Impact of transient stress and stress enzymes on development

Stress enzymes triggered by transient stress mediate reprioritization of developmental and homeostatic events to flexibly accomplish the next essential developmental event. This review analyzes recent studies on stress and stress enzyme function during early mammalian development and describes the diverse consequences that result from measurement, analysis of function, and management of stress and stress enzymes during development.     

Oxidative stress,antioxidants and stress tolerance

Traditionally, reactive oxygen intermediates (ROIs) were considered to be toxic by-products of aerobic metabolism, which were disposed of using antioxidants. However, in recent years, it has become apparent that plants actively produce ROIs as signaling molecules to control processes such as programmed cell death, abiotic stress responses, pathogen defense and systemic signaling. Recent advances including microarray studies and the development of mutants with altered ROI-scavenging mechanisms provide new insights into how the steady-state level of ROIs are controlled in cells. In addition, key steps of the signal transduction pathway that senses ROIs in plants have been identified. These raise several intriguing questions about the relationships between ROI signaling, ROI stress and the production and scavenging of ROIs in the different cellular compartments.     

Getting stress out of stressed‐out stress granules

Amyotrophic lateral sclerosis (ALS) pathology is linked to the aberrant aggregation of specific proteins, including TDP‐43, FUS, and SOD1, but it is not clear why these aggregation events cause ALS. In this issue of The EMBO Journal, Mateju et al (2017) report a direct link between misfolded proteins accumulating in stress granules and the phase transition of these stress granules from liquid to solid. This discovery provides a model connecting protein aggregation to stress granule dysfunction.     

Pelvic stress

Biomechanics testing simulated stress concentrations in the acetabulum resulting from a blow to the right trochanter, as commonly occurs in recreational and passenger contexts. Developing tolerance criteria for the pelvis is addressed in this paper in terms of (1) the load distribution and energy transmission to the pelvis via both soft tissues and the femur, (2) the instability of the femur-pelvis complex, and (3) the difficulty of predicting stress using simple, experimentally derived, parameters.     

Formaldehyde stress

Formaldehyde, one of the most toxic organic compounds, is produced and processed in human cells. The level of human endogenous formaldehyde is maintained at a low concentration (0.01–0.08 mmol L⁻¹ in blood) under physiological conditions, but the concentration increases during ageing (over 65 years old). Clinical trials have shown that urine formaldehyde concentrations are significantly different between elderly Alzheimer’s patients (n=91) and normal elderly volunteers (n=38) (P<0.001). Abnormally high levels of intrinsic formaldehyde lead to dysfunction in cognition such as learning decline and memory loss. Excess extracellular and intracellular formaldehyde could induce metabolic response and abnormal modifications of cellular proteins such as hydroxymethylation and hyperphosphorylation, protein misfolding, nuclear translocation and even cell death. This cellular response called formaldehyde stress is dependent upon the concentration of formaldehyde. Chronic impairments of the brain resulted from formaldehyde stress could be one of the mechanisms involved in the process of senile dementia during ageing.     

Transient sequestration of TORC1 into stress granules during heat stress

The target of rapamycin complex 1 (TORC1) is a central kinase that coordinates nutrient availability with eukaryotic cell growth. Although TORC1 signaling is repressed by various stresses in yeast, the underlying mechanisms remain elusive. Here we report that TORC1 signaling upon heat stress is regulated by stress granules (SGs), which are cytoplasmic foci formed under certain stresses. Ectopic formation of SGs achieved by Pbp1 overexpression in unstressed cells sequesters TORC1 in this compartment, thereby blunting TORC1 signaling. Upon heat stress, a physiological SG-inducing condition, TORC1 is also recruited to SGs, which delays reactivation of TORC1 signaling during recovery from heat stress. Moreover, TORC1 reactivation is directed through SG disassembly, suggesting that SGs act as a key determinant for TORC1 reactivation during recovery from heat stress. Furthermore, this mechanism contributes to reduction of heat-induced mutations. Thus, TORC1 signaling is coupled to heat-induced SGs to protect cells from DNA damage.     

Plasma beta-endorphin and stress hormones in stress and adaptation

The experiments on white rats have shown that the induction of 4 hour stress produces an acute increase in beta-endorphin level, as well as characteristic changes in ACTH, cortisol, insulin, thyroxin and triiodothyronine concentrations. Different types of adaptation (training with short stress periods or injection of rhodiola rosea extract) promote a moderate increase in the amount of serum immunoreactive beta-endorphin, preventing its subsequent stress-induced elevation. Adaptation is characterized by a decrease or total prevention of hormonal changes peculiar to stress. The role of opioid neuropeptides in enhancing stress tolerance and the effect of adaptation factors are discussed.     

Oxidative stress markers in patients with post-traumatic stress disorder

Recent study data support the role of oxidative stress in diverse psychiatric disorders. Oxidative stress results from an oxidant/antioxidant imbalance, an excess of oxidants and/or a depletion of antioxidants. There are numerous studies that indicate that free radicals (FRs) damage neurons, and then play an important role in the pathophysiology of schizophrenia and depression. Active oxygen can cause considerable damage and disrupt the important physiological functions of proteins, lipids, enzymes and DNA. The aim of our study was to investigate the possible differences in the concentration of tromboxane B2, 8-OHdG and protein carbonyls, as significant markers of oxidative damage, and urate, albumin and total protein concentrations as antioxidative molecules in PTSD patients in comparison to the healthy control group. The study included 74 male participants who were active soldiers in the Croatian armed forces from 1991 to 1995. 46 subjects with chronic and current PTSD were recruited from the Department of Psychiatry of Dubrava University Hospital during 2010, 28 healthy subjects were recruited in the same period during the regular medical examination at the Dubrava University Hospital. Study results have shown that there is no statistically significant difference in urinary concentrations of 8-OHdG, serum thromboxane B2, and serum urates between two studied groups. Statistically significant difference of the protein carbonyl concentrations was examined. Concentrations were significantly lower in the PTSD group than in the control group. The clinical significance of these results was examined using ROC analysis. The obtained ROC curves did not separate the groups in a satisfactory manner.     

Acute heat stress induces oxidative stress in broiler chickens

The stress responses and possible oxidative damage in plasma, liver and heart were investigated in broiler chickens acutely exposed to high temperature. Eighty 5-week old broiler chickens were exposed to 32 degrees C for 6h. The extent of lipid peroxidation, activities of superoxide dismutase and total antioxidant power in plasma, liver and heart tissues were investigated. Meanwhile, the blood metabolites such as glucose, urate, triiodothyronine, thyroxine, corticosterone, ceruloplasmin and creatine kinase were measured before and after 3 and 6h of heat exposure. The results showed that oxidative stress could be induced in 5-week old broiler chickens by acute heat exposure (32 degrees C, 6h). The results suggest that the elevated body temperature can induce the metabolic changes that are involved in the induction of oxidative stress. The liver is more susceptible to oxidative stress than heart during acute heat exposure in broiler chickens. The oxidative stress should be considered as part of the stress response of broiler chickens to heat exposure.