Natural antioxidant functionalization for fabricating ambient-stable black phosphorus nanosheets toward enhancing flame retardancy and toxic gases suppression of polyurethane.

Herein, as a natural antioxidant, tannin (TA) is firstly used to functionalize black phosphorous (BP) nanosheets to improve the ambient stability and toxic suppression, thus decreasing the fire hazards of polymer materials. Compared to pure BP nanosheets, higher temperature for thermal oxidation decomposition is achieved for TA-BP nanosheets, directly confirming the ambient stability of TA-BP nanosheets. Meanwhile, from high resolution TEM and XPS results, TA-BP nanosheets after being exposed at air for 10 days present well-organized crystal structure and low POx bonds content. Cone calorimeter results illustrate that the incorporation of 2.0 wt% TA-BP nanosheets significantly decreases the peak value of heat release rate (-56.5 %), total heat release (-43.0 %), CO2 concentration (-57.3 %) of TPU composite. Meanwhile, with addition of low to 1.5 wt%, the release of highly-toxic CO gas is significantly suppressed, confirmed by lower peak value (0.52 mg/m3) and decreased total release amount (-55.1 %). The obviously enlarged tensile strength (36.7 MPa) and desirable elongation at break (622 %) are also observed. This strategy not only firstly adopts bio-based antioxidant to impart excellent environmental stability for BP nanosheets, but also promotes the promising potentials of BP nanosheets in the fire safety application of polymer composites.

Contradictory effects of mitochondria- and non-mitochondria-targeted antioxidants on hepatocarcinogenesis by altering DNA repair in mice.

Conflicting effects of antioxidant supplementation on cancer prevention or promotion is of great concern to healthy people and cancer patients. Despite recent studies about antioxidants accelerating the progression of lung cancer and melanoma, antioxidants may still play a role in cancer prevention. Both tumor and antioxidants types influence the actual efficacy. However, little is known about the impact of different types of antioxidants on primary hepatocellular carcinoma (HCC), including non-mitochondrial- and mitochondrial-targeted antioxidants. Utilizing mouse models of chemical hepatocarcinogenesis, we showed that administration of non-mitochondria-targeted antioxidants N-acetylcysteine (NAC) and the soluble vitamin E analog, Trolox, prevented tumorigenesis, whereas administration of mitochondria-targeted antioxidants SS-31 (the mitochondria-targeted peptide) and Mito-Q (a derivative of ubiquinone) facilitated tumorigenesis. RNA sequencing revealed that NAC and SS-31 caused very different changes in the oxidation-reduction state and DNA damage response. In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them. Interestingly, partial recovery of SS-31-scavengened mitochondrial reactive oxygen species (mtROS) could alleviate SS-31-aggravated DNA damage. Localization of ATM between mitochondria and nuclei was altered after NAC and SS-31 treatment. Furthermore, blockage of phospho-ATR (p-ATR) led to the recurrence of NAC-ameliorated DEN HCC. In contrast, reactivation of p-ATR blocked SS-31-promoted DEN HCC. Conclusion: These results demonstrate that the type of antioxidants plays a previously unappreciated role in hepatocarcinogenesis, and provide a mechanistic rationale for exploring the therapeutic use of antioxidants for liver cancer. (Hepatology 2018;67:623-635).