Foliar δ15N values characterize soil N cycling and reflect nitrate or ammonium preference of plants along a temperate grassland gradient

The natural abundance of stable 15N isotopes in soils and plants is potentially a simple tool to assess ecosystem N dynamics. Several open questions remain, however, in particular regarding the mechanisms driving the variability of foliar δ15N values of non-N2 fixing plants within and across ecosystems. The goal of the work presented here was therefore to: (1) characterize the relationship between soil net mineralization and variability of foliar Δδ15N (δ15Nleaf − δ15Nsoil) values from 20 different plant species within and across 18 grassland sites; (2) to determine in situ if a plant’s preference for NO3− or NH4+ uptake explains variability in foliar Δδ15N among different plant species within an ecosystem; and (3) test if variability in foliar Δδ15N among species or functional group is consistent across 18 grassland sites. Δδ15N values of the 20 different plant species were positively related to soil net mineralization rates across the 18 sites. We found that within a site, foliar Δδ15N values increased with the species’ NO3− to NH4+ uptake ratios. Interestingly, the slope of this relationship differed in direction from previously published studies. Finally, the variability in foliar Δδ15N values among species was not consistent across 18 grassland sites but was significantly influenced by N mineralization rates and the abundance of a particular species in a site. Our findings improve the mechanistic understanding of the commonly observed variability in foliar Δδ15N among different plant species. In particular we were able to show that within a site, foliar δ15N values nicely reflect a plant’s N source but that the direction of the relationship between NO3− to NH4+ uptake and foliar Δδ15N values is not universal. Using a large set of data, our study highlights that foliar Δδ15N values are valuable tools to assess plant N uptake patterns and to characterize the soil N cycle across different ecosystems

DNA damage by lipid peroxidation products: implications in cancer, inflammation and autoimmunity

Oxidative stress and lipid peroxidation (LPO) induced by inflammation, excess metal storage and excess caloric intake cause generalized DNA damage, producing genotoxic and mutagenic effects. The consequent deregulation of cell homeostasis is implicated in the pathogenesis of a number of malignancies and degenerative diseases. Reactive aldehydes produced by LPO, such as malondialdehyde, acrolein, crotonaldehyde and 4-hydroxy-2-nonenal, react with DNA bases, generating promutagenic exocyclic DNA adducts, which likely contribute to the mutagenic and carcinogenic effects associated with oxidative stress-induced LPO. However, reactive aldehydes, when added to tumor cells, can exert an anticancerous effect. They act, analogously to other chemotherapeutic drugs, by forming DNA adducts and, in this way, they drive the tumor cells toward apoptosis. The aldehyde-DNA adducts, which can be observed during inflammation, play an important role by inducing epigenetic changes which, in turn, can modulate the inflammatory process. The pathogenic role of the adducts formed by the products of LPO with biological macromolecules in the breaking of immunological tolerance to self antigens and in the development of autoimmunity has been supported by a wealth of evidence. The instrumental role of the adducts of reactive LPO products with self protein antigens in the sensitization of autoreactive cells to the respective unmodified proteins and in the intermolecular spreading of the autoimmune responses to aldehyde-modified and native DNA is well documented. In contrast, further investigation is required in order to establish whether the formation of adducts of LPO products with DNA might incite substantial immune responsivity and might be instrumental for the spreading of the immunological responses from aldehyde-modified DNA to native DNA and similarly modified, unmodified and/or structurally analogous self protein antigens, thus leading to autoimmunity