The ingestion of nucleic acids (NAs) as a nutritional supplement or in genetically modified food has attracted the attention of researchers in recent years. Discussions over the fate of NAs led us to study their digestion in the stomach. Interestingly, we found that NAs are digested efficiently by human gastric juice. By performing digests with commercial, recombinant and mutant pepsin, a protein-specific enzyme, we learned that the digestion of NAs could be attributed to pepsin rather than to the acidity of the stomach. Further study showed that pepsin cleaved NAs in a moderately site-specific manner to yield 3′-phosphorylated fragments and the active site to digest NAs is probably the same as that used to digest protein. Our results rectify the misunderstandings that the digestion of NAs in the gastric tract begins in the intestine and that pepsin can only digest protein, shedding new light on NA metabolism and pepsin enzymology.

Astaxanthin is an excellent antioxidant that can form unstable aggregates in biological or artificial systems. The changes of astaxanthin properties caused by molecular aggregation have gained much attention recently. Here, water-dispersible astaxanthin H- and J-aggregates were fabricated and stabilized by a natural DNA/chitosan nanocomplex (respectively noted as H-ADC and J-ADC), as evidenced by ultraviolet and visible spectrophotometry, Fourier transform infrared spectroscopy, and Raman spectroscopy. Compared with J-ADC, H-ADC with equivalent astaxanthin loading capacity and encapsulation efficiency showed smaller particle size and similar zeta potential. To explore the antioxidant differences between astaxanthin H- and J-aggregates, H-ADC and J-ADC were subjected to H₂O₂-pretreated Caco-2 cells. Compared with astaxanthin monomers and J-aggregates, H-aggregates showed a better cytoprotective effect by promoting scavenging of intracellular reactive oxygen species. Furthermore, in vitro 1,1-diphenyl-2-picrylhydrazyl and hydroxyl free radical scavenging studies confirmed a higher efficiency of H-aggregates than J-aggregates or astaxanthin monomers. These findings give inspiration to the precise design of carotenoid aggregates for efficient utilization.

In this research, astaxanthin-rich nanopowder was prepared by nanoencapsulation and freeze-drying techniques with enhanced bioavailability and antioxidant activities. The nanopowder showed a maximum solubility of 230 mg mL⁻¹ with an astaxanthin content as high as 2.9%. Compared with free astaxanthin, the astaxanthin-loaded nanopowder exhibited a more efficient antioxidant effect: an oral dose of 0.9 mg per kg BW significantly reduced the malondialdehyde and protein carbonyl contents, and increased the glutathione content as well as the superoxide dismutase activities in alcohol-induced acute hepatic injured mice, and maintained these oxidative stress indicators at a normal level for a longer period when treated with nanoencapsulated-astaxanthin than free astaxanthin. Simulated gastrointestinal tract studies demonstrated that the nanopowder with pH and DNase I-dependent dissociation properties delivered astaxanthin efficiently to the small intestine. Astaxanthin-rich nanopowder with a dose as high as 2.4 mg per kg BW (equivalent to astaxanthin) showed no chronic toxicity to mice in terms of hematology and pathological histology, indicating its impressive biocompatibility for biomedical applications. Pharmacokinetics and relative bioavailability (207%) of the nanopowder further proved that DNA/chitosan nanocarriers significantly improved the delivery efficiency of astaxanthin. With enhanced bioavailability and antioxidant activities, this novel type of astaxanthin-loaded nanopowder is expected to find broad application in the food and drug industry.

Lung cancer ranks as the most common type of cancer in males worldwide. Although great advances have been achieved in chemotherapy and radiotherapy, the long‑term survival rate of lung cancer patients has not improved significantly. Dissemination of lung cancer in the thoracic cavity and metastatic spread to the liver, bone and brain are characteristic of non‑small cell lung cancer (NSCLC), constituting the primary source of morbidity and mortality in lung cancer. Increasing evidence also indicates that the CXC chemokine receptor 4 (CXCR4)/chemokine CXC motif ligand 12 (CXCL12) chemokine axis is important for the cell invasion and migration of lung cancer. CXCR4 is a G protein‑coupled receptor with a major role in lymphocyte homing. Its ligand, CXCL12, is secreted by target organs and functions as a highly efficient chemotactic factor for T cells, monocytes, pre‑B cells, dendritic cells and myeloid bone marrow‑derived cells. In the current study, recombinant CXCR4‑specific small interfering RNA‑pBSilence1.1 plasmids were constructed and transfected into the A549 NSCLC cell line in vitro. Reverse transcription polymerase chain reaction and western blotting revealed that CXCR4 was downregulated in transfected cells compared with control cells. The results of MTT and Transwell migration assays indicated that the specific downregulation of CXCR4 inhibited cell growth, invasiveness and migration. Thus, siRNA targeting of CXCR4 may effectively inhibit the effect of CXCL12/CXCR4 on increasing the metastatic potential of NSCLC.