA assay, differed between the BEAS-2B and A549 cell lines following treatment with BUOx. While BUOx did not cause a significant increase in ROS production at either tested dose on the BEAS-2B cell line, a significant increase in ROS production was seen at a 10-ppm dose in the A549s. This suggests that BUOx's mechanism of action may vary between different cell types and selectively cause oxidative stress in cancer cells. Overall, these findings suggest that BUOx may be an effective and safe alternative to current oxygen therapies, especially for the treatment of acute pulmonary dysfunctions associated with hypoxia. Further research is required to confirm BUOx's effects on oxidative stress and its potential as an anti-cancer agent.
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