Effects of organophosphorus flame retardant EHDPP on mouse retinal photoreceptor cells: Oxidative stress, apoptosis, and proinflammatory response.

2-Ethylhexyl diphenyl phosphate (EHDPP) is a frequently utilized organophosphorus flame retardant (OPFR) and has been extensively detected in environmental media. Prolonged daily exposure to EHDPP has been linked to potential retinal damage, yet the adverse impacts on the retina are still generally underexplored. In this research, we explored oxidative stress, inflammation, and the activating mechanisms initiated by EHDPP in mouse retinal photoreceptor (661 W) cells following a 24 h exposure period. Our research demonstrated that EHDPP led to a decline in cell viability that was directly proportional to its concentration, with the median lethal concentration (LC50) being 88 µM. Furthermore, EHDPP was found to elevate intracellular and mitochondrial levels of reactive oxygen species (ROS), trigger apoptosis, induce cell cycle arrest at the G1 phase, and modulate the expression of both antioxidant enzymes (Nrf2, HO-1, and CAT) and pro-inflammatory mediators (TNF-α, IL-1ß, and IL-6) within 661 W cells. These findings indicate that retinal damage triggered by EHDPP exposure could be mediated via the Nrf2/HO-1 signaling pathway in these cells. Collectively, our investigation revealed that oxidative stress induced by EHDPP is likely a critical factor in the cytotoxic response of 661 W cells, potentially leading to damage in retinal photoreceptor cells.

Mitochondria-targeted SkQ1 nanoparticles for dry eye disease: Inhibiting NLRP3 inflammasome activation by preventing mitochondrial DNA oxidation.

Dry eye disease (DED) is a multifactorial ocular surface disorder mutually promoted by reactive oxygen species (ROS) and ocular surface inflammation. NLRP3 is the key regulator for inducing ocular surface inflammation in DED. However, the mechanism by which ROS influences the bio-effects of NLRP3, and the consequent development of DED, largely remains elusive. In the present study, we uncovered that robust ROS can oxidate mitochondrial DNA (ox-mtDNA) along with loss of mitochondria compaction causing the cytosolic release of ox-mtDNA and subsequent co-localization with cytosolic NLRP3, which can promote the activation of NLRP3 inflammasome and stimulate NLRP3-mediated inflammation. Visomitin (also known as SkQ1), a mitochondria-targeted anti-oxidant, could reverse such a process by in situ scavenging of mitochondrial ROS. To effectively deliver SkQ1, we further developed a novel mitochondria-targeted SkQ1 nanoparticle (SkQ1 NP) using a charge-driven self-assembly strategy. Compared with free SkQ1, SkQ1 NPs exhibited significantly higher cytosolic- and mitochondrial-ROS scavenging activity (1.7 and 1.9 times compared to levels of the free SkQ1 group), thus exerting a better in vitro protective effect against H2O2-induced cell death in human corneal epithelial cells (HCECs). After topical administration, SkQ1 NPs significantly reduced in vivo mtDNA oxidation, while suppressing the expressions of NLRP3, Caspase-1, and IL-1ß, which consequently resulted in better therapeutic effects against DED. Results suggested that by efficiently scavenging mitochondrial ROS, SkQ1 NPs could in situ inhibit DED-induced mtDNA oxidation, thus blocking the interaction of ox-mtDNA and NLRP3; this, in turn, suppressed NLRP3 inflammasome activation and NLRP3-mediated inflammatory signaling. Results suggested that SkQ1 NPs have great potential as a new treatment for DED.

Highly selective and sensitive determination of uranyl ion by the probe of CdTe quantum dot with a specific size.

Determination of trace amounts of uranyl ions is of great significance to environment and human health, but challenging. In this paper, we demonstrate a new approach for highly effective determination of uranyl ions by the probe of CdTe quantum dot (QD) with a specific size. The selectivity is relied on the probe of CdTe quantum dots; the selectivity, which was a function of QDs size, was optimum at 6.8 nm. The probe has a detection limit of 7.88 × 10-9 mol L-1 and responded linearly to uranyl ion concentration in the range of 2.36 × 10-8 mol L-1 ~ 4.00 × 10-7 mol L-1. The mechanism can be probably attributed to the fact that uranyl ions could react with Te(0) on the surface of the quantum dots as large as 6.8 nm, resulting in fluorescence quenching. This work provides a new approach to detect uranyl ions in the aqueous solution by doing strip and real sample tests, and indicated the promise of this approach for real-time and in-situ detection of uranyl ions.

Phosphonate and carboxylic acid co-functionalized MoS2 sheets for efficient sorption of uranium and europium: Multiple groups for broad-spectrum adsorption.

It is significant to develop novel materials and techniques for efficient removal of radionuclides from radioactive wastes due to the radioactive and chemical toxicity. In this paper, we report a strategy for broad-spectrum adsorption of radionuclides by multiple groups-decorated adsorbents. Specifically, the adsorbents were prepared by grafting diethyl-(4-vinylbenzyl) phosphonate and maleic anhydride copolymers onto molybdenum disulfide sheets for the sorption of uranium(VI) and europium(III). The sorption efficiencies exhibited a dependency on pH, contact time and initial concentrations. The sorption reached the equilibrium within 60 min and followed a pseudo-second-order kinetic model. The maximum sorption capacities of the sorbents were 448.4 mg/g and 171.2 mg/g at pH 4.0 and 298.15 K for uranium(VI) and europium(III), respectively. The sorbent possessed a high efficiency of 98% in five sorption-desorption cycles without damage in chemical structures. XPS spectra showed that the sorption of uranium(VI) and europium(III) on the sorbents were originated from the interaction between multiple groups (such as sulfur, COOH, PO and PO) and uranium/europium. This work demonstrates that the adsorbent can be utilized as a promising material for the separation of broad-spectrum radionuclides from an aqueous solution.