Exogenously spermidine alleviates damage from drought stress in the photosystem II of tall fescue

Drought stress is one of the major limiting factors to crop productivity around the globe. It has been well documented that spermidine (Spd) plays an important key role in plant growth and development, especially in the defense response to stress. The objective of this study was to explore the effect of Spd on protecting photosynthetic apparatus in tall fescue under drought stress. Spd application significantly improved the OJIP (fluorescence rise kinetics O-J-I-P) curve compared to non-Spd application during drought. Exogenous Spd exhibited higher F_J (fluorescence value at the J-step (2 ms) of OJIP) and F_P (maximal recorded fluorescence intensity, at the peak P of OJIP) than non-Spd application. Moreover, normalised total complementary area (S_m) and the number of Q_A (primary quinone acceptor of PS II) reduction events (N) significantly reduced after the application of Spd in tall fescue under drought stress. In terms of quantum yields and efficiencies and specific energy fluxes, exogenous Spd notably decreased the values of efficiency of electron transfer from Q_B (secondary quinone acceptor of PS II) to PSI acceptors (δR₀), absorption flux per RC (ABS/RC) and trapping flux per RC (TR₀/RC) compared to the non-Spd application without watering. All the above suggested that exogenous Spd facilitated the photosynthetic system of tall fescue in drought. These observations involved in the electron transport capacity of photosystem II assist in understanding better the protective role of exogenous Spd in tall fescue under drought stress.

Docosahexanoic acid signals through the Nrf2–Nqo1 pathway to maintain redox balance and promote neurite outgrowth

Evidence suggests that n-3 polyunsaturated fatty acids (PUFA) may act as activators of the Nrf2 antioxidant pathway. The antioxidant response in-turn promotes neuronal differentiation and neurite outgrowth. Nrf2 has recently been suggested to be a cell intrinsic mediator of DHA signaling. In the current study, we assessed whether DHA mediated axodendritic development was dependent on activation of the Nrf2-pathway and whether Nrf2 protected from agrochemical-induced neuritic retraction. Expression profiling of the DHA-enriched Fat-1 mouse brain relative to WT showed a significant enrichment of genes associated with neuronal development and neuronal projection and genes associated with the Nrf2-transcriptional pathway. Moreover, we found that primary cortical neurons treated with DHA showed a dose dependent increase in Nrf2 transcriptional activity and Nrf2-target gene expression. DHA-mediated activation of Nrf2 promoted neurite outgrowth and inhibited oxidative stress induced neuritic retraction evoked by exposure to agrochemicals. Finally, we provide evidence that this effect is largely dependent on induction of the Nrf2-target gene NAD(P)H: (quinone acceptor) oxidoreductase 1 (NQO1), and that silencing of either Nrf2 or Nqo1 blocks the effects of DHA on the axodendritic compartment. Collectively, these data support a role for the Nrf2-NQO1 pathway in DHA-mediated axodendritic development and protection from agrochemical exposure.

β-Lapachone Induces Acute Oxidative Stress in Rat Primary Astrocyte Cultures that is Terminated by the NQO1-Inhibitor Dicoumarol

β-lapachone (β-lap) is reduced in tumor cells by the enzyme NAD(P)H: quinone acceptor oxidoreductase 1 (NQO1) to a labile hydroquinone which spontaneously reoxidises to β-lap, thereby generating reactive oxygen species (ROS) and oxidative stress. To test for the consequences of an acute exposure of brain cells to β-lap, cultured primary rat astrocytes were incubated with β-lap for up to 4 h. The presence of β-lap in concentrations of up to 10 µM had no detectable adverse consequences, while higher concentrations of β-lap compromised the cell viability and the metabolism of astrocytes in a concentration- and time-dependent manner with half-maximal effects observed for around 15 µM β-lap after a 4 h incubation. Exposure of astrocytes to β-lap caused already within 5 min a severe increase in the cellular production of ROS as well as a rapid oxidation of glutathione (GSH) to glutathione disulfide (GSSG). The transient cellular accumulation of GSSG was followed by GSSG export. The β-lap-induced ROS production and GSSG accumulation were completely prevented in the presence of the NQO1 inhibitor dicoumarol. In addition, application of dicoumarol to β-lap-exposed astrocytes caused rapid regeneration of the normal high cellular GSH to GSSG ratio. These results demonstrate that application of β-lap to cultured astrocytes causes acute oxidative stress that depends on the activity of NQO1. The sequential application of β-lap and dicoumarol to rapidly induce and terminate oxidative stress, respectively, is a suitable experimental paradigm to study consequences of a defined period of acute oxidative stress in NQO1-expressing cells.

Genotypic Variability of Photosynthetic Parameters in Maize Ear-Leaves at Different Cadmium Levels in Soil

Excess of cadmium (Cd) in soil leads to a number of adverse effects which challenge agricultural production. Aims of this study were to investigate variations in Cd content in leaves (Zea mays L.) of different maize genotypes and to detect effects of Cd on photosynthesis through chlorophyll a fluorescence. Pot vegetation experiments with four maize genotypes and four different soil Cd levels were repeated for two years. Chlorophyll fluorescence, photosynthetic pigments and inductively coupled plasma (ICP) analysis for ear-leaf Cd and zinc (Zn) and soil Cd were carried out. Significant differences between genotypes were found for leaf Cd, where higher Cd soil concentrations resulted in higher Cd leaf concentrations. Cd uptake into maize leaves increased with increasing Cd levels in soil, which was genotype-dependent and higher and lower Cd accumulating groups were formed. Changes in chlorophyll fluorescence caused by elevated Cd levels in soil were mostly visible as changes in dissipation energy, yields of primary photosystem II photochemistry and electron transport. Decrease of reaction centers per antenna chlorophyll and increased variable fluorescence at J step (VJ) resulted in decrease of performance indexes in the highest Cd concentration. Decreases in chlorophyll fluorescence parameters suggest reduced functionality of reaction centers and problems in re-oxidation of primary quinone acceptor (QA).

Effects of low temperature and cold-acclimation on photoinhibition and singlet oxygen production in four natural accessions of Arabidopsis

To understand the effects of low temperature and cold-acclimation on reactive oxygen species and photoinhibition of photosystem II (PSII), light-induced inactivation of PSII was measured at 22 and 4 °C from four Arabidopsis thaliana accessions (Rschew, Tenela, Columbia-0 and Coimbra) grown under optimal conditions. Photoinhibition was also measured at 4 °C from plants cold-acclimated at 4 °C for two weeks. Measurements were done in the absence and presence of lincomycin that blocks PSII repair, and PSII activity was assayed with the ratio of variable to maximum chlorophyll a fluorescence (FV/FM) and with light-saturated rate of oxygen evolution using a quinone acceptor. Of the non-acclimated accessions, Rschew was the most tolerant to photoinhibition and Coimbra the least; the rate constants of photoinhibition of the most sensitive accession were 1.3-1.9 times as high as those of the tolerant ones. The damaging reaction of photoinhibition in non-acclimated plants was slower or equal at 4 °C than at 22 °C. The rate constants of photoinhibition of cold-acclimated plants, at 4 °C, were 0.55 to 1.25 times as high as those of non-acclimated plants; the protective effect of cold-acclimation on photoinhibition was consistent in Columbia-0 and Coimbra whereas Rschew and Tenela were either slightly more tolerant or susceptible, depending on the method used to assay photoinhibition. Production of singlet oxygen, measured from thylakoid membranes isolated from non-acclimated and cold-acclimated plants, did not decrease due to cold-acclimation, nor did singlet oxygen production correlate with the rate of photoinhibition or with flavonol contents of the leaves.

Galangin Activates Nrf2 Signaling and Attenuates Oxidative Damage, Inflammation, and Apoptosis in a Rat Model of Cyclophosphamide-Induced Hepatotoxicity

Cyclophosphamide (CP) is a widely used chemotherapeutic agent; however, its clinical application is limited because of its multi-organ toxicity. Galangin (Gal) is a bioactive flavonoid with promising biological activities. This study investigated the hepatoprotective effect of Gal in CP-induced rats. Rats received Gal (15, 30 and 60 mg/kg/day) for 15 days followed by a single dose of CP at day 16. Cyclophosphamide triggered liver injury characterized by elevated serum transaminases, alkaline phosphatase (ALP) and lactate dehydrogenase (LDH), and histopathological manifestations. Increased hepatic reactive oxygen species, malondialdehyde, nitric oxide, and oxidative DNA damage along with declined glutathione and antioxidant enzymes were demonstrated in CP-administered rats. CP provoked hepatic nuclear factor-kappaB (NF-κB) phosphorylation and increased mRNA abundance of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) both expression and serum levels. Gal prevented CP-induced liver injury, boosted antioxidants and suppressed oxidative stress, DNA damage, NF-κB phosphorylation and pro-inflammatory mediators. Gal diminished Bax and caspase-3, and increased B-cell lymphoma-2 (Bcl-2) in liver of CP-administered rats. In addition, Gal increased peroxisome proliferator-activated receptor gamma (PPARγ) expression and activated hepatic nuclear factor erythroid 2-related factor 2 (Nrf2) signaling showed by the increase in Nrf2, NAD(P)H: quinone acceptor oxidoreductase-1 (NQO-1) and heme oxygenase 1 (HO-1) in CP-administered rats. These findings suggest that Gal prevents CP hepatotoxicity through activation of Nrf2/HO-1 signaling and attenuation of oxidative damage, inflammation and cell death. Therefore, Gal might represent a promising adjuvant therapy to prevent hepatotoxicity in patients on CP treatment.

Red-shifted delayed fluorescence at the expense of photoluminescence quantum efficiency – an intramolecular charge-transfer molecule based on a benzodithiophene-4,8-dione acceptor

A donor–acceptor compound using a thiophene based quinone acceptor displays strongly red-shifted delayed emission but limited quantum efficiency.