Prevention of cardiac contractile function disorders during prolonged stress by preliminary adaptation to short-term stress exposure

Studies of contractile function of an isolated right auricle in Wistar rats have demonstrated that long-term immobilization stress (fixation in the lying position for 6 h) results in the decreased extensibility of the auricle and pronounced depression of the developed tension. Preliminary adaptation of the animals to short-term immobilization stress (daily fixation in the lying position for 1 h over 10 days) per se insignificantly affects the extensibility and contractile function of the auricle but in effect it reduces its adrenoreactivity and completely prevents the post-stressor rigidity of the auricle and its function abnormality after long-term stress.     

Interrelations between sympathetic adrenal and opioid systems--regulatory mechanism determining cardiac resistance to stress damage]

The present paper has analyzed relationship between sympatico-adrenal and opioid systems in the pathogenesis of stress heart damage. Based on the our own results and other investigator data the authors make a conclusion that namely relationship between opioid and sympatico-adrenal systems both on the level of the brain and on the periphery determines a degree of the heart resistance to the injury action of severe stress. Myocardial protection by opioids at stress was found to be mediated by the peripheral mu-opioid receptors and was associated with decrease in an activity of sympatico-adrenal system and a inhibition of its effector part. On contrary central opioid system activation leads to an increase in stress heart damage via an increase in sympathetical influence on the myocardium.     

Ammonium enhances resistance to salinity stress in citrus plants

In this work, we demonstrate that NH?? nutrition in citrange Carrizo plants acts as an inducer of resistance against salinity conditions. We investigated its mode of action and provide evidence that NH?? confers resistance by priming abscisic acid and polyamines, and enhances H?O? and proline basal content. Moreover, we observed reduced Cl? uptake as well as enhanced PHGPx expression after salt stress. Control and N-NH?? plants showed optimal growth. However, N-NH?? plants displayed greater dry weight and total lateral roots than control plants, but these differences were not observed for primary root length. Our results revealed that N-NH?? treatment induces a similar phenotypical response to the recent stress-induced morphogenetic response (SIMRs). The hypothesis is that N-NH?? treatment triggers mild chronic stress in citrange Carrizo plants, which might explain the SIMR observed. Moreover, we observed modulators of stress signaling, such as H?O? in N-NH?? plants, which could acts as an intermediary between stress and the development of the SIMR phenotype. This observation suggests that NH?? treatments induce a mild stress condition that primes the citrange Carrizo defense response by stress imprinting and confers protection against subsequent salt stress.     

Natural adaptation to environmental stress via physiological clock-regulation of stress resistance in Drosophila

In the present study we describe a novel mechanism by which populations, in an interplay between physiology and behaviour, can evolve adaptation to environmental extremes. Comparing Drosophila populations from different climate zones, we found diel shifts in high temperature resistance after maintenance at 25 °C for several generations. Resistance changes that co-occurred with field and laboratory activity of the populations are controlled by the physiological clock and appear to be a consequence of local adaptation to the thermal profiles of the environment of origin.     

Myocardial contraction in the reverse development of adaptation to short-term exposure to stress

Contractile function of an isolated right atrium was studied in short-term stressor effects-adapted male Wistar rats at different times after adaptation was completed. Adaptation to short-term stressor effects was shown to produce a restricted decrease of myocardial contractility shortly after adaptation was completed. At the 3d day another decrease of contractile function was noted. However, contractile function returned to the control level by the 5th day. At the same time adaptation completely prevented the impairment of myocardial contractility, induced by prolonged stress. The protective effect was seen immediately after adaptation, by days 3 and 5 after it, being reduced by day 10. It is assumed that at the 5th day after adaptation, the animals experience the post-adaptation state marked by disappearance of the negative adaptation effect and by remarkable protective effect of adaptation. As a result, all the characteristics of myocardial contractility evaluated after prolonged stress experienced by the animals at the 5th day following short-term stressor effects do not differ from control parameters.     

Prior exposure to restraint stress enhances 7,12-dimethylbenz(a)anthracene (DMBA) induced DNA damage in rats

Over the years, several lines of evidence have emerged supporting the role of stress in the development and progression of cancer. Stress can cause an increase in the production of reactive oxygen species (ROS) and decrease in the in vivo antioxidant defense systems. A ROS-induced DNA damage in peripheral lymphocytes, liver and skin cells may be revealed by Comet assay. To test whether DNA is damaged by stress/DMBA/stress and DMBA, rats were exposed to multiple doses of DMBA in the presence and absence of restraint stress, and DNA damage was evaluated. Insignificant differences were detected in all the three cells tested (peripheral lymphocytes, liver and skin cells) between control and stress treatment in terms of frequencies of damaged DNA. The extent of DNA migration was enhanced in DMBA treated rats in a dose dependent manner. Pre-stress DMBA treatment showed still higher frequencies of damage in comparison with control, stress alone or DMBA alone groups. Thus, prior exposure to stress clearly enhanced the DMBA induced DNA damage, especially so in the skin cells (target organ of the carcinogen application) than liver and peripheral lymphocytes as observed on the basis of the extent of DNA migration (tail DNA) during single cell gel electrophoresis.     

Effect of preliminary adaptation to short-term stress exposure on the resistance of the spontaneously contracting myocardium to a lipid peroxidation inducer

Contractile function of the isolated right atrium was studied in male Wistar rats adapted to short-term stressor exposures at varying times after adaptation was completed. Adaptation to short-term stressor exposures induced a limited decrease in myocardial contractility immediately after adaptation was over. On the 3d day an additional reduction in the characteristics of contractile function was still observed. However, by the 5th day the characteristics recovered to the control level. At the same time adaptation completely prevented the derangement of myocardial contractility, induced by exposure to a prolonged stress. That protective effect was observed as early as adaptation was completed, on days 3 and 5 after adaptation, and became lessened on the 10th day. It is assumed that on the 5th day after adaptation the animals are in a postadaptation state where the untoward effect of adaptation disappears whereas the protective effect is demonstrable to a full extent. As a result all the characteristics of myocardial contractility following a prolonged stress on the 5th day after completion of short-term stressor exposures differed in no way from the control parameters.     

Oxidative stress generated damage to DNA by gastrointestinal exposure to insoluble particles

There is growing concern that gastrointestinal exposure to particles is associated with increased risk of toxicity to internal organs and carcinogenicity. The mechanism of action is related to particle-induced oxidative stress and oxidation of DNA. Observations from animal models indicate that gastrointestinal exposure to single-walled carbon nanotubes (SWCNT), fullerenes C60, carbon black, titanium dioxide and diesel exhaust particles generates oxidized DNA base lesions in organs such as the bone marrow, liver and lung. Oral exposure to nanosized carbon black has also been associated with increased level of lipid peroxidation derived exocyclic DNA adducts in the liver, suggesting multiple pathways of oxidative stress for particle-generated damage to DNA. At equal dose, diesel exhaust particles (SRM2975) generated larger levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine in rat liver than carbon black (Printex 90) did, whereas exposure to fullerenes C60 and SWCNT was the least potent. This ranking of samples was also observed for oxidatively damaged DNA in cultured cells. The extent of translocation from the gut is largely unresolved. However, there is evidence indicating that gastrointestinal exposure to particulate matter is associated with oxidative damage to DNA and this might be associated with increased risk of cancer.     

Comparative assessment of the effect of adaptation to stress exposure and high altitude hypoxia on heart resistance to reperfusion injury after total ischemia]

Experiments on isolated Wistar rat hearts perfused according to Langendorff showed that adaptation to stress exposure limited the depression of contraction amplitude and contracture and possessed an antiarrhythmic effect in reperfusion. Furthermore, adaptation to stress exposure efficiently limited reperfusion damage to sarcolemma. It was shown that adaptation to hypoxia did not result in any increase in the heart resistance to reperfusion damage following total ischemia. Possible mechanisms of differences in the protective effects of adaptation to stress exposure and hypoxia are discussed.     

l-Carnitine enhances resistance to oxidative stress by reducing DNA damage in Ataxia telangiectasia cells

In this study, the modulating effect of l-carnitine on tert-butyl-hydroperoxide-induced DNA damage was compared with that of mannitol, a well known scavenger of hydroxyl radicals, both in normal and Ataxia telangiectasia mutated (ATM)-deficient lymphoblastoid cell lines established from A. telangiectasia (A-T) patients. The alkaline version of the comet assay was employed to measure the frequency of single-strand breaks (SSBs) and alkali-labile sites induced by t-butyl-OOH immediately after treatment and at different recovery times in normal and A-T cell lines, with and without pre-treatment with l-carnitine. In addition, both the yield of induced chromosomal damage and the effect on cell proliferation were evaluated. Our results show that pre-treatment of cells with l-carnitine produced an enhancement of the rate and extent of DNA repair in A-T cell lines at early recovery time; furthermore, in samples pre-treated with l-carnitine a reduction of all types of chromosomal aberration was observed, both in A-T and in wild-type cell lines. The reducing effect of l-carnitine pre-treatment on oxidative DNA damage was more prominent than that of pre-treatment with mannitol. In conclusion, we demonstrated a protective effect of l-carnitine on oxidative stress-induced DNA damage in A-T cells, suggesting its possible role in future pharmacological applications in A-T therapy.     

Loss of adaptation to oxidative stress as a mechanism for aortic damage in aging rats

Cells are armed with a vast repertoire of antioxidant defence mechanisms to prevent the accumulation of oxidative damage. The cellular adaptive response is an important antioxidant mechanism against physiological and pathophysiological oxidative alterations in a cell's microenvironment. The aim of this paper was to study, in the rat aorta, whether this adaptive response and the inflammation associated with oxidative stress were expressed throughout the aging process. We examined the rat aorta, as it is a very sensitive tissue to oxidative stress. Male Wistar rats of 1.5, 3, 12, 18 and 24 months of age were used. Superoxide anion (O2(-)) generation; levels of two antioxidant enzymes, superoxide dismutase (SOD) and catalase; and the levels of prostaglandin E2 (PGE2), an inflammatory marker, were measured. The results for rats at different ages were compared with those for 3 months of age. A balance between production of O2(-) and SOD activity was found in the aorta of rats from 1.5 to 12 months old. Oxidative stress was present in the aorta of old animals (18-24 months), due to a failure in the mechanisms of adaptation to oxidative stress. The observed increase in PGE2 levels in these rats reflected an inflammatory response. All together suggest that vascular oxidative stress and the inflammatory process observed in the old groups of rats could be closely related to vascular aging. Our results also remark the importance of the adaptative response to oxidative stress.     

Effects of adaptation to exposure to short-term stress on indices of resistance of energy metabolism and contractile function of the myocardium to acute hypoxic hypoxia and reoxygenation

Effect of preliminary adaptation to immobilization stress with progressive duration from 15 min. to 1 h (every second day, 8 sessions) on the resistance of indices of myocardial energy metabolism and contractile function to acute hypoxic hypoxia and subsequent reoxygenation was studied. It was shown, that adaptation to short-term stress exposure by some way provided the retention of activities of important enzymes like creatine-phosphokinase and phosphorylase under the harmful action of acute hypoxia and subsequent reoxygenation. At the same time, the ATP restoration and the CP super-restoration were observed during reoxygenation. This effect, in its turn, was accompanied by a more pronounced super-restoration of the heart contractile function than in control.     

Pulmonary exposure to diesel exhaust particles enhances coagulatory disturbance with endothelial damage and systemic inflammation related to lung inflammation

Pulmonary exposure to diesel exhaust particles (DEP) enhances lung inflammation related to bacterial endotoxin (lipopolysaccharide [LPS]) in mice. Severe lung inflammation can reportedly induce coagulatory abnormalities and systemic inflammation. This study examined the effects of components of DEP on lung inflammation, pulmonary permeability, coagulatory changes, systemic inflammatory response, and lung-to-systemic translocation of LPS in a murine model of lung inflammation. ICR mice were divided into six experimental groups that intratracheally received vehicle, LPS (2.5 mg/kg), organic chemicals in DEP (DEP-OC; 4 mg/kg) extracted with dicloromethane), residual carbonaceous nuclei of DEP (washed DEP: 4 mg/kg), DEP-OC + LPS, or washed DEP + LPS. Both DEP components exacerbated lung inflammation, vascular permeability, and the increased fibrinogen and E-selectin levels induced by LPS. With overall trends, the exacerbation was more prominent with washed DEP than with DEP-OC. Washed DEP + LPS significantly decreased activated protein C and antithrombin-III and elevated circulatory levels of interleukin (IL)-6, keratinocyte chemoattractant (KC), and LPS as compared with LPS alone, whereas DEP-OC + LPS elevated IL-6, KC, and LPS without significance. These results show that DEP components, especially washed DEP, amplify the effects if LPS on the respiratory system and suggest that they contribute to the adverse health effects of particulate air pollution on the sensitive populations with predisposing vascular and/or pulmonary diseases, including ischemic vascular diseases and respiratory infection.