Reactive oxygen species (ROS) and ROS-dependent (redox regulation) signaling pathways and transcriptional activities are thought to be critical in stem cell self-renewal and differentiation during growth and organogenesis. Aberrant ROS burst and dysregulation of those ROS-dependent cellular processes are strongly associated with human diseases including many cancers. ROS levels are elevated in cancer cells partially due to their higher metabolism rate. In the past 15 years, the concept of cancer stem cells (CSCs) has been gaining ground as the subpopulation of cancer cells with stem cell-like properties and characteristics have been identified in various cancers. CSCs possess low levels of ROS and are responsible for cancer recurrence after chemotherapy or radiotherapy. Unfortunately, how CSCs control ROS production and scavenging and how ROS-dependent signaling pathways contribute to CSCs function remain poorly understood. This review focuses on the role of redox balance, especially in ROS-dependent cellular processes in cancer stem cells (CSCs). We updated recent advances in our understanding of ROS generation and elimination in CSCs and their effects on CSC self-renewal and differentiation through modulating signaling pathways and transcriptional activities. The review concludes that targeting CSCs by manipulating ROS metabolism/dependent pathways may be an effective approach for improving cancer treatment.

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The objective of this study was to prepare antioxidant peptides from duck meat hydrolysate (DMH) using Protamex. The DPPH(•) scavenging activity, hydroxyl radical ((•)OH) scavenging activity, and Fe(2+)-chelating ability of DMH were investigated. DMH was separated into three groups, MWCO-1 (69.57%), MWCO-2 (9.53%), and MWCO-3 (8.21%), by ultrafiltration. MWCO-3 exhibited the highest DPPH(•) scavenging activity (83.17 ± 0.73%) and was subsequently fractionated by using gel filtration chromatography to obtain fraction B (40.90%). Fraction B5 (6.71%) obtained from ion exchange chromatography exhibited the highest DPPH(•) scavenging activity (93.63 ± 0.13%) and contained seven peptides which were characterized by LC-MS/MS. Among these peptides, LQAEVEELRAALE showed the highest DPPH(•) scavenging activity (93.36 ± 0.53%) and Fe(2+)-chelating ability (87.13 ± 0.47%) and IEDPFDQDDWGAWKK exhibited the highest (•)OH scavenging activity (46.51 ± 0.16%). The results presented here indicated that DMH could serve as a suitable source of antioxidant peptides.

Alzheimer's disease is the most common neurodegenerative disease. Until now, there has been no specific medicine that can cure Alzheimer's disease or effectively reverse the disease process. A good dietary pattern is an efficient way to prevent or delay the progression of the disease. Evidence suggests that diet may affect β-amyloid production and tau processing or may regulate inflammation, metabolism, and oxidative stress associated with Alzheimer's disease, which can be exerted by gut microbiota. The gut microbiota is a complex microbial community that affects not only various digestive diseases but also neurodegenerative diseases. Studies have shown that gut microbial metabolites, such as pro-inflammatory factors, short-chain fatty acids, and neurotransmitters, can affect the pathogenesis of Alzheimer's disease. Clinical studies suggested that the gut microbial composition of patients with Alzheimer's disease is different, in particular to lower abundances of Eubacterium rectale and Bacteroides fragilis, which have an antiinflammatory activity. The purpose of this review is to summarize the neuropathological pathogenesis of Alzheimer's disease, and the modulation of dietary patterns rather than single dietary components on Alzheimer's disease through the gut−brain axis was discussed.

The objectives of this study were to determine the effects of dietary glycyl-glutamine (Gly-Gln) on postweaning growth, small intestinal morphology, and immune response of stressed or nonstressed piglets. Pigs (n = 144; initially 4.49 kg and 14 d of age) were randomly allocated to 24 pens (6 pigs/pen) in an environmentally controlled nursery and assigned to Escherichia coli lipopolysaccharide (LPS) challenge (PBS vs. LPS) and Gly-Gln supplementation (0 vs. 0.15%) in a 2 x 2 factorial arrangement of treatments with 6 pens/treatment. The LPS was the stress-inducing agent, and it was injected on d 7 and 14 of the 21-d experiment. Inflammatory challenge with LPS reduced ADG (P < 0.05) and tended to reduce ADFI (P = 0.06) of piglets from d 7 to 21 of the experiment. Supplementation of Gly-Gln increased ADG and G:F from d 0 to 21 (P < 0.05). On d 21 (1 wk after the second LPS injection), there was an LPS challenge x diet Gly-Gln interaction for ADFI (P < 0.05), but it was difficult to ascertain whether Gly-Gln increased ADFI. A trend for an LPS challenge x diet Gly-Gln interaction was observed for ADG (P = 0.07). There were no differences in lymphocyte proliferation among treatments. The LPS challenge increased crypt depth (CD) of the duodenum and decreased the ratio of villus height (VH) to CD of the ileum (P < 0.05) on d 14 (1 wk after the first LPS injection), whereas dietary supplementation of Gly-Gln increased VH of the ileum and VH:CD of the duodenum (P < 0.05). The concentration of peripheral blood IL-1beta was increased by injection of LPS (P < 0.05) and was decreased by dietary Gly-Gln supplementation during the experimental period (P < 0.05); however, there was no interaction of LPS challenge x Gly-Gln addition for IL-1beta concentration. Concentrations of peripheral blood IL-2 tended to increase at d 14 (P = 0.09) and soluble IL-2 receptor tended to decrease at d 7 (P = 0.06) in piglets supplemented with Gly-Gln; therefore, the peripheral blood IL-2/soluble IL-2 receptor system tended to favor the secretion of IL-2 during the first 2 wk of the experiment. In conclusion, considerable suppression of growth and immune function occurred in early weaning piglets challenged with LPS, and such depression could be alleviated by dietary Gly-Gln supplementation independent of the LPS challenge.