Night-Warming Priming at the Vegetative Stage Alleviates Damage to the Flag Leaf Caused by Post-anthesis Warming in Winter Wheat (Triticum aestivum L.)

The asymmetric warming in diurnal and seasonal temperature patterns plays an important role in crop distribution and productivity. Asymmetric warming during the early growth periods of winter wheat profoundly affects its vegetative growth and post-anthesis grain productivity. Field experiments were conducted on winter wheat to explore the impact of night warming treatment in winter (Winter warming treatment, WT) or spring (Spring warming treatment, ST) on the senescence of flag leaves and yield of wheat plants later treated with night warming during grain filling (Warming treatment during grain filling, FT). The results showed that FT decreased wheat yield by reducing the number of grains per panicle and per 1,000-grain weight and that the yield of wheat plants treated with FT declined to a greater extent than that of wheat plants treated with WT + FT or ST + FT. The net photosynthetic rate, chlorophyll content, and chlorophyll fluorescence parameters of the flag leaves of wheat plants treated with WT + FT or ST + FT were higher than those under the control treatment from 0 to 7 days after anthesis (DAA) but were lower than those under the control treatment and higher than those of wheat plants treated with FT alone from 14 to 28 DAA. The soluble protein and Rubisco contents in the flag leaves of wheat plants treated with WT + FT or ST + FT were high in the early grain-filling period and then gradually decreased to below those of the control treatment. These contents were greater in wheat plants treated with WT + FT than in wheat plants treated with ST + FT from 0 to 14 DAA, whereas the opposite was true from 21 to 28 DAA. Furthermore, WT + FT and ST + FT inhibited membrane lipid peroxidation by increasing superoxide dismutase and peroxidase activities and lowering phospholipase D (PLD), phosphatidic acid (PA), lipoxygenase (LOX), and free fatty acid levels in the early grain-filling period, but their inhibitory effects on membrane lipid peroxidation gradually weakened during the late grain-filling period. Night-warming priming alleviated the adverse effect of post-anthesis warming on yield by delaying the post-anthesis senescence of flag leaves.

Dietary supplementation with manganese and selenium offer protection against cadmium-induced oxidative damage to rat liver and kidney

The present study determined the effect of pre-supplementation with manganese (Mn) and selenium (Se) on biomarkers of oxidative stress in the liver and kidneys of rats exposed to a mild dose of cadmium. Sixteen Male Wistar strain rats (180-200 g b. wt) were divided into four groups (control, Cd alone, Mn + Se + Cd and Mn + Se). The rats used as the control received a normal rat diet and tap water throughout the study while the Cd alone rats received a normal rat diet and then exposed to a single daily oral dose of cadmium (3 mg CdCl2/kg) in drinking water for three days. Mn + Se + Cd rats were pretreated with Mn (3 mg MnCl2/kg/day) and Se (3mg SeO2/kg/day) for seven days and thereafter received a single daily oral dose of cadmium (3 mg CdCl2/kg) in drinking water for three days while Mn + Se rats were exposed to only Mn (3 mg MnCl2/kg/day) and Se (3mg SeO2/kg/day) for seven days. At the end of the experiment tissue cadmium concentration, membrane lipid peroxidation, glutathione content, and activities of antioxidant enzymes catalase, superoxide dismutase, and glutathione peroxidase were determined in the liver and kidney samples. The results showed that pretreatment with Mn and Se effectively countered Cd-induced cadmium accumulation, membrane lipid peroxidation, depletion of the non-enzymic antioxidant, glutathione, and induction of the antioxidant enzymes catalase, superoxide dismutase and glutathione peroxidase in the liver and kidney. It can be concluded that pre-supplementation with Mn and Se significantly reversed Cd-induced deleterious alterations in the liver and kidney tissue of the rats.

Enhancement of membrane lipid peroxidation in lung cancer cells irradiated with monoenergetic X-rays at the K-shell resonance absorption peak of phosphorus

The aim of this study was to determine whether membrane lipid peroxidation in mammalian cells is enhanced by X-ray irradiation at the K-shell resonance absorption peak of phosphorus. A549 and wild-type p53-transfected H1299 (H1299/wtp53) cell lines derived from human lung carcinoma were irradiated with monoenergetic X-rays at 2.153 keV, the phosphorus K-shell resonance absorption peak, or those at 2.147 or 2.160 keV, which are off peaks. Immunofluorescence staining for 4-hydroxy-2-nonenal (HNE), a lipid peroxidation product, was used as marker for protein modification. In both cell lines, the HNE production was significantly enhanced after irradiation at 2.153 keV compared to sham-irradiation. The enhancement (E) was calculated as the ratio of the fluorescence intensity of irradiated cells to that of sham-irradiated cells. In both the cell lines, E2.153 was significantly larger than E2.147 and no significant difference between E2.147 and E2.160 was observed. The extra enhancement at 2.153 keV was possibly caused by energy transition within the phosphorus K-shell resonance absorption. Our results indicate that membrane lipid peroxidation in cells is enhanced by the Auger effect after irradiation at the K-shell resonance absorption peak of phosphorus rather than by the photoelectric effect of the constituent atoms in the membrane lipid at 2.147 keV.

Decreased Na+/K+-ATPase Activity and Altered Susceptibility to Peroxidation and Lipid Composition in the Erythrocytes of Metabolic Syndrome Patients with Coronary Artery Disease

Background: The increased generation of reactive oxygen species that occurs in the case of a metabolic syndrome (MetS) may be responsible for the increased oxidative injury to erythrocyte membranes in coronary artery disease (CAD). Therefore, we studied the effects of MetS on both indexes of oxidative damage and biochemical properties of erythrocyte membranes in CAD patients. Methods: We analyzed the markers of oxidative stress, Na+/K+-ATPase activity, total cholesterol content of erythrocyte membranes (CEM), and fatty acid compositions of the erythrocyte membrane in 82 patients with stable CAD and 39 non-CAD subjects. Results: The CAD patients had higher levels of CEM, membrane lipid peroxidation, erythrocyte superoxide dismutase (SOD) activity, and Na+/K+-ATPase activity compared with non-CAD subjects. The Na+/K+-ATPase activity was correlated negatively with membrane lipid peroxidation, and positively with the CEM. In CAD patients with MetS compared with those without MetS, we found that the membrane lipid peroxidation and CEM were increased, whereas the n-3 fatty acids content, SOD activity, Na+/K+-ATPase activity were decreased. Conclusion: These findings suggest an impairment of erythrocyte membrane biochemical properties in stable CAD patients as a consequence of oxidative injury that may contribute to the development of CAD. In addition, MetS may be related to increased oxidative injury to erythrocyte membranes.