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Multiple Stresses (multiple + stress)
Selected AbstractsWhole effluent toxicity testing,usefulness, level of protection, and risk assessmentENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 1 2000Peter M. Chapman Abstract The general status of whole effluent toxicity (WET) tests is assessed relative to their generally accepted purpose of identifying, characterizing, and eliminating toxic effects of effluents on aquatic resources. Although WET tests are useful, they are not perfect tools (no perfect tools exist). Imperfections include the innate variability of these tests, due both to biotic and anthropogenic factors; the reality of species differences both between the laboratory and the field and within the field; and differences between the laboratory and the receiving environment. Whole effluent toxicity tests may be overprotective (because of their conservative nature, the absence of environmental and ecological processes that could ameliorate exposure, and sensitivity to noncontaminant effects), underprotective (because the most sensitive species cannot be tested, multiple stresses tend to be present in the receiving environment, and failure to account for food chain effects or all possible endpoints), or offer an uncertain level of protection (intermittent doses and mixtures in the environment, adaptations, and hormesis). The implication of hormesis and inverted U-shaped dose responses for WET testing are reviewed in particular detail. Comparisons to field conditions indicate that WET tests are not reliable predictors of effects or lack of effects in the receiving environment. Whole effluent toxicity tests are only the first stage in a risk assessment and as such identify hazard, not risk. Identification of risk requires discarding the concept of independent applicability. The appropriate use of WET tests is identified in the context of their advantages and disadvantages. [source] The Legionella pneumophila Dps homolog is regulated by iron and involved in multiple stress toleranceJOURNAL OF BASIC MICROBIOLOGY, Issue S1 2009Ming-jia Yu Abstract Iron homeostasis is essential to almost all organisms. In this study, we identified the putative homolog of the iron-storage protein-encoding gene, dpsL, in the intracellular pathogen Legionella pneumophila and demonstrated its expression under iron-limited conditions and its responses to multiple stresses. Quantitative real-time PCR analysis indicated that the expression of dpsL was enhanced under iron limitation regardless of the growth phase. Compared with the wild-type cells, the cells devoid of dpsL were heat and H2O2 -sensitive. In contrast to the dps mutants of other bacteria, the growth of the dpsL mutant in an iron-deprived medium was delayed but finally reached the same cell density as wild-type cells during the stationary phase of growth. The finding that the dpsL mutant is salt resistant suggested the involvement of DpsL in virulence. (© 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source] Reduced expression of alpha-1,2-mannosidase I extends lifespan in Drosophila melanogaster and Caenorhabditis elegansAGING CELL, Issue 4 2009Ya-Lin Liu Summary Exposure to sub-lethal levels of stress, or hormesis, was a means to induce longevity. By screening for mutations that enhance resistance to multiple stresses, we identified multiple alleles of alpha-1,2-mannosidase I (mas1) which, in addition to promoting stress resistance, also extended longevity. Longevity enhancement is also observed when mas1 expression is reduced via RNA interference in both Drosophila melanogaster and Caenorhabditis elegans. The screen also identified Edem1 (Edm1), a gene downstream of mas1, as a modulator of lifespan. As double mutants for both mas1 and Edm1 showed no additional longevity enhancement, it appeared that both mutations function within a common pathway to extend lifespan. Molecular analysis of these mutants revealed that the expression of BiP, a putative biomarker of dietary restriction (DR), is down-regulated in response to reductions in mas1 expression. These findings suggested that mutations in mas1 may extend longevity by modulating DR. [source] Yeast Yak1 kinase, a bridge between PKA and stress-responsive transcription factors, Hsf1 and Msn2/Msn4MOLECULAR MICROBIOLOGY, Issue 4 2008Peter Lee Summary Hsf1 and Msn2/Msn4 transcription factors in Saccharomyces cerevisiae play important roles in cellular homeostasis by activating gene expression in response to multiple stresses including heat shock, oxidative stress and nutrient starvation. Although it has been known that nuclear import of Msn2 is inhibited by PKA-dependent phosphorylation, the mechanism for PKA-dependent regulation of Hsf1 is not well understood. Here we demonstrate that Yak1 kinase, which is under the negative control of PKA, activates both Hsf1 and Msn2 by phosphorylation when PKA activity is lowered by glucose depletion or by overexpressing Pde2 that hydrolyses cAMP. We show that Yak1 directly phosphorylates Hsf1 in vitro, leading to the increase in DNA binding activity of Hsf1. We also demonstrate that Yak1 phosphorylates Msn2 in vitro, but does not affect DNA binding activity of Msn2 or nuclear localization of Msn2 upon glucose depletion. These results suggest a central role for Yak1 in mediating PKA-dependent inhibition of Hsf1 and Msn2/Msn4. [source] Isoprenoid emission in trees of Quercus pubescens and Quercus ilex with lifetime exposure to naturally high CO2 environment,PLANT CELL & ENVIRONMENT, Issue 4 2004F. RAPPARINI ABSTRACT The long-term effect of elevated atmospheric CO2 on isoprenoid emissions from adult trees of two Mediterranean oak species (the monoterpene-emitting Quercus ilex L. and the isoprene-emitting Quercus pubescens Willd.) native to a high-CO2 environment was investigated. During two consecutive years, isoprenoid emission was monitored both at branch level, measuring the actual emissions under natural conditions, and at leaf level, measuring the basal emissions under the standard conditions of 30 °C and at light intensity of 1000 µmol m,2 s,1. Long-term exposure to high atmospheric levels of CO2 did not significantly affect the actual isoprenoid emissions. However, when leaves of plants grown in the control site were exposed for a short period to an elevated CO2 level by rapidly switching the CO2 concentration in the gas-exchange cuvette, both isoprene and monoterpene basal emissions were clearly inhibited. These results generally confirm the inhibitory effect of elevated CO2 on isoprenoid emission. The absence of a CO2 effect on actual emissions might indicate higher leaf temperature at elevated CO2, or an interaction with multiple stresses some of which (e.g. recurrent droughts) may compensate for the CO2 effect in Mediterranean ecosystems. Under elevated CO2, isoprene emission by Q. pubescens was also uncoupled from the previous day's air temperature. In addition, pronounced daily and seasonal variations of basal emission were observed under elevated CO2 underlining that correction factors may be necessary to improve the realistic estimation of isoprene emissions with empirical algorithms in the future. A positive linear correlation of isoprenoid emission with the photosynthetic electron transport and in particular with its calculated fraction used for isoprenoid synthesis was found. The slope of this relationship was different for isoprene and monoterpenes, but did not change when plants were grown in either ambient or elevated CO2. This suggests that physiological algorithms may usefully predict isoprenoid emission also under rising CO2 levels. [source] | ||||||||||