Modulation Of Antioxidant Capacity Research Articles

Exogenous Proline Improves Salt Tolerance of Alfalfa through Modulation of Antioxidant Capacity, Ion Homeostasis, and Proline Metabolism.

Alfalfa (Medicago sativa L.) is an important forage crop, and its productivity is severely affected by salt stress. Although proline is a compatible osmolyte that plays an important role in regulating plant abiotic stress resistance, the basic mechanism of proline requires further clarification regarding the effect of proline in mitigating the harmful effects of salinity. Here, we investigate the protective effects and regulatory mechanisms of proline on salt tolerance of alfalfa. The results show that exogenous proline obviously promotes seed germination and seedling growth of salt-stressed alfalfa. Salt stress results in stunted plant growth, while proline application alleviates this phenomenon by increasing photosynthetic capacity and antioxidant enzyme activities and decreasing cell membrane damage and reactive oxygen species (ROS) accumulation. Plants with proline treatment maintain a better K+/Na+ ratio by reducing Na+ accumulation and increasing K+ content under salt stress. Additionally, proline induces the expression of genes related to antioxidant biosynthesis (Cu/Zn-SOD and APX) and ion homeostasis (SOS1, HKT1, and NHX1) under salt stress conditions. Proline metabolism is mainly regulated by ornithine-δ-aminotransferase (OAT) and proline dehydrogenase (ProDH) activities and their transcription levels, with the proline-treated plants displaying an increase in proline content under salt stress. In addition, OAT activity in the ornithine (Orn) pathway rather than Δ1-pyrroline-5-carboxylate synthetase (P5CS) activity in the glutamate (Glu) pathway is strongly increased under salt stress, made evident by the sharp increase in the expression level of the OAT gene compared to P5CS1 and P5CS2. Our study provides new insight into how exogenous proline improves salt tolerance in plants and that it might be used as a significant practical strategy for cultivating salt-tolerant alfalfa.

Opportunities for plant-derived enhancers for iron, zinc, and calcium bioavailability: A review.

Understanding of the mechanism of interactions between dietary elements, their salts, and complexing/binding ligands is vital to manage both deficiency and toxicity associated with essential element bioavailability. Numerous mineral ligands are found in both animal and plant foods and are known to exert bioactivity via element chelation resulting in modulation of antioxidant capacity or micobiome metabolism among other physiological outcomes. However, little is explored in the context of dietary mineral ligands and element bioavailability enhancement, particularly with respect to ligands from plant-derived food sources. This review highlights a novel perspective to consider various plant macro/micronutrients as prospective bioavailability enhancing ligands of three essential elements (Fe, Zn, and Ca). We also delineate the molecular mechanisms of the ligand-binding interactions underlying mineral bioaccessibility at the luminal level. We conclude that despite current understandings of some of the structure-activity relationships associated with strong mineral-ligand binding, the physiological links between ligands as element carriers and uptake at targeted sites throughout the gastrointestinal (GI) tract still require more research. The binding behavior of potential ligands in the human diet should be further elucidated and validated using pharmacokinetic approaches and GI models.

Seaweed-derived bioactives as potential energy regulators in obesity and type 2 diabetes.

There is epidemiological evidence that dietary intake of seaweeds is associated with a lower prevalence of chronic diseases. While seaweeds are of high nutritious value, due to their high content of fiber, polyunsaturated fatty acids and minerals, they also contain an abundance of bioactive compounds. There is a growing body of scientific data that these bioactive moieties exert effects that could correct the metabolic dysregulation that is present in obesity and Type 2 diabetes (T2D). In this review we describe how the molecular mechanisms, specific to different tissues, that underly obesity and T2D are influenced by both seaweed extracts and seaweed-derived bioactive molecules. In obesity, modulation of antioxidant capacity and reduction of intracellular ROS levels within tissues, and regulation of signaling pathways involved in enhancing browning of white adipose tissue, have been highlighted as key mechanism and identified as a potential target for optimal energy metabolism. In T2D, management of post-prandial blood glucose by modulating α-glucosidase or α-amylase activities, modulation of the AMPK signaling pathway, and similarly to obesity, reduction of ROS and NO production with subsequent increased expression of antioxidant enzymes have been shown to play a key role in glucose metabolism and insulin signaling. Future studies aimed at discovering new therapeutic drugs from marine natural products should, therefore, focus on bioactive compounds from seaweed that exert antioxidant activity and regulate the expression of key signaling pathways involved in glucose homeostasis, mechanisms that are common to both obesity and T2D management. In addition, more data is required to provide evidence of clinical benefit.

Coffee Consumption and Oxidative Stress: A Review of Human Intervention Studies.

Research on the potential protective effects of coffee and its bioactives (caffeine, chlorogenic acids and diterpenes) against oxidative stress and related chronic disease risk has been increasing in the last years. The present review summarizes the main findings on the effect of coffee consumption on protection against lipid, protein and DNA damage, as well as on the modulation of antioxidant capacity and antioxidant enzymes in human studies. Twenty-six dietary intervention studies (involving acute and chronic coffee intake) have been considered. Overall, the results suggest that coffee consumption can increase glutathione levels and improve protection against DNA damage, especially following regular/repeated intake. On the contrary, the effects of coffee on plasma antioxidant capacity and antioxidant enzymes, as well as on protein and lipid damage, are unclear following both acute and chronic exposure. The high heterogeneity in terms of type of coffee, doses and duration of the studies, the lack of information on coffee and/or brew bioactive composition, as well as the choice of biomarkers and the methods used for their evaluation, may partially explain the variability observed among findings. More robust and well-controlled intervention studies are necessary for a thorough understanding of the effect of coffee on oxidative stress markers in humans.

Expression of redox-regulating molecules rather than mitochondrial biogenesis correlate with susceptibility to apoptotic stimuli in human CD62L T cell subsets (P1034)

Abstract Ex vivo-expanded CD8+ T cells used for adoptive immunotherapy generally acquire an effector memory-like phenotype (TEM cells) and exhibit impaired in vivo persistence and anti-tumor efficacy, compared to T cells with central memory-like phenotype (TCM cells). However, the intrinsic and metabolic factors that attribute to this differential outcome of T cell subsets are not well understood. Here we show that CD62Lhi TCM-like T cells exhibited increased expression of cell surface sulphydryl groups (-SH; thiols), compared to TEM phenotype like CD62Llo TEM-like T cells. This increase in thiols coincided with an up-regulation of the redox-regulating anti-oxidant proteins catalase, SOD1, NRF2 and inversely correlated to the generation of ROS, RNS, extent of T cell proliferation and glycolytic enzymes. Further, we observed that T cells pretreated with rapamycin, a drug that favors the generation of a CD62Lhi TCM-like phenotype of T cells and renders reduced susceptibility to apoptosis, also up-regulated thiol expression and level of anti-oxidative genes. Conversely, thiol donor L-NAC pretreatment reduced mTOR activation. However, both rapamycin and L-NAC treated T cells showed a decrease in oxygen consumption rate, key glycolytic enzymes and expression of PGC1α, a key regulator of mitochondrial biogenesis. These data suggest that modulation of anti-oxidant capacity, mitochondrial metabolism and glycolytic pathway of T cell subsets could increase persistence and improve immunotherapy.