Stress-induced Decrease Research Articles

Involvement of the JIN1/MYC2 Transcription Factor in Inducing Salt Resistance in Arabidopsis Plants by Exogenous Hydrogen Sulfide

The JIN1/MYC2 transcription factor, which is currently considered to be the key in jasmonate signaling, is also involved in the transduction of abscisic acid signals and, probably, in the effects of other intermediaries involved in the formation of plants’ adaptive responses. Arabidopsisjin1 mutants were used to study its possible involvement in protective effects of hydrogen sulfide (H2S) against salt stress. The treatment of wild-type Arabidopsis plants (Col-0) with the donor of hydrogen sulfide (50 μmol NaHS) led to an increase in their salt resistance, which was expressed in a decrease in oxidative damages, a decrease in water deficit, and preservation of a pool of photosynthetic pigments under 150 mmol NaCl. The treatment of Col-0 plants with NaHS prevented the stress-induced decrease in the activity of antioxidant enzymes, i.e., superoxide dismutase and catalase, and contributed to the increase in the activity of guaiacol peroxidase. In addition, leaves’ proline content in wild-type plants treated with the H2S donor was lower and sugar was higher after salt stress than in untreated plants. The treatment of jin1 mutants did not contribute to their salt resistance and did not have a noticeable effect on the functioning of the studied protective systems. The obtained results make it possible to assume the involvement of the JIN1/MYC2 transcription factor in the effects of hydrogen sulfide and/or intermediaries of its signaling pathways involved in the formation of plants’ adaptive responses to salt stress.

Modulation of depression-related behaviors by adiponectin AdipoR1 receptors in 5-HT neurons

The adipocyte-derived hormone adiponectin has a broad spectrum of functions beyond metabolic control. We previously reported that adiponectin acts in the brain to regulate depression-related behaviors. However, its underlying neural substrates have not been identified. Here we show that adiponectin receptor 1 (AdipoR1) is expressed in the dorsal raphe nucleus (DRN) and colocalized with tryptophan hydroxylase 2 (TPH2), a marker of serotonin (5-HT) neurons. Selective deletion of AdipoR1 in 5-HT neurons induced anhedonia in male mice, as indicated by reduced female urine sniffing time and saccharin preference, and behavioral despair in female mice and enhanced stress-induced decrease in sucrose preference in both sexes. The expression levels of TPH2 were downregulated with a concurrent reduction of 5-HT-immunoreactivity in the DRN and its two major projection regions, the hippocampus and medial prefrontal cortex (mPFC), in male but not female mice lacking AdipoR1 in 5-HT neurons. In addition, serotonin transporter (SERT) expression was upregulated in both DRN projection fields of male mice but only in the mPFC of female mice. These changes presumably lead to decreased 5-HT synthesis and/or increased 5-HT reuptake, thereby reducing 5-HT transmission. The augmented behavioral responses to the selective serotonin reuptake inhibitor fluoxetine but not desipramine, a selective norepinephrine reuptake inhibitor, observed in conditional knockout male mice supports deficient 5-HT transmission underlying depression-related phenotypes. Our results indicate that adiponectin acts on 5-HT neurons through AdipoR1 receptors to regulate depression-related behaviors in a sex-dependent manner.

Striatal reactivity to reward under threat-of-shock and working memory load in adults at increased familial risk for major depression: A preliminary study

Anhedonia, a core symptom of Major Depressive Disorder (MDD), manifests as a lack or loss of motivation as reflected by decreased reward responsiveness, at both behavioral and neural (i.e., striatum) levels. Exposure to stressful life events is another important risk factor for MDD. However, the mechanisms linking reward-deficit and stress to MDD remain poorly understood. Here, we explore whether the effects of stress exposure on reward processing might differentiate between Healthy Vulnerable adults (HVul, i.e., positive familial MDD) from Healthy Controls (HCon). Furthermore, the well-described reduction in cognitive resources in MDD might facilitate the stress-induced decrease in reward responsiveness in HVul individuals. Accordingly, this study includes a manipulation of cognitive resources to address the latter possibility. 16 HVul (12 females) and 16 gender- and age-matched HCon completed an fMRI study, during which they performed a working memory reward task. Three factors were manipulated: reward (reward, no-reward), cognitive resources (working memory at low and high load), and stress level (no-shock, unpredictable threat-of-shock). Only the reward anticipation phase was analyzed. Imaging analyses focused on striatal function. Compared to HCon, HVul showed lower activation in the caudate nucleus across all conditions. The HVul group also exhibited lower stress-related activation in the nucleus accumbens, but only in the low working memory (WM) load condition. Moreover, while stress potentiated putamen reactivity to reward cues in HVul when the task was more demanding (high WM load), stress blunted putamen reactivity in both groups when no reward was at stake. Findings suggest that HVul might be at increased risk of developing anhedonic symptoms due to weaker encoding of reward value, higher difficulty to engage in goal-oriented behaviors and increased sensitivity to negative feedback, particularly in stressful contexts. These findings open new avenues for a better understanding of the mechanisms underlying how the complex interaction between the systems of stress and reward responsiveness contribute to the vulnerability to MDD, and how cognitive resources might modulate this interaction.

Investigating the deformation mechanisms of a highly metastable high entropy alloy using in-situ neutron diffraction

The present study correlates the effect of enhanced metastability on both the well-understood γ-f.c.c. stacking fault energy (SFE) and deformation mechanisms in the ε-h.c.p. phase of a metastable high entropy alloy (HEA). The SFE of a Fe40Mn20Cr15Co20Si5 alloy (CS-HEA) was experimentally determined to be ∼6.31 mJ m−2 using in-situ neutron diffraction. The relatively low-measured SFE of the CS-HEA results in a high fraction of the ε-h.c.p. phase (58 %) triggering significant stress partitioning to ε-h.c.p. and a marginal fraction of γ-f.c.c. → ε-h.c.p. transformation (∼25 %). The ε-h.c.p. phase accommodated a significant amount of strain marked by the large stress-induced decrease of c/a ratio (from ∼1.619 to 1.588), which was accompanied by activation of non-basal deformation modes, such as deformation twinning and pyramidal slip. Using in-situ neutron diffraction, we show by decreasing SFE and stabilization of large fractions of ε-h.c.p., activation of non-basal deformation modes are responsible for high work hardenability in absence of significant γ-f.c.c. → ε-h.c.p. transformation.

Antidepressive Effects of Kamishoyosan through 5-HT1AReceptor and PKA-CREB-BDNF Signaling in the Hippocampus in Postmenopausal Depression-Model Mice.

Females are well known to suffer disproportionately more than males from stress-related neuropsychiatric disorders, especially during perimenopausal and postmenopausal periods. In addition to a decline in serum estradiol levels, environmental stress and social stress likely contribute to the development of neuropsychiatric symptoms in perimenopausal and postmenopausal women. Kamishoyosan (KSS) is a traditional Japanese Kampo medicine, composed of a specified mixture of 10 crude compounds derived from plant sources, widely used for various neuropsychiatric symptoms in perimenopausal and postmenopausal women. However, the molecular mechanisms underlying KSS-mediated attenuation of neuropsychological symptoms and stress-response behaviors in perimenopausal and postmenopausal women remain unknown. In the present study, we first established a mouse model for postmenopausal depression-like signs using chronic water-immersion and restraint-stressed ovariectomized (OVX) mice to investigate the underlying molecular mechanism of KSS. We found that continuous administration of KSS to these mice normalized the activation of the hypothalamic-pituitary-adrenal (HPA) axis, ameliorated stress-induced depressive behavior, and prevented a decrease of neurogenesis in the hippocampus. As previous studies have implicated dysfunction of the hippocampal 5-HT1A receptor (5-HT1AR) in depressive disorders, we also evaluated the effect of KSS on 5-HT1AR expression and the protein kinase A- (PKA-) cAMP response element-binding- (CREB-) brain-derived neurotrophic factor (BDNF) signaling pathway in the hippocampus in this model. The level of 5-HT1AR in the hippocampus decreased in chronic stress-exposed OVX mice, while KSS treatment normalized the stress-induced decrease in 5-HT1AR expression in the hippocampus of chronic stress-exposed OVX mice. Furthermore, we found that KSS treatment upregulated the expression levels of phosphorylated PKA (p-PKA), phosphorylated CREB (p-CREB), and BDNF in the hippocampus in chronic stress-exposed OVX mice. These results suggest that KSS improves neuropsychiatric symptoms through 5-HT1AR and PKA-CREB-BDNF signaling in the hippocampus in postmenopausal women.

Oxidative stress mediates heat-induced changes of tight junction proteins in porcine sertoli cells via inhibiting CaMKKβ-AMPK pathway

Heat stress causes reversible changes in tight junction proteins in immature Sertoli cells via inhibition of the AMPK signaling pathway; these effects are accompanied by an increase in the early apoptotic rate and decrease in the cell viability of Sertoli cells. Since heat stress is known to also cause oxidative damage, in the present study, we investigated whether the earlier mentioned effects of heat stress were brought about via the induction of oxidative stress in boar Sertoli cells. Immature Sertoli cells obtained from 3-week-old piglets were subjected to heat treatment (43 °C, 30 min), and the percentage of ROS-positive cells, the malonaldehyde (MDA) concentration, and the activity of the antioxidases, including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were measured. Next, the Sertoli cells were treated with N-acetyl-l-cysteine (NAC) (1 mmol/L, 2 h), an antioxidant agent, before they were exposed to heat stress. The effects of NAC on ROS accumulation, MDA levels, antioxidase activity, the CaMKKβ-AMPK signaling pathway and expression of tight junction proteins were assessed. The results showed that heat stress reversibly increased the percentage of ROS-positive cells and MDA levels, and decreased the activity of SOD, GSH-Px, and CAT. Pretreatment with NAC abrogated these effects of heat stress. Additionally, NAC reversed the heat stress-induced decrease in the expression of CaMKKβ and dephosphorylation of AMPK. NAC also obviously rescued the heat stress-induced downregulation of tight junction proteins (claudin-11, JAM-A, occludin, and ZO-1) both at the mRNA and protein level. In conclusion, the findings indicate that oxidative damage participates in heat stress-induced downregulation of tight junction proteins in Sertoli cells by inhibiting the CaMKKβ-AMPK axis. Further, NAC reversed the effects of heat stress on tight junction proteins; this means that it has potential as a protective agent that can prevent reproductive dysfunction in boars under conditions of heat stress.

Downregulation of SIRT2 by Chronic Stress Reduces Expression of Synaptic Plasticity-related Genes through the Upregulation of Ehmt2

Silent information regulator 2 (Sirtuin2 / SIRT2) is a NAD+-dependent deacetylase that regulates the cellular oxidative stress response. It modulates transcriptional silencing and protein stability through deacetylation of target proteins including histones. Previous studies have shown that SIRT2 plays a role in mood disorders and hippocampus-dependent cognitive function, but the underlying neurobiological mechanism is poorly understood. Here, we report that chronic stress suppresses SIRT2 expression in the hippocampus. Molecular and biochemical analyses indicate that the stress-induced decrease in the SIRT2 expression downregulates synaptic plasticity-related genes in the hippocampus through the increase of euchromatic histone-lysine N-methyltransferase 2 (Ehmt2) (also known as G9a). shRNA-mediated knockdown of SIRT2 in the dentate gyrus alters the expression of synaptic plasticity-related genes in a way similar to those induced by chronic stress, and produces depression-like behaviors. Our results indicate that SIRT2 plays an important role in the response to stress, thereby modulating depression-like behaviors.

Mindful Sensation Seeking: An Examination of the Protective Influence of Selected Personality Traits on Risk Sport-Specific Stress.

Stress often has a negative influence on sports performance. Stress-induced decreases in performance can be especially disastrous for risk sports athletes, who often put their life at risk when practicing their sport. Therefore, it is of great importance to identify protective factors in stressful situations in risk sports. On average, risk sports athletes score extremely high on the personality trait sensation seeking. At the same time, theoretical considerations about dispositional mindfulness suggest that mindful athletes can handle stress more effectively. The main goal of this experiment is to examine the influence of sensation seeking and mindfulness on the stress response to a risk sport-specific stressor. To induce stress, 88 male students completed the Heidelberg Risk Sport-Specific Stress Test (HRSST) which utilizes fear of falling as the stressful event during a climbing exercise. Psychological (anxiety) and physiological (cortisol) responses were measured at multiple time points before and after the HRSST to determine the severity of the stress response. In reaction to the stressor, a significant increase in self-reported state anxiety, but no significant increase in cortisol were observed. The mindfulness subscale external observation correlated positively with anxiety in the climbing wall, sensation seeking and the anxiety scales after the jump correlated negatively and sensation seeking predicted anxiety subscales after the jump in hierarchical regression analyses. However, mindfulness did not predict anxiety measures. Neither sensation seeking nor mindfulness correlated significantly with cortisol levels. The results suggest that high sensation seekers perceive a risk sport-specific stressor as less stressful. The missing physiological response might be explained by the Cross-Stressor-Adaptation-Hypothesis and particularities of the sample. Good internal observers might be especially aware of their need of stimulation and new experiences, which in turn might explain the higher experience-seeking scores. Future studies should further examine the role of mindfulness in stressful situations and the interaction of its subscales with sensation seeking. The current experiment offers new possibilities for adjoining research fields at the interface between sports sciences, psychology and medicine: The findings can be transferred to high risk professions such as police officers, firefighters and military forces (e.g., for selection processes or for interventions).

Amelioration effects of Kaempferol on immune response following chronic intermittent cold-stress

Cold-stress causes disturbance of the homeostatic regulation of animals, and gradually impairs the immune and antioxidant functions of animals. Therefore, increasing the effectiveness of the immune response and antioxidant function are the most attractive strategies against cold-stress. Kaempferol (KPF) exerts both an anti-inflammatory and antioxidant pharmacological effect. However, nor much is known of the effects of KPF on providing protection from cold-induced intestinal oxidative damage and improving immunity. This study investigated the effects of KPF on immune factors and intestinal antioxidation in the blood of cold-stressed mice.KPF was solubilized in diluted saline before administration. The mice were randomly divided into 4 groups: (1) control, (2) cold-stress, (3) KPF 25 mg/kg, and (4) cinnamon (CAM) 30 mg/kg groups. Groups (2)–(4) were exposed to cold stress once a day for 7 days. Cold-stress was achieved by exposing the mice to a temperature of −15 °C and 70 ± 10% humidity for 60 min, once a day. The histopathological changes in the small intestine of the mice were analyzed. The T lymphocyte populations in blood were measured using flow cytometry. The level of SLC6a4, 5-HT3 and 5-HTT in small intestine tissue was assessed using RT-PCR analysis. Cow blood samples were obtained for the hematological analysis.Kaempferol (KPF) (25 mg/kg) regularized the intestinal antioxidant activity in the cold stress animals. KPF was able to significantly (P < .05) return intestinal SLC6a4, 5-HT3 and 5-HTT levels to normal after it had increased due to cold-stress. KPF treatment prevented the cold stress-induced decrease in blood CD4+T cells and decrease CD8+T cells levels in mice. Improved hematological profiles were additionally observed on treatment cows with KPF.KPF compared favorably with cinnamon in cold stress management, suggesting cold stress disturbs the anti-inflammatory effect of KPF. Thus, KPF contributes to suppress the activated pro-inflammatory cytokines, IL-9, IL-13, CD8+T and neurochemicals, and to increase anti-inflammatory cytokines and CD4+T levels.

Relevance of number and physiological status of conspecifics in preventing stress-induced decreases in newly proliferated cells and neuroblasts.

The presence of three conspecifics prevents stress-induced decreases in newly proliferated cells and neuroblasts in mouse dentate gyrus (DG). In this study, we sought to determine how many conspecifics are required to exert these protective effects against stress. In addition, we manipulated the physiological status of those conspecifics in the context of their stress-buffering effects and used airborne oxytocin exposure as a substitute for the presence of conspecifics. Bromodeoxyuridine staining was used to indicate the newly proliferated cells and co-staining with doublecortin to reveal the proliferative neuroblasts. Presentation of three intact and lipopolysaccharide-treated conspecifics prevented the stress-induced decreases in the number of newly proliferated cells and neuroblasts in DG. Presentation of one saline- or oxytocin (OT)-treated conspecific did not exert observable stress-buffering effects. In contrast, airborne oxytocin prevented the stress-induced decreases in DG cell proliferation and early neurogenesis, while pretreatment with L-371,257, a selective OT receptor antagonist, abolished the buffering effects of OT. Physical interaction with the conspecifics and conspecifics' sickness, at best, play a minor role in mediating the buffering effects against stress-induced decreases in DG cell proliferation or early neurogenesis. Moreover, stress-buffering effects are negligible with the presence of only one conspecific. Finally, airborne OT produced stress-buffering effects possibly via its stimulation of OT receptors. Oxytocin merits further study as a substitute for the stress-buffering effects of companions.

Edaravone prevents memory impairment in an animal model of post-traumatic distress.

Post-traumatic stress disorder (PTSD) is a mental health problem that develops in a proportion of individuals after experiencing a potential life-threatening traumatic stress event. Edaravone is a free radical scavenger, with a neuroprotective effect against cognitive impairment in several animal models. In the present study, the protective effect of edaravone on PTSD-induced memory impairment was investigated. Single prolonged stress was used as an animal model of PTSD, comprising 2 h of restrain, 20-min forced swimming, 15-min rest, and 1-2-min diethyl ether exposure. Concurrently, edaravone was given at a dose of 6 mg/kg/day, intraperitoneally, for 21 days. The radial arm water maze was used to assess learning and memory. Antioxidant biomarkers were measured in hippocampus tissues. Chronic administration of edaravone prevented impairment of short-term and long-term memory. Edaravone also prevented the stress-induced decrease in the ratio of reduced glutathione/oxidized glutathione and the activities of glutathione peroxidase and catalase enzymes in the hippocampus, as well as increases in the levels of oxidized glutathione and thiobarbituric acid reactive substances. In conclusion, edaravone ameliorated oxidative stress and cognitive impairment associated with a PTSD model, probably by supporting antioxidant mechanism in the hippocampus.

Melatonin treatment affects changes in adrenal gene expression of catecholamine biosynthesizing enzymes and norepinephrine transporter in the rat model of chronic-stress-induced depression.

This study investigated the effects of melatonin treatment on adrenal catecholamine content, synthesis, uptake, and vesicular transport induced by the chronic unpredictable mild stress (CUMS) model of depression in rats. This entailed quantifying the norepinephrine, epinephrine, mRNA, and protein levels of tyrosine hydroxylase (TH), dopamine-β-hydroxylase (DBH), phenylethanolamine N-methyltransferase (PNMT), norepinephrine transporter (NET), and vesicular monoamine transporter 2 (VMAT2) in the adrenal medulla. CUMS caused a significant depletion of norepinephrine stores and protein levels of TH, DBH, and NET, whereas the gene expression of PNMT was increased. It was observed that melatonin treatment in the CUMS rats prevented the stress-induced decrease in norepinephrine content and the protein expression of TH, DBH, and NET in the adrenal medulla of chronically stressed rats. The present study demonstrates the stimulatory effect of melatonin on adrenomedullary synthesis, the uptake and content of catecholamine in the rat model of chronic stress-induced depression.

Short-term antidepressant treatment has long-lasting effects, and reverses stress-induced decreases in bone features in rats

Antidepressants are among the most-prescribed class of drugs in the world and though weight gain is a common outcome of antidepressant treatment, that effect is not well understood. We employed an animal model comprised of 2 weeks of chronic restraint stress with antidepressant treatment, followed by diet-induced obesity. We showed that short-term antidepressant treatment had long-lasting effects, not only leading to weight gain, but also enhancing trabecular and cortical bone features in rats; therefore, weight gain in this model was different from that of the classic diet-induced obesity. Late in the post-restraint recovery period, antidepressant-treated animals were significantly heavier and had better bone features than saline-treated controls, when assessed in the distal femoral metaphysis. The propensity to gain weight might have influenced the rate of catch-up growth and bone allometry, as heavier animals treated with fluoxetine also had enhanced bone features when compared to non-stressed animals. Therefore, short-term antidepressant treatment ameliorated the long-term effects of stress on body growth and bone. Growth and bone structural features were associated with leptin levels, and the interaction between leptin levels and antidepressant was significant for bone mineral content, suggesting that short-term antidepressants in the context of long-term diet-induced obesity modified the role of leptin in bone formation. To our knowledge this is the first study reporting that short-term antidepressant treatment has long-lasting effects in restoring the effects of chronic stress in body weight and bone formation. Our findings may be relevant to the understanding and treatment of osteoporosis, a condition of increasing prevalence due to the aging population.

Micro-scale investigation on coupling of gas diffusion and mechanical deformation of shale

The nanopore structure usually exhibit complex geometry in the shale formation. The interactions between gas and pore structure in such heterogeneous property impacts the properties of shale gas transport in micro-scale. The precise description of this shale gas flow processes in detail is impossible if the micropore is not properly characterized. Thus, this study provides a simulation approach to model the complex geometry of nanopore structures in the shale formation. Based on SEM image segmentation of the shale matrix, the geometry of three compositions (nanopore, kerogen, and matrix) are explicitly simulated. Mass storage, transport mechanisms, and geomechanical properties are fully modeled in the micro-scale model. It demonstrates that the conventional dual porosity model fails to capture the storage and transport mechanisms in micro-scale by comparison with the micro-scale model. The simulation results reveal that stress-induced decrease of the diffusion coefficient is both time-dependent and space-dependent. The reduction of the diffusion coefficient can significantly cut down the adsorbed gas production in kerogen. It results in the low recovery rate of shale gas that a large proportion of adsorbed gas is unable to liberate. Moreover, the later stage of gas production is depended on the supply of adsorbed gas in kerogen.

ANTIDEPRESSANT-LIKE ACTIVITY OF FLOWERS OF TECOMELLA UNDULATA IN MICE SUBJECTED TO CHRONIC UNPREDICTABLE MILD STRESS

Objective: Flowers of Tecomella undulata have been reported to be a rich source of flavonoids such as rutin and quercetin. The present study was designed to evaluate the effect of ethanol extract of flowers of T. undulata on chronic unpredictable mild stress (CUMS)-induced depression in Swiss young male albino mice.Methods: The mice were subjected to CUMS for 21 successive days. Ethanol extract of the flowers (50, 100, and 200 mg/kg, p.o.) and fluoxetine (20 mg/kg, p.o.) per se was administered for 21 successive days to separate groups of unstressed and stressed mice. Tail suspension test (TST) and sucrose preference test were used to evaluate the effect of the extract on depression-like behavior in mice.Results: Extract of flowers of T. undulata (100 and 200 mg/kg) significantly decreased immobility period of stressed mice in TST, indicating significant antidepressant-like activity of the extract. Stress-induced reduced sucrose preference was significantly restored by the extract. There was no significant effect on locomotor activity of mice by the extract and fluoxetine. The extract significantly reversed stress-induced increase in brain malondialdehyde levels; plasma nitrite and corticosterone levels; and also significantly reversed the stress-induced decrease in reduced glutathione and catalase levels. There was no significant effect of the extract on brain MAO-A activity in both unstressed and stressed mice.Conclusion: These results indicated that ethanol extract of flowers of T. undulata showed significant antidepressant-like activity in mice subjected to CUMS, probably through alleviation of oxidative stress and decrease in plasma corticosterone levels.

ANTIDEPRESSANT-LIKE ACTIVITY OF FLOWERS OF TECOMELLA UNDULATA IN MICE SUBJECTED TO CHRONIC UNPREDICTABLE MILD STRESS

Objective: Flowers of Tecomella undulata have been reported to be a rich source of flavonoids such as rutin and quercetin. The present study was designed to evaluate the effect of ethanol extract of flowers of T. undulata on chronic unpredictable mild stress (CUMS)-induced depression in Swiss young male albino mice.Methods: The mice were subjected to CUMS for 21 successive days. Ethanol extract of the flowers (50, 100, and 200 mg/kg, p.o.) and fluoxetine (20 mg/kg, p.o.) per se was administered for 21 successive days to separate groups of unstressed and stressed mice. Tail suspension test (TST) and sucrose preference test were used to evaluate the effect of the extract on depression-like behavior in mice.Results: Extract of flowers of T. undulata (100 and 200 mg/kg) significantly decreased immobility period of stressed mice in TST, indicating significant antidepressant-like activity of the extract. Stress-induced reduced sucrose preference was significantly restored by the extract. There was no significant effect on locomotor activity of mice by the extract and fluoxetine. The extract significantly reversed stress-induced increase in brain malondialdehyde levels; plasma nitrite and corticosterone levels; and also significantly reversed the stress-induced decrease in reduced glutathione and catalase levels. There was no significant effect of the extract on brain MAO-A activity in both unstressed and stressed mice.Conclusion: These results indicated that ethanol extract of flowers of T. undulata showed significant antidepressant-like activity in mice subjected to CUMS, probably through alleviation of oxidative stress and decrease in plasma corticosterone levels.

Effect of Hydrogen Sulfide Donor on Antioxidant State of Wheat Plants and Their Resistance to Soil Drought

Effects of plant treatment with a donor of hydrogen sulfide—sodium hydrosulfide—on the state of antioxidative and osmoprotective systems of young plants of winter wheat (Triticum aestivum L.) cv. Doskonala under conditions of soil drought (progressive decrease in soil moisture down to 25–30% of the total moisture capacity) were studied. Spraying of plants with NaHS solutions (0.1–0.5 mM) before the drought significantly alleviated the growth suppression and favored the conservation of the chlorophyll pool under drought conditions. The beneficial effect of sodium hydrosulfide on plants was eliminated by their simultaneous treatment with hydroxylamine, which is a scavenger of hydrogen sulfide. The plant pretreatment with NaHS prevented the drought-induced accumulation of hydrogen peroxide and that of a lipid peroxidation product (malonic dialdehyde) in leaves. Such pretreatment also promoted an increase in the activity of superoxide dismutase (SOD) and prevented a stress-induced decrease in activities of catalase and guaiacol peroxidase in the leaves. Furthermore, the hydrogen sulfide donor elevated the concentration of proline and considerably increased levels of anthocyanins and UV-absorbing flavonoids under the drought. It is concluded that the plant drought protection afforded by the hydrogen sulfide donor depends to large extent on SOD and flavonoid compounds.

Postoperative CD4 counts predict anastomotic leaks in patients with penetrating abdominal trauma

IntroductionThe influence of trauma- and surgical stress-induced decrease of CD4 count on anastomotic leaks after penetrating abdominal trauma has to date not been investigated. A prospective study was performed to explore the effect of CD4 count 24 h after surgery on the anastomotic leak rate and to identify risk factors for anastomotic leaks. MethodsThis was a prospective study including 98 patients with small or large bowel resection and subsequent anastomosis due to penetrating abdominal trauma. Univariate analysis identified risk factors for the development of anastomotic leak and also investigated the predictive value of the CD4 count for this complication. ResultsOf the 98 patients 23 patients (23%) were HIV-infected. The overall leak rate was 13%. Univariate analysis including all potential risk factors with p-values<0.05 identified six factors leading to a significantly higher rate of anastomotic complications: postoperative CD4 count<250 cells/μl, postoperative albumin <30 g/L, penetrating abdominal trauma index≥25, gunshot wound as mechanism of injury, blood transfusion requirement >6units and delayed anastomosis after damage control surgery. Survival rates were analysed with the χ2 test and did not show a significantly higher mortality rate in patients with low CD4 count. The negative impact of trauma and subsequent surgery on the cell mediated immunity was demonstrated by the fact that 55 (73%) of the HIV-negative patients had a CD4 count less than 500 cells/μl 24 h postoperatively. HIV-infection had no significant influence on the leak rate, however all HIV infected patients that developed an anastomotic leak died. ConclusionA low post-operative CD4 count is a predictor for anastomotic leaks irrespective of HIV-serostatus. Low postoperative serum albumin, high injury severity, gunshot wound as mechanism of injury, blood transfusion requirement >6 units and delayed anastomosis were further risk factors for anastomotic complications. Postoperative CD4 count and serum albumin should be considered in the decision making process of performing an anastomosis or diverting stoma for patients after “clip and drop” of the bowel as part of damage control surgery.

Pretreatment with NaCl Promotes the Seed Germination of White Clover by Affecting Endogenous Phytohormones, Metabolic Regulation, and Dehydrin-Encoded Genes Expression under Water Stress.

This study was designed to examine the effects of NaCl pretreatment on the seed germination of white clover (Trifolium repens cv. Ladino) under water stress induced by 19% polyethylene glycol (PEG) 6000. Lower concentrations of NaCl (0.5, 1, and 2.5 mM) pretreatment significantly alleviated stress-induced decreases in germination percentage, germination vigor, germination index, and radicle length of seedlings after seven days of germination under water stress. The soaking with 1 mM of NaCl exhibited most the pronounced effects on improving seed germination and alleviating stress damage. NaCl-induced seeds germination and growth could be associated with the increases in endogenous gibberellic acid (GA) and indole-3-acetic acid (IAA) levels through activating amylases leading to improved amylolysis under water stress. Seedlings pretreated with NaCl had a significantly lower osmotic potential than untreated seedlings during seed germination, which could be related to significantly higher soluble sugars and free proline content in NaCl-treated seedlings under water stress. For antioxidant metabolism, NaCl pretreatment mainly improved superoxide dismutase, peroxidase, ascorbate peroxidase, and glutathione reductase activities, transcript levels of FeSOD, APX, and DHAR, and the content of ascorbic acid, reduced glutathione, and oxidized glutathione during seed germination under water stress. The results indicated that seeds soaking with NaCl could remarkably enhance antioxidant metabolism, thereby decreasing the accumulation of reactive oxygen species and membrane lipid peroxidation during germination under water stress. In addition, NaCl-upregulated dehydrin-encoded genes SK2 expression could be another important mechanism of drought tolerance during seeds germination of white clover in response to water stress.

Rieske iron-sulfur protein of cytochrome-b6f is involved in plant recovery after drought stress

The aim of the study was to determine molecular basis of plant photosynthetic activity during soil drought and under rapid (unfavorable) and gradual (favorable) rehydration. We analyzed the content of proteins associated with the photosynthetic apparatus and photosynthetic fixation of CO2. The experiment involved two genotypes of triticale showing complete and incomplete recovery from drought stress.The reason for irreversible changes in the activity of the photosynthetic apparatus was stress-induced decrease in the content of Rieske protein (PetC) of cytochrome complex b6f. Intensification of metabolic processes during rehydration and following overload the electron transport chain led to electron transfer from primary acceptors QA/QB in PSII and ferredoxin in PSI to oxygen. The resulting reactive oxygen species oxidized proteins and inhibited synthesis of those controlling the photosynthetic apparatus and carbon fixation. The consequence was a reduction of quantum yield of electron transport to their final acceptors in PSI and lowering of plant photosynthetic activity and biomass. Simultaneous utilization of H2O2 during saturation of cell wall with phenolic compounds ensured restoration of desired level of proteins controlling the photosynthetic apparatus and photosynthetic carbon fixation, as well as high photosynthetic activity.