Significance: Oxidative stress and oxidative damage are central hypothetical mechanisms for the adverse effects of airborne particulate matter (PM). Activation of inflammatory cells capable of generating reactive oxygen and nitrogen species is another proposed damage pathway. Understanding the interplay between these responses can help us understand the adverse health effects attributed to breathing polluted air. Critical issues: Reactive oxygen species (ROS) are generated during phagocytosis of the particles, leading to enhancement of oxidative stress and triggering the inflammatory response. The activation of inflammatory signaling pathways results in the release of cytokines, and other mediators that can further induce ROS production by activating endogenous enzymes, leading to a positive feedback loop, which can aggravate the effects triggered by PM exposure. Recent advances: The consequences of PM exposure on different organs results in oxidative damage, decreased function, and inflammation, which can lead to the development/exacerbation of proinflammatory disorders. Mitochondrial damage is also an important event in PM-induced cytotoxicity. Future directions: Further research is required to elucidate the exact mechanisms by which PM exposure results in adverse health effects, in terms of the relationship between the redox responses triggered by the presence of the particles and the inflammation observed in the different organs, so the development/exacerbation of PM-associated health problems can be prevented.

: Purpose:  The goal of the present study is to establish the antioxidant status in the brain of a high pressure–induced rat model.Methods:  Ocular hypertension was induced in rats (n = 12) cauterizing two episcleral veins under a surgical microscope. A sham procedure (n = 12) was performed in the control group. The markers evaluated in the brain 7 days after surgery were as follows: spontaneous chemiluminescence, protein carbonylation, nitrite concentration, total reactive antioxidant potential (TRAP), ascorbic acid, glutathione, vitamin E and activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase.Results:  Chemiluminescence in glaucoma was 55% higher than in controls (393 ± 20 cpm/mg protein, p < 0.001). Protein carbonylation in glaucoma was 93% higher than in controls (1.15 ± 0.18 nmol/mg protein, p < 0.001). Nitrite concentration was 5.30 ± 0.25 μM for glaucoma (controls 4.41 ± 0.24 μM, p < 0.05). Total reactive antioxidant potential decreased by 42% in glaucoma (controls 153 ± 14 μM Trolox, p < 0.001). Ascorbic acid was 67 ± 26 μM for glaucoma (controls 275 ± 22 μM, p < 0.001). Vitamin E was 0.58 ± 0.05 μmol/g organ for glaucoma (controls 1.10 ± 0.06 μmol/g organ, p < 0.01). Glutathione was 1.98 ± 0.13 μmol/g organ for glaucoma (controls 8.19 ± 0.71 μmol/g organ, p < 0.001). Superoxide dismutase and GPx were increased in glaucoma by 42 and 59%, respectively (p < 0.05).Conclusions:  Reactive oxygen and nitrogen species were increased in glaucoma, the increase in chemiluminescence, protein carbonylation and nitrite levels could be evidenced by this situation. The decrease in nonenzymatic antioxidants and a compensatory increase in SOD and GPx activity may have been a consequence of an increase in oxidative processes.

Background/Objectives: Glaucoma is the leading cause of irreversible blindness worldwide and oxidative stress is considered to play a key role in its development. While antioxidants offer a promising approach to mitigating oxidative stress, their clinical application is often hindered by bioavailability and absorption challenges. Entrapment antioxidants within liposomes may overcome these issues, enhancing their stability and delivery. The aim of this study was to develop a novel composite liposomal formulation for glaucoma treatment, designed to enhance lipoic acid bioavailability and administration through its incorporation into the lipid bilayer. Methods: Liposomes were prepared via lipid film hydration and extrusion. To characterize them, the following analyses were performed: FTIR spectroscopy, liposomal bilayer melting temperature (Tm), TEM, DLS, Z-potential, antioxidant activity, and cytotoxicity assays. Results: The efficient incorporation of lipoic acid into the liposomes’ lipid bilayer was confirmed by FTIR. This incorporation resulted in an increase in the Tm, from 37.0 °C for liposomes to 40.0 °C for liposomes with lipoic acid (L-LA). TEM images confirmed that the spherical morphology of the lipid vesicles remained unchanged following LA incorporation. Dynamic Light Scattering analysis revealed effective diameters of 423 ± 36 nm for L liposomes and 404 ± 62 nm for L-LA liposomes. Notably, the Z-potential shifted from +4.7 ± 0.4 mV (L) to −0.4 ± 0.3 mV (L-LA). Furthermore, L-LA exhibited significant antioxidant activity (31.6 ± 0.4%) compared with L (5.3 ± 0.3%) and biocompatibility, suggesting its potential for therapeutic applications. Conclusions: In summary, biocompatible composite liposomes with antioxidant capacity were successfully developed, resulting in promising candidates for neuroprotective glaucoma therapy.