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PubMed2000

Formation and stability of the bacteriophage lambda replication complexes in UV-irradiated Escherichia coli.

Bacteriophage lambda replication complex, containing the phage-encoded O initiator protein protected from proteases by other elements of this complex, is a stable structure that can be inherited by one of the two daughter lambda DNA copies after a replication round in Escherichia coli. In normal growth conditions in bacteria bearing a plasmid derived from bacteriophage lambda, such a complex may be stable for many cell generations. However, it was found that this stable structure is disassembled under certain conditions, namely, after heat shock. Therefore, we asked whether other environmental stresses may cause disassembly of the lambda replication complex. We found that UV irradiation of the host cells prevented formation of the stable lambda replication complex (though not preventing phage replication), while the same UV doses did not affect the stability of the replication complex assembled prior to the irradiation. These results indicate that the stable lambda replication complex, although sensitive to heat shock, is resistant to some other environmental stresses and that formation of at least two types of lambda replication complexes is possible. Both stable and unstable lambda replication complexes are functional because replication of lambda DNA under conditions preventing formation of the stable complex proceeds efficiently.

Bacteriolysis↗
PubMed1991

Infection with adeno-associated parvovirus leads to increased sensitivity of mammalian cells to stress.

Infection of the SV40-transformed Syrian hamster cells Elona with adeno-associated parvovirus type 5 (AAV-5) affects the cellular stress response. Stress-induced growth delay becomes permanent and this promotes cell death. AAV DNA is replicated in the absence of helper virus. Induction of an incomplete stress response by cycloheximide treatment still results in replication of viral DNA but not in virus-mediated growth arrest. Thus, the reactions that induce AAV DNA replication and that direct growth delay are different and replication of AAV DNA is not sufficient to induce growth arrest and cell death. Additional steps that lead to effects resembling inhibition of protein synthesis are required. The possibility that they may have their origin in the action of AAV rep proteins is discussed.

Animals↗
PubMed1996

Changes in taste and satiety in dietary-restrained women following stress.

Stress has been shown to increase food consumption in women with high levels of dietary restraint (restrainers) but decrease consumption in nonrestrainers. The present study was designed to replicate the differential eating pattern following stress and measure physiological and subjective responses to food over repeated taste presentations. Restrained (N = 16) and nonrestrained (N = 16) women were given eight taste presentations of a food followed by an ad lib taste test. Between taste trials, half of the restrainers and nonrestrainers performed a variation of the Stroop stressor while remaining subjects sat quietly. Salivation to the food cue was measured at each trial as well as ratings of food liking, hunger, fullness, and arousal. Results showed significant effects of restraint on food liking and stress condition on hunger. Restrainers increased liking ratings over taste trials whereas ratings for nonrestrainers increased and then decreased to baseline levels by the last trial (p = 0.05). Nonstressed subjects showed an increase in hunger ratings, whereas ratings for stressed subjects did not show any stable directional pattern (p = 0.04). Salivary responses decreased for all groups (p = 0.01). A significant interaction of restraint by stress for intake was found (p = 0.03); restrainers increased consumption following stress whereas nonrestrainers decreased consumption as compared with controls. The data suggest that the Stroop task can influence intake in restrainers, but the changes in intake did not directly correspond to the changes observed during the presentations of the taste cues and stressor.

Adolescent↗
PubMed2005

Cognitive behavioral stress management effects on mood, social support, and a marker of antiviral immunity are maintained up to 1 year in HIV-infected gay men.

Numerous herpesvirus infections are associated with clinically relevant outcomes as well as an accelerated HIV replication rate and subsequent disease progression. Stress management interventions may improve markers of cellular immune control over latent herpesvirus infections and these changes appear to be mediated by perceptions of increased social support availability. We examined the effects of a group-based cognitive behavioral stress management (CBSM) intervention on distress, dysphoria, perceived social support, and herpesvirus immunoglobulin G (IgG) antibody titers during the 6 to 12 months following the intervention. Of those who were initially randomized, 49 HIV-infected men were followed during the 6- to 12-month period after randomization to either a 10-week CBSM intervention (n = 31) or a modified wait-list control condition (n = 18). Measures of distress, dysphoria, social support, and blood samples for herpesvirus IgG titers were taken at baseline, immediately following CBSM and at 6- to 12-month follow-up. Men in CBSM displayed maintenance of previously observed intervention effects on dysphoria, reliable alliance support, and herpesvirus IgG antibody titers (i.e., Epstein-Barr virus capsid antigen; EBV-VCA). Intervention-related changes in EBV-VCA were unrelated to changes in lymphocyte subsets (i.e., CD4+, CD8+, and CD4+:CD8+) or changes in measures of dysphoria and social support during the investigation period. Data indicate that HIV-infected men participating in a CBSM intervention maintain better psychosocial status and immunologic control of latent EBV infection up to 1 year after its conclusion.

Adult↗
PubMedDate not supplied

Replicative senescence and the art of counting.

The idea that aging is largely the result of (endogenous) stress appears to be at odds with the concept of biological 'clocks', which seem to programme and terminate cellular aging processes. Here, data are reviewed that show that telomeres, the major clock identified in human cells so far, do in fact measure stress and damage accumulation much more than simple mitotic time. Telomere shortening is significantly stress-dependent due to a telomere-specific damage repair deficiency. This identifies telomere-driven human cell replicative senescence as a stress response with high potential importance for human aging.

Biological Clocks↗
PubMed2006

Flashbulb memories and posttraumatic stress reactions across the life span: age-related effects of the German occupation of Denmark during World War II.

A representative sample of older Danes were interviewed about experiences from the German occupation of Denmark in World War II. The number of participants with flashbulb memories for the German invasion (1940) and capitulation (1945) increased with participants' age at the time of the events up to age 8. Among participants under 8 years at the time of their most traumatic event, age at the time correlated positively with the current level of posttraumatic stress reactions and the vividness of stressful memories and their centrality to life story and identity. These findings were replicated in Study 2 for self-nominated stressful events sampled from the entire life span using a representative sample of Danes born after 1945. The results are discussed in relation to posttraumatic stress disorder and childhood amnesia.

Age Factors↗
PubMed1980

A description and analysis of the operation and validity of the psychological stress evaluator.

A detailed description and analysis are presented of the psychological stress evaluator (PSE), an instrument purported to measure accurately and to portray graphically differential levels of stress in human speech. In addition, two studies are presented that attempt to validate this instrument against better known measures of stress or A-state anxiety. The PSE measures were compared with heart rate and State Trait Anxiety Inventory (STAI) A-state scores obtained under conditions where the level of stress was experimentally manipulated through threat of shock or the presentation of taboo words. The first study revealed that PSE, STAI, and heart rate measures accurately reflect different levels of stress and are significantly correlated with one another. The second study failed to replicate the validity of the PSE. This failure to replicate is attributed to lower levels of induced stress and a reduction in baseline measures of stress.

Acoustics↗
PubMed2004

Mitochondrial oxidative stress in human hepatoma cells exposed to stavudine.

The toxicity of nucleoside reverse transcriptase inhibitors (NRTIs) is linked to altered mitochondrial DNA (mtDNA) replication and subsequent disruption of cellular energetics. This manifests clinically as elevated concentrations of lactate in plasma. The mechanism(s) underlying how the changes in mtDNA replication lead to lactic acidosis remains unclear. It is hypothesized that mitochondrial oxidative stress links the changes in mtDNA replication to mitochondrial dysfunction and ensuing NRTIs toxicity. To test this hypothesis, changes in mitochondrial function, mtDNA amplification efficiency, and oxidative stress were assessed in HepG2-cultured human hepatoblasts treated with the NRTI stavudine (2',3'-didehydro-2',3'-deoxythymidine or d4T) for 48 h. d4T produced significant mitochondrial dysfunction with a 1.5-fold increase in cellular lactate to pyruvate ratios. In addition, d4T caused a dose-dependent decrease in mtDNA amplification and a correlative increase in abundance of markers of mitochondrial oxidative stress. Manganese (III) meso-tetrakis (4-benzoic acid) porphyrin, MnTBAP, a catalytic antioxidant, ameliorated or reversed d4T-induced changes in cell injury, energetics, mtDNA amplification, and mitochondrial oxidative stress. In conclusion, d4T treatment elevates mitochondrial reactive oxygen species (ROS), enhances mitochondrial oxidative stress, and contributes mechanistically to NRTI-induced toxicity. These deleterious events may be potentiated in acquired immunodeficiency syndrome (AIDS) by human immunodeficiency virus (HIV) infection itself, coinfection (e.g., viral hepatitis), aging, substance, and alcohol use.

Carcinoma, Hepatocellular↗
PubMed1998

The structure of supercoiled intermediates in DNA replication.

We studied the structure of replication intermediates accumulated by Tus-induced arrest of plasmid DNA replication at termination sites. For intermediates generated both in vitro with purified components and in vivo, superhelical stress is distributed throughout the entire partially replicated molecule; daughter DNA segments are wound around each other, and the unreplicated region is supercoiled. Thus, unlinking of parental DNA strands by topoisomerases can be carried out both behind and in front of the replication fork. We explain why previous studies with prokaryotic and eukaryotic replication intermediates discerned only supercoiling in the unreplicated portion.

DNA Replication↗
PubMed1994

Aldehyde-induced protein-DNA crosslinks disrupt specific stages of SV40 DNA replication.

Aldehydes with specific protein-DNA crosslinking ability disrupted simian virus 40 (SV40) DNA replication to cause replication fork failure by the 40S intermediate pathway, in which replicating viral genomes become inactivated and torsionally stressed. In contrast, aldehydes without detectable protein-DNA crosslinking ability had no effect on SV40 DNA replication during the 10 min exposure times employed. This indicates that protein-DNA crosslinks block either DNA polymerase or the entire replication complex. Replication failure by the 40S pathway is known to initiate recombinational events in the damaged SV40 replicons. Similar events in cellular replicons may play a role in the clastogenic effects of formaldehyde. In addition, formaldehyde and acrolein caused accumulation of catenated (topologically linked) SV40 daughter chromosomes--a signature of topoisomerase II inhibition.

Acrolein↗
PubMed2001

Increasing Saccharomyces cerevisiae stress resistance, through the overactivation of the heat shock response resulting from defects in the Hsp90 chaperone, does not extend replicative life span but can be associated with slower chronological ageing of nondividing cells.

Recent studies on Drosophila and Caenorhabditis elegans indicate that increases in stress resistance result in a longer chronological life span, an effect that must operate primarily on the postmitotic tissues of the adult. Stress resistance can be increased through decreases in Hsp90 chaperone activity, since Hsp90 acts to downregulate the activity of heat shock transcription factor. This study investigated whether the increases in stress resistance associated with reduced Hsp90 chaperone activity influence ageing in the budding yeast Saccharomyces cerevisiae, ageing being measured either as the replicative (nonchronological) senescence of budding cells or as the chronological ageing of non-dividing (stationary phase) cultures. Overactivation of the heat shock response caused no slowing of replicative senescence. In some situations though it was associated with a longer chronological life span of stationary cells, the yeast equivalent of the postmitotic state. This is consistent with the idea that stress resistance exerts its life span-extending effects primarily in postmitotic cells and tissues.

Carrier Proteins↗
PubMed1992

Alterations in EEG amplitude, personality factors, and brain electrical mapping after alpha-theta brainwave training: a controlled case study of an alcoholic in recovery.

A controlled case study was conducted of effects of EEG alpha and theta brainwave training with a recovering alcoholic patient who experienced craving and fear of relapse after 18 months of abstinence. Training consisted of six sessions of thermal biofeedback to increase central nervous system (CNS) relaxation. Effects were documented with pretreatment and post-treatment personality testing, 20-channel digitized EEG evaluations both under relaxed conditions and under stress, minute-by-minute physiologic recordings of autonomic and EEG data during each training session, blood pressure, and heart rate indications taken both during relaxation and under stress, and by clinical observation. Results replicated those of a previous controlled study with chronic alcoholic patients not abstinent prior to treatment. New findings include post-treatment indications of more relaxed CNS functioning under stress, and of reduced autonomic activation both during relaxation and under stress. Brain-mapping indications of anxiety associated with painful cold-pressor stimulation were seen only in the pretest readings; at post-test the brain map indicated pain-associated EEG activity in the contralateral somatosensory area, but no apparent anxiety-associated EEG activity. At 4 months post-treatment the patient's wife and colleagues report the patient appears to function in a more relaxed way under the impact of stress, and he reports no longer experiencing craving for alcohol. Overall, support is provided for the possibility that alpha and theta brainwave training may be a useful intervention for the abstinent alcoholic experiencing stress-related craving and fear of relapse.

Adult↗
PubMed1993

Inhibition of vesicular stomatitis virus replication by delta 12-prostaglandin J2 is regulated at two separate levels and is associated with induction of stress protein synthesis.

delta 12-Prostaglandin J2 (delta 12-PGJ2), a naturally occurring dehydration product of prostaglandin D2, is shown to suppress the replication of vesicular stomatitis virus (VSV) in two different epithelial monkey cell lines. A significant delay in the virus-induced cytopathic effect and a dramatic inhibition of virus production can be obtained at doses which do not inhibit protein synthesis in uninfected cells, and induce the synthesis of heat shock proteins (HSPs) in both uninfected and VSV-infected cells. delta 12-PGJ2 is shown to block VSV replication at two separate levels in the early and late phase of the virus replication cycle. Treatment started soon after VSV infection greatly suppresses viral (but not cellular) protein synthesis and prevents the virus-induced shut-off of host cell protein synthesis. This effect is accompanied by the induction of HSP synthesis. delta 12-PGJ2-treatment in a late phase of the virus replication cycle, when all virus proteins have been synthesized, still causes a dramatic block of infectious virus production. This block is accompanied by a decrease in [3H]glucosamine incorporation into the virus glycoprotein G, at concentrations which do not alter glucosamine uptake by the cells, suggesting that a defect in virus protein glycosylation could be responsible for the antiviral activity. Finally, delta 12-PGJ2 causes a decrease of glucosamine incorporation into at least two host cell polypeptides, while the majority of cellular proteins are unaffected and glycosylation of a 47 kDa cellular protein is strongly induced. These selective alterations of protein glycosylation suggest that delta 12-PGJ2 affects a specific group of glycosylated proteins. The finding that cyclopentenone prostaglandins act on different events during the virus cycle explains the effectiveness of these compounds in controlling the replication of different types of viruses and presents an attractive new approach to antiviral chemotherapy.

Animals↗
PubMed2005

Cyclic nucleotide kinases and tachyzoite-bradyzoite transition in Toxoplasma gondii.

The ability of Toxoplasma gondii to cycle between the tachyzoite and bradyzoite life stages in intermediate hosts is key to parasite survival and the pathogenesis of toxoplasmosis. Studies from a number of laboratories indicate that differentiation in T. gondii is a stress-induced phenomenon. The signalling pathways or molecular mechanisms that control formation of the latent bradyzoite stage are unknown and specific effectors of differentiation have not been identified. We engineered a reporter parasite to facilitate simultaneous comparison of differentiation and replication after various treatments. Chloramphenicol acetyltransferase (CAT), expressed constitutively from the alpha-tubulin promoter (TUB1), was used to quantitate parasite number. beta-galactosidase (beta-GAL), expressed from a bradyzoite specific promoter (BAG1), was used as a measure of bradyzoite gene expression. Sodium nitroprusside, a well-known inducer of bradyzoite differentiation, reduced reporter parasite replication and caused bradyzoite differentiation. Stress-induced differentiation in many other pathogens is regulated by cyclic nucleotide kinases. Specific inhibitors of the cAMP dependent protein kinase and apicomplexan cGMP dependent protein kinase inhibited replication and induced differentiation. The beta-GAL/CAT reporter parasite provides a method to quantify and compare agents that cause differentiation in T. gondii.

1-Methyl-3-isobutylxanthine↗
PubMed2007

A history of human-like dieting alters serotonergic control of feeding and neurochemical balance in a rat model of binge-eating.

OBJECTIVE: This study replicated a model of stress-induced binge-eating in rats with a history of caloric restriction (HCR), tested their response to SSRI (fluoxetine) treatment, and explored changes in brain monoamine levels. METHOD: Young female rats with no-HCR/no-Stress, no-HCR/Stress, HCR/no-Stress, and HCR+Stress (binge-eating) were treated with fluoxetine. Post-mortem levels of serotonin, dopamine, and metabolites were assessed from brain regions key to feeding and reward. RESULTS: A 3 mg/kg dose of fluoxetine without effect in the no-HCR groups suppressed intake of HCR groups, normalizing the binge-eating of HCR/Stress rats. No differences in monoamines were detected in the hypothalamus or tegmentum but a strong positive relationship between accumbens serotonin and dopamine turnover in no-HCR rats was absent in rats with HCR. CONCLUSION: Despite lack of hunger, a history of human-like dieting alters serotonin function in ways suggesting consequences not only to feeding but also control of reward and mood that are dependent on dopamine/serotonin interactions.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2006

The p53 tumor suppressor participates in multiple cell cycle checkpoints.

The process of cell division is highly ordered and regulated. Checkpoints exist to delay progression into the next cell cycle phase only when the previous step is fully completed. The ultimate goal is to guarantee that the two daughter cells inherit a complete and faithful copy of the genome. Checkpoints can become activated due to DNA damage, exogenous stress signals, defects during the replication of DNA, or failure of chromosomes to attach to the mitotic spindle. Abrogation of cell cycle checkpoints can result in death for a unicellular organism or uncontrolled proliferation and tumorigenesis in metazoans (Nyberg et al., 2002). The tumor suppressor p53 plays a critical role in each of these cell cycle checkpoints and is reviewed here.

Animals↗
PubMed1983

Cyclophosphamide-induced in vivo sister chromatid exchange in Mus Musculus. II: Effect of age and genotype on sister chromatid exchange, micronuclei and metaphase index.

In vivo cyclophosphamide-induced sister chromatid exchanges (SCEs) micronuclei, and metaphase indices were assessed in two age groups (10.8 +/- 0.9 weeks' an 33.1 +/- 1.3 weeks' old) of female mice from three genetic strains (C3H/S, C57BL/6J, and Balb/c). In general, older animals showed diminished SCE induction over their younger counterparts. The relative difference between individuals of the two ages is strain-dependent. Unlike C57BL/6J and Balb/c, strain C3H/S showed significantly lower SCE values in the older animals at every cyclophosphamide treatment. It may reflect on the possible involvement of genetic determinant(s) for the component(s) of SCE formation during aging. Frequencies of micronuclei, however, were consistently higher in older animals than in their younger counterparts. Furthermore, cytotoxicity of cyclophosphamide, as reflected in metaphase indices, was also higher in older animals. Lower metaphase indices associated with higher micronuclei levels in older individuals may suggest a decline in the rate of cellular replication in these animals. Furthermore, the lower metaphase indices associated with lower SCE values, and increasing micronuclei levels accompanied by decreasing SCE frequencies in older animals, may reflect reduced DNA repair ability during aging. These results support the hypothesis of genotype-dependent decline in the rate of DNA repair and replication during aging, particularly under stressed conditions.

Aging↗
PubMed2005

Chemoprevention of genome, transcriptome, and proteome alterations induced by cigarette smoke in rat lung.

Post-genomic methodologies have provided novel tools for evaluating safety and efficacy of cancer chemopreventive agents. We exposed rats to environmental cigarette smoke (ECS) for 28 days, with or without oral administration of N-acetylcysteine (NAC). As assessed by 32P-postlabelling, ECS caused a 10-fold increase of DNA adduct levels, which were significantly reduced by NAC. Of 518 proteins tested by antibody microarray, ECS stimulated 56 activities involved in stress response, protein removal, cell replication, apoptosis, phagocytosis, and immune response. NAC alone did not change the amounts of any protein, whereas it significantly decreased the amounts of 6 ECS-induced proteins. The intensity of expression of 278 related genes, assessed by cDNA microarray, was significantly correlated with protein amounts. These observed molecular alterations, which can be attenuated by NAC, represent in part adaptive responses and in part reflect mechanisms contributing to the pathogenesis of smoke-related diseases, including lung cancer, asthma, chronic bronchitis, and emphysema.

Animals↗