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In this study, a novel fabrication method was used to synthesize phenolic resin/phosphate hybrid coatings using aluminum dihydrogen phosphate (Al(H2PO4)3, hereafter denoted as Al), SC101 silica sol (Si) as the primary film-forming agent, and phenolic resin (PF) as the organic matrix. This approach culminated in the formation of Al+Si+PF organo–inorganic hybrid coatings. Fourier-transform infrared spectroscopy (FT-IR) and X-ray photoelectron spectroscopy (XPS) results confirmed the successful integration of hybrid structures within these coatings. The crystalline structure of the coatings post-cured at various temperatures was elucidated using X-ray diffraction (XRD). Additionally, the surface and cross-sectional morphologies were meticulously analyzed using scanning electron microscopy (SEM), offering insights into the microstructural properties of the coatings. The coatings' porosities under diverse thermal and temporal regimes were quantitatively evaluated using advanced image processing techniques, revealing a significant reduction in porosity to a minimum of 5.88% following a thermal oxidation process at 600 °C for 10 h. The antioxidant efficacy of the phosphate coatings was rigorously assessed through cyclic oxidation tests, which revealed their outstanding performance. Specifically, at 300 °C across 300 h of cyclic oxidation, the weight losses recorded for phosphate varnish and the phenolic resin-infused phosphate coatings were 0.15 mg·cm−2 and 0.09 mg·cm−2, respectively. Furthermore, at 600 °C and over an identical period, the weight reduction was noted as 0.21 mg·cm−2 for phosphate varnish and 0.085 mg·cm−2 for the hybrid coatings, thereby substantiating the superior antioxidation capabilities of the phenolic resin hybrid coatings in comparison to the pure phosphate varnish. [ABSTRACT FROM AUTHOR]

The Ca 2+ buffering capacity of mitochondria maintains the balance of cell physiological activities. The exogenous reactive oxygen species (ROS) can be used to break the balance, resulting in mitochondrial dysfunction and irreversible cell apoptosis. Herein, the CaCO 3 -based tumor microenvironment (TME) responsive nanoplatform (CaNP CAT+BSO @Ce6-PEG) was designed for oxygen/GSH depletion-boosted photodynamic therapy (PDT) and mitochondrial Ca 2+ -overloading synergistic therapy. In acidic TME, CaCO 3 decomposed and released the cargos (catalase (CAT), buthionine sulfoximine (BSO), chlorin e6 (Ce6), and Ca 2+ ). The tumor hypoxia and reductive microenvironment could be significantly reversed by CAT and BSO, which greatly enhanced the PDT efficacy. The generated 1 O 2 during PDT process not only directly killed cancer cells but also destroyed the Ca 2+ buffering capacity, leading to the mitochondrial Ca 2+ -overloading. The increased Ca 2+ concentration promoted the process of oxidative phosphorylation and inhibited the production of adenosine triphosphate (ATP), resulting in the acceleration of cell death. Under the joint action of enhanced PDT and mitochondrial Ca 2+ -overloading, the CaNP CAT+BSO @Ce6-PEG NPs showed remarkable synergistic effects in tumor inhibition without any side effects. STATEMENT OF SIGNIFICANCE: In the manuscript, a CaCO 3 -based nano-platform for tumor microenvironment response was designed. With the decomposition of CaNP CAT+BSO @Ce6-PEG NPs in the acidic tumor microenvironment, the released catalase (CAT) and buthionine sulfoximine (BSO) could relieve the tumor hypoxia and inhibit GSH production. Under 660 nm laser irradiation, the photodynamic effect was enhanced and caused apoptosis. Meanwhile, the Ca 2+ buffering capacity was destroyed which led to the mitochondrial Ca 2+ -overloading. The synergistic effect of enhanced PDT and mitochondrial Ca 2+ -overloading made the CaNP CAT+BSO @Ce6-PEG NPs present remarkable antitumor performance., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.)