Causes of stress

Academic Institutions offering higher education in Arts and Science Colleges are undergoing a process of change is similar to that of business organisations, more particularly during the last few decades when the industries have to confront hectic competitions.

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Stress is the “wear and tear” our minds and bodies experience as we attempt to cope with our continually changing environment. Stress mainly occurs when the pressure is greater than the resource.

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We have examined the effects of widely used stress-inducing agents on protein synthesis and on regulatory components of the translational machinery. The three stresses chosen, arsenite, hydrogen peroxide and sorbitol, exert their effects in quite different ways. Nonetheless, all three rapidly ( 30 min) caused a profound inhibition of protein synthesis. In each case this was accompanied by dephosphorylation of the eukaryotic initiation factor (eIF) 4E-binding protein 1 (4E-BP1) and increased binding of this repressor protein to eIF4E. ...

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Mitochondrial functional and structural impairment and generation of oxidative stress have been implicated in aging, various diseases and chemotherapies. This study analyzed azidothymidine (AZT)-caused failures in mitochondrial functions, in redox regulation and activation of the HIV-1 gene expression. We monitored intracellular concentrations of ATP and glutathione (GSH) as the indicators of energy production and redox conditions, respectively, during the time-course experiments with U937 and MOLT4 human lymphoid cells in the presence of AZT (0.05 mgÆmL)1) or H2O2 (0.01 mM) for 15–25 days.

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Exposure of mammalian cells to oxidant stress causes early (iron catalysed) lysosomal rupture followed by apoptosis or necrosis. Enhanced intracellular production of reactive oxygen species (ROS), presumably of mitochondrial origin, is also observed when cells are exposed to nonoxidant pro-apoptotic agonists of cell death. We hypothesized that ROS generation in this latter case might promote the apoptotic cascade and could arise from effects of released lysosomal materials on mitochondria.

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Mortality in the host armyworm larvaePseudaletia separata parasitized by the parasitic waspCotesia kariyaiwas dra-matically increased when they were simultaneously infected by the entomopathogen Serratia marcescens. Previous studies have shown that this strong insecticidal effect is due to a metalloprotease-like insecticide (MPLI)released from S. marcescensenterobacter. This study was conducted to elucidate the exact cause of the mortality resulting from MPLI.

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Halobacterium salinarumdisplays four distinct kinetic forms of M-intermediate in its bacteriorhodopsin photocycle. In wild-type, there are mainly two species with time constants near 2 and 5 ms. Under various kinds of stress, two other species arise with time constants near 10 and 70 ms. We show that these four species are interconvertible. Increases in membrane hydrophobicity convert the slower to faster forms. Perturbations caused by Triton X-100 or mutations convert faster to slower forms.

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The ability of yeasts to grow in the presence of weak organic acid preservatives is an important cause of food spoilage. Many of the determinants of acetate resistance inSac-charomyces cerevisiae differ from the determinants of resistance to the more lipophilic sorbate and benzoate. Interestingly,we show in this study that hypersensitivity to both acetate and sorbate results when the cells have auxo-trophic requirements for aromatic amino acids.

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Plasma concentrations of free fatty acids are increased in metabolic syn-drome, and the increased fatty acids may cause cellular damage via the induction of oxidative stress. The present study was designed to determine whether the increase in fatty acids can modify the free sulfhydryl group in position 34 of albumin (Cys34) and enhance the redox-cycling activity of the copper–albumin complex in high-fat diet-induced obese mice.

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Rare, inherited mutations causing familial forms of Parkinson’s disease have provided insight into the molecular mechanisms that underlie the genetic and sporadic forms of this disease. Loss of protein function result-ing from autosomal-recessive mutations in PTEN-induced putative kinase 1 (PINK1), Parkin and DJ-1 has been linked to mitochondrial dysfunction, accumulation of abnormal and misfolded proteins, impaired protein clear-ance and oxidative stress.

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Oxidative stress, followed by the apoptotic death of pancreaticbcells, is considered to be one of causative agents in the evolution of the type 2 dia-betic state; therefore, the protection ofbcells can comprise an efficacious strategy for preventing type 2 diabetes. In the present study, RIN-m5F cells (i.e. the rat insulinoma bcell line) were stimulated with streptozotocin, resulting in a time- and concentration-dependent release of lactate dehydrogenase.

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There is strong evidence thatb-amyloid (Ab) causes oxidative stress and induces mitochondrial dysfunction in the pathogenesis of Alzheimer’s dis-ease. Mitochondrial transcription factor A (Tfam) has multiple roles in the maintenance of mtDNA. To study the protective roles of Tfam against amyloid neurotoxicity, we established SH-SY5Y cell lines stably over-expressing Tfam and exposed them to 10lmAb1-42 for 24 h.

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Hydrogen peroxide (H2O2) is a well known oxidative stress inducer causing apoptosis of many cells. Previously, we have shown that heat shock pre-treatment blocked the release of the second mitochondria-derived activator of caspase (Smac) to the cytosol and inhibited apoptosis of C2C12 myo-blast cells in response to H2O2.

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Fatty aldehyde dehydrogenase (FALDH; also known as ALDH3A2 or ALDH10) oxidizes medium- or long-chain aliphatic aldehydes. FALDH deficiency in humans is known to be the cause of Sjo¨gren–Larsson syn-drome, in which individuals display neurological symptoms and cutaneous abnormality.

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There is growing concern about the safety of engineered nanoparticles, which are produced for various industrial applications. Quantum dots are colloidal semiconductor nanoparticles that have unique luminescence char-acteristics and the potential to become attractive tools for medical imaging. However, some of these particles can cause oxidative stress and induce cell death.

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The Ca 2+ -dependent response to oxidative stress caused by H2O2 ortert-butylhydroperoxide (tBOOH) was investigated inSaccharomyces cerevisiae cells expressing transgenic cytosolic aequorin, a Ca 2+ -dependent photopro-tein. Both H2O2 and tBOOH induced an immediate and short-duration cytosolic Ca 2+ increase that depended on the concentration of the stres-sors.

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Cells have evolved complex and overlapping mechanisms to protect their proteins from aggregation. However, several reasons can cause the failure of such defences, among them mutations, stress conditions and high rates of protein synthesis, all common consequences of heterologous protein pro-duction.

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Arsenic is a strong stimulus of heme oxygenase (HO)-1 expression in experimental studies in response to oxidative stress caused by a stimulus. A functional GT-repeat polymorphism in the HO-1 gene promoter was inversely correlated to the development of coronary artery disease in diabetics and development of restenosis following angioplasty in patients. The role of this potential vascular protective factor in carotid atherosclerosis remains unclear. We previously reported a graded association of arsenic...

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Cushing's Syndrome is a disease caused by an excess of cortisol production or by excessive use of cortisol or other similar steroid (glucocorticoid) hormones. Cortisol is a normal hormone produced in the outer portion, or cortex, of the adrenal glands, located above each kidney. The normal function of cortisol is to help the body respond to stress and change. It mobilizes nutrients, modifies the body's response to inflammation, stimulates the liver to raise the blood sugar, and it helps control the amount of water in the body.

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