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Local oxidative stress in diseases or injury severely hinders cell homeostasis and organ regeneration. Antioxidant therapy is an effective strategy for oxidative stress treatment. Biomaterials with good biocompatibility and reactive oxygen species (ROS) scavenging ability are good choices for antioxidant therapeutics. However, there are few natural biomaterials that are identified with both biocompatibility and strong antioxidant activity. Here, we show, for the first time, that silk fibroin (SF) is a strong antioxidant, which can eliminate ROS in both cells and zebrafish. We further demonstrate that the β-sheet structures turn into a random coiled structure when SF is treated with hydrogen peroxide. The content of β-sheet structures can be increased by heating, thus enhancing the antioxidation properties of SF. Therefore, SF can serve as a good antioxidant biomaterial for therapeutics, and its β-sheet structure-based antioxidation mechanism provides a novel theoretical basis, which could be a new cue for more antioxidant biomaterial discovery and identification.

Cadmium (Cd) is a toxic element that endangers crop growth and affects food safety and human health. Therefore, the study of Cd mitigation technology is important. Ultrasonic treatment can improve crop growth and enhance their ability to resist various abiotic stresses. In this study, the effect of ultrasonic treatment on alleviating sugarcane Cd stress was studied in a barrel experiment using sugarcane varieties ‘ROC22’ and ‘LC05‐136’ as test materials. Sugarcane buds without ultrasonic treatment and with ultrasonic treatment (20–40 kHz mixed frequency ultrasound for 2 min, dry treatment) were planted in soil with Cd contents of 0, 50, 100, 250, and 500 mg·kg−1. Compared with non-ultrasonic treatment, Ultrasonic treatment significantly increased the activities of antioxidant enzymes in sugarcane, significantly increased the content of osmoregulation substances, significantly reduced the content of superoxide anion (the highest decreases reached 11.55%) and malondialdehyde (the highest decreases reached 20.59%), and significantly increased the expression level of metallothionein (MT)-related genes, with the expression of ScMT1 increased by 8.80–37.49% and the expression of ScMT2–1–5 increased by 1.55–69.33%. In addition, ultrasonic treatment significantly reduced the Cd contents in sugarcane roots, stems, leaves, bagasse, and juice (the highest reduction in Cd content was 49.18%). In general, ultrasonic treatment regulated the metabolism of reactive oxygen species and MT-related gene expression in sugarcane, increased the Cd tolerance of sugarcane, promoted photosynthesis in sugarcane leaves, improved root morphology, enhanced sugarcane growth, and increased cane and sugar yield.

Ammonia, as one of the primary water pollutants in aquaculture, has been shown to induce a wide range of ecotoxicological effects on aquatic animals. In order to investigate the antioxidant and innate immune responses in crustaceans disrupted by ammonia, red swamp crayfish (Procambarus clarkii) were exposed to 0, 15, 30, and 50 mg/L total ammonia nitrogen for 30 d, the alterations of antioxidant responses as well as innate immunity were studied. The results showed that the severity of hepatopancreatic injury were aggravated by the increasing ammonia levels, which were mainly characterized by tubule lumen dilatation and vacuolization. The swollen mitochondria and disappeared mitochondria ridges suggested that oxidative stress induced by ammonia targets the mitochondria. Concurrently, enhanced MDA levels, and decreased GSH levels as well as the decreased transcription and activity of antioxidant enzymes, including SOD, CAT, and GPx were noticed, which suggested that high concentrations of ammonia exposure induce oxidative stress in P. clarkii. Furthermore, a significant decrease of the hemolymph ACP, AKP, and PO along with the significant downregulation of immune-related genes (ppo, hsp70, hsp90, alf1, ctl) jointly indicated that ammonia stress inhibited the innate immune function. Our findings demonstrated that sub-chronic ammonia stress induced hepatopancreatic injury and exert suppressive effects on the antioxidant capacity as well as innate immunity of P. clarkii. Our results provide a fundamental basis for the deleterious effects of ammonia stress on aquatic crustaceans.

Red swamp crayfish (Procambarus clarkii) has increasingly become a high-value freshwater product in China. During the intensive cultivation, excessive ammonia exposure is an important lethal factor of crayfish. We investigated the toxic effects and mechanisms of ammonia on crayfish at two different developmental stages. A preliminary ammonia stress test showed a 96-h LC50 of 135.10 mg/L and 299.61 mg/L for Stage_1 crayfish (8.47 ± 1.68 g) and Stage_2 crayfish (18.33 ± 2.41 g), respectively. During a prolonged ammonia exposure (up to 96 h), serum acid phosphatase and alkaline phosphatase showed a time-dependent decrease. Histological assessment indicated the degree of hepatopancreatic injury, which was mainly characterized as tubule lumen dilatation, degenerated tubule, vacuolization and dissolved hepatic epithelial cell, increased with exposure time. Enhanced malondialdehyde level and reduced antioxidant capacity of hepatopancreas were also observed. The mRNA expression and activity of catalase and superoxide dismutase showed an initial up-regulation within 24 h, and then gradually down-regulated with the exposure time. In the post-treatment recovery period, the Stage_2 crayfish exerted a stronger antioxidant and detoxification capacity than that of the Stage_1 crayfish, and thus quickly recovered from the ammonia exposure. Our findings provide a further understanding of the adverse effects of ammonia stress and suggest guidelines for water quality management during crayfish farming.

Objective: To explore the role of long non-coding RNA DLEU1 in the tumorigenesis and progression of non-small cell lung cancer (NSCLC) and the underlying mechanisms. Methods: The expression of DLEU1 in NSCLC tumor tissues and adjacent normal tissues was evaluated using bioinformatics analysis and qPCR. The effects of DLEU1 overexpression or deficiency on cell proliferation, apoptosis, migration and invasion were explored experimentally. Additionally, the impact of DLEU1 up-regulation on tumourigenesis was also assessed in vivo. Results: The expression of DLEU1 was up-regulated in NSCLC tumor tissues. DLEU1 overexpression promoted the proliferation, migration, and invasion, but inhibited the apoptosis of NSCLC cells by upregulating CDK1 expression, binding with SRC and altering the expression of P70(S6K), MMP2 and E-cadherin. Besides, xenograft tumors in nude mice demonstrated that DLEU1 overexpression accelerated tumor growth. Conclusions: DLEU1 promoted tumorigenesis and progression of NSCLC, and might be a promising therapeutic target for NSCLC.