Oxygen

Compounds known as liquid organic hydrogen carriers (LOHCs) offer a promising pathway for storing hydrogen. Beyond the use of pure hydrocarbons, the incorporation of oxygen atoms offers a way to modify thermodynamic properties and potentially improve suitability for hydrogen storage. This study explores the effect of oxygen functionalization in aromatic ethers and lactones on the reaction equilibrium of reversible hydrogenation. To address this question, reaction enthalpies and entropies are calculated using both experimental and theoretically determined pure substance data. The equilibrium position shift in the hydrogenation of furan derivatives has been shown to follow a similar trend to that of their hydrocarbon counterparts upon the addition of aromatic rings. This shift is, however, more pronounced in the case of the furan-based systems. The effect is reflected in increasing Gibbs reaction energies during the dehydrogenation process. Both the formation of lactones and the addition of a second ring to the furan core leads to a further increase in the Gibbs reaction energy. The highest value is observed for dibenzofuran, with a Gibbs reaction energy of 36.6 kJ∙mol⁻¹ at 500 K. These findings indicate that, from a thermodynamic perspective, hydrogen release is feasible at temperatures below 500 K, which is an important feature for the potential application as a hydrogen storage system.

Experimental evidence indicates that aqueous extracts of the Cistus genus have significant antioxidant properties, suggesting their potential as food fortifiers. In the present study, the antioxidant capacity and total phenolic content of lyophilized Cistus creticus extract were examined before and after in vitro digestion. Three concentrations of Cistus creticus extract were evaluated before and after in vitro gastrointestinal digestion, along with yogurt products fortified with these extracts, examined after digestion. Biochemical and cellular analyses were performed to assess these properties. The results showed statistically significant differences in total antioxidant capacity and total phenolic content, with values increasing from the lowest to the highest concentration studied, for both the lyophilized extracts and fortified yogurts after digestion. Additionally, cellular antioxidant activity after digestion was concentration-dependent (p < 0.05) within the range 25–500 mg/mL for both the extracts and fortified yogurts. In conclusion, based on the high phenolic content and the increased antioxidant capacity observed in epithelial cells, 250 mg of extract per 200 g of yogurt was proposed as the optimal fortification dose.

Amiodarone (AMD) is an effective antiarrhythmic drug whose long-term use is limited by multi-organ toxicities linked to oxidative stress. This review synthesizes current evidence on how AMD induces reactive oxygen species (ROS) generation in vitro and in vivo, and the mechanistic pathways involved. AMD promotes ROS production through both direct and indirect mechanisms. Directly, AMD accumulates in mitochondria and impairs the electron transport chain, leading to electron leakage and superoxide formation. It also undergoes redox cycling, forming radical intermediates that trigger lipid peroxidation and deplete cellular antioxidants. AMD and its metabolites inhibit antioxidant enzymes (SOD, CAT, GPx) expression and/or activities and reduce glutathione level, compounding oxidative injury. Indirectly, AMD activates signaling pathways that exacerbate ROS generation. This compound can induce pro-inflammatory mediators such as TNF-α and modulate nuclear receptors such as AhR, PXR, CAR, and PPARs, altering the expression of metabolic enzymes and endogenous antioxidants. These processes are time- and dose-dependent: short exposures at low concentrations may transiently scavenge radicals, whereas chronic or higher-dose exposures consistently lead to net ROS accumulation. The oxidative effects of AMD vary by tissue and experimental models. In chronic models, organs such as the lung and liver show pronounced ROS-mediated injury, whereas acute or cell-based systems typically exhibit subtler changes. AMD-induced toxicity arises from multifactorial oxidative stress involving mitochondrial dysfunction, increased radical formation, depletion of antioxidant defenses, and activation of pro-oxidant signaling pathways. Recognizing these pathways suggests that antioxidant and mitochondria-targeted co-therapies could ameliorate the side effects of AMD.