Causes of root growth retardation induced by ultraviolet-B irradiation of shoots in Barley seedlings

In barley seedlings (Hordeum vulgare L.) during two days after irradiation of shoots with UV-B (0.5 W/m², 6 h), the rate of elongation of primary roots decreased 2–3 times compared to that in control plants. The modulus of elasticity of roots (ε) increased at most twofold in 12 h after the onset of irradiation; the hydraulic conductivity (L _p) diminished by a factor of two in 12 h, and the root osmotic pressure gradually decreased by 0.08 MPa in 24 h. Changes in ε and L _p were shown to be related to oxidative stress in growing roots, which was evidenced from the increase in H₂O₂ level up to 15-fold increase in 6 h and in activity of guaiacol peroxidase (3.5-fold in 12 h). After 48 h, the characteristics of oxidative metabolism and root characteristics ε and L _p became identical in untreated and treated plants. On the third day, the rate of root growth in treated plants reached its initial value. It is concluded that the main causes of retardation of root growth under these conditions were as follows: the increase in cell wall rigidity related to formation of oxidative cross-links in the apoplast and the decrease in root osmotic pressure due to limited transport of assimilates from irradiated leaves. After the intensity of UV-B irradiation applied to shoots was enhanced (1.6 W/m², 4 h), another physiological status of roots was observed on the 2nd day characterized by twofold increase in L _p, tenfold decreased root elongation rate, and by a progressing increase of root diameter in growing roots. The comparison of root responses induced by irradiation of shoots with the root responses to sodium salicylate and ABA suggests that both agents might participate in the transmission of signals from irradiated leaves to roots.     

Hill coefficient-based stochastic switch-like signal directly governs damage-recovery dynamics in freshwater fish in response to pulse copper

Growing evidence demonstrates that fluctuating metal stressors can have profound impact on the ecophysiological responses in aquatic species. However, how environmental stochasticity affects the complex damage-recovery dynamics in organisms remains difficult to predict. The objective of this paper was to investigate the stochastic behavior in the damage-recovery dynamics in tilapia in response to pulse waterborne copper (Cu). We developed a mathematical framework that allows discrimination between damage and recovery processes in tilapia exposed to designed pulse Cu scenarios. We built deterministic nonlinear models for the damage-recovery dynamics that produce response surfaces describing killing/recovery rate–Cu-pulse interval interactions. Here we showed that the stochastic switching behavior arose from competition among killing, recovery rates, and Cu pulse frequency. This competition resulted in an ultrasensitivity appeared in whole body, gills, muscle, liver, and kidney with Hill coefficients of ≥7, 4, 7, 5, and 5, respectively, at Cu 3 mg L⁻¹, dilution rate 0.05 h⁻¹, and pulse interval 72 h, indicating that a stochastic switch-like response was generated. We argue that the role of gill-associated Hill coefficient as a direct signal of the stochastic switch-like response in the damage-recovery dynamics in response to pulse metal stressor can serve as a sensitive indicator for risk detection in fluctuating environments. Our approach constitutes a general method to identify the stochastic switch-like response for aquatic species exposed to fluctuating metal stressors, which may help to predict and, eventually, expand our understanding of the damage-recovery dynamics. Finally, we implicate that Hill coefficient-based switch-like signal and its damage with hazard response can be linked in an information theoretic framework to handle environmental stochasticity.     

Quercetin supplementation does not alter antioxidant status in humans

Abstract

This study measured the influence of ingesting quercetin on plasma measures for oxidative stress and antioxidant capacity. Male and female subjects (n = 1002) varying in age (18–85 years) and body mass index (BMI) (16.7–52.7 kg/m²) were studied. Subjects were randomized to one of three groups using double-blinded methods: placebo, 500 mg or 1000 mg quercetin/day with 125 mg or 250 mg vitamin C/day, respectively. Pre- and post-study fasting blood samples show that plasma quercetin increased in a dose-responsive manner. The pattern of change in plasma F₂-isoprostanes, oxidized low density lipoprotein, reduced glutathione, ferric reducing ability of plasma (FRAP) and oxygen radical absorbance capacity (ORAC) did not differ between supplementation groups or after adjustment for gender, age, BMI and disease status. In summary, quercetin supplementation over 12 weeks in doses of 500 mg or 1000 mg/day significantly increased plasma quercetin levels, but had no influence on several measures of oxidative stress and antioxidant capacity.     

Ginsenoside Rg1 protects H9c2 cells against nutritional stress-induced injury via aldolase /AMPK/PINK1 signalling

Insufficient nutrients supply will greatly affect the function of cardiac myocytes. The adaptive responses of cardiac myocytes to nutritional stress are not fully known. Ginsenoside Rg1 is one of the most pharmacologically active components in Panax Ginseng and possesses protective effects on cardiomyocyte. Here, we investigate the effects of ginsenoside Rg1 on H9c2 cells which were subjected to nutritional stress. Nutritional stress-induced by glucose deprivation strongly induced cell death and this response was inhibited by ginsenoside Rg1. Importantly, glucose deprivation decreased intracellular ATP levels and mitochondrial membrane potential. Ginsenoside Rg1 rescued ATP levels and mitochondrial membrane potential in nutrient-starved cells. For molecular mechanisms, ginsenoside Rg1 increased the expressions of PTEN-induced kinase 1 (PINK1) and p-AMPK in glucose deprivation treated H9c2 cells. Reducing the expression of aldolase in H9c2 cells inhibited ginsenoside Rg1′s actions on PINK1 and p-AMPK. Further, the nutritional stress mice were used to verify the mechanisms obtained in vitro. Ginsenoside Rg1 increased the expressions of aldolase, p-AMPK, and PINK1 in starved mice heart. Taken together, our results reveal that ginsenoside Rg1 limits nutritional stress-induced H9c2 cells injury by regulating the aldolase /AMP-activated protein kinase/PINK1 pathway.     

Human Health Risk Assessment of Soils Contaminated with Metal(loid)s by Using DGT Uptake: A Case Study of a Former Korean Metal Refinery Site

The human health risk of soils contaminated with As, Pb, Cu, and Zn was evaluated based on pseudo-total concentrations of metal(loid)s, the physiologically based extraction test (PBET), and diffusive gradients in thin films (DGT). Non-carcinogenic (NCR) and carcinogenic (CR) risks exceeded the U.S. Environmental Protection Agency criteria under both the residential and non-residential scenarios. Human bioavailable concentrations (PBET) were much lower than pseudo-total concentrations. The Hazardous Index of NCR (HI (NCR)) for the PBET in the studied soils was 67% and 94% less than that for pseudo-total concentration, respectively, under the non-residential and residential scenarios. Similarly, CR for the PBET was also 65% and 93% less for the two soils. The concentration of metal(loid)s accumulated in the DGT resin was highly correlated with the PBET-extractable concentration (R² > 0.649). Therefore, for both the CR and HI (NCR), the DGT-calculated risk was linearly related to the PBET-calculated risk for the studied soils under both scenarios. The results suggest that DGT uptake and PBET-extracted concentrations are good surrogates for risk estimation and that both J1 and J2 soils require remediation before their use for residential or non-residential purposes.     

The mechanism of water-stress-induced embolism in two species of chaparral shrubs

The mechanism of water-stress-induced embolism of xylem was investigated in Malosma laurina and Heteromeles arbutifolia, two chaparral shrub species of southern California. We tested the hypothesis that the primary cause of xylem dysfunction in these species during dehydration was the pulling of air through the pores in the cell walls of vessels (pores in pit membranes) as a result of high tensions on xylem water. First, we constructed vulnerability-to-embolism curves for (i) excised branches that were increasingly dehydrated in the laboratory and (ii) hydrated branches exposed to increasing levels of external air pressure. Branches of M. laurina that were dehydrated became 50% embolized at a xylem pressure potential of -1.6 MPa, which is equal in magnitude but opposite in sign to the +1.6 MPa of external air pressure that caused 50% embolism in hydrated stems. Dehydrated and pressurized branches of H. arbutifolia reached a 50% level of embolism at -6.0 and +6.4 MPa, respectively. Secondly, polystyrene spheres ranging in diameter from 20 to 149 nm were perfused through hydrated stem segments to estimate the pore size in the vessel cell walls (pit membranes) of the two species. A 50% or greater reduction in hydraulic conductivity occurred in M. laurina at perfusions of 30, 42, 64 and 82 nm spheres and in H. arbutifolia at perfusions of 20 and 30 nm spheres. Application of the capillary equation to these pore diameters predicted 50% embolism at xylem tensions of -2.2 MPa for M. laurina and -6.7 MPa for H. arbutifolia, which are within 0.7 MPa of the actual values. Our results suggest that the size of pores in pit membranes may be a factor in determining both xylem efficiency and vulnerability to embolism in some chaparral species. H. arbutifolia, with smaller pores and narrower vessels, withstands lower water potentials but has lower transport efficiency. M. laurina, with wider pores and wider vessels, has a greater transport efficiency but requires a deeper root system to help avoid catastro-phically low water potentials.     

Staphylococcus aureus dry stress survivors have a heritable fitness advantage in subsequent dry exposure

Staphylococcus aureus is a major cause of hospital-acquired infections. The ability to survive on abiotic surfaces is an important characteristic that facilitates transmission between human hosts. We found that S. aureus survivors of dry surface incubation are resistant to subsequent dry stress exposure. Survivors also had reduced sensitivity to the disinfectant chlorhexidine gluconate, but not to ethanol. By using a set of mutants in cardiolipin synthase genes, we further demonstrated that the housekeeping cardiolipin synthase, Cls2, was significant for survival on dry surface. Taken together, this study provides insights into S. aureus survival outside of a host.