Morphine-Induced Degradation of the Host Defense Barrier

Frenklakh, L; Bhat, Rajani; Bhaskaran, Madhu; Sk, Sharma; Sharma, Mukut; Dinda, Amit Kumar; Singhal, Pravin C.

doi:10.1007/s10620-006-3132-0

Cited by 19 publications

(15 citation statements)

References 18 publications

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“…Hoechst-33342 is a nuclear stain that labels nuclei blue and can be used as an apoptotic marker. 36 Apoptotic cells appear as a strong bright blue color due to the chromatin condensation characteristic of apoptotic cells, while normal healthy cells appear a uniform blue. Hoechst-33342 can enter intact cells without the need for cell membrane permeability, which helps in the identification of early apoptotic cells.…”

Section: Apoptotic Assaymentioning

confidence: 99%

Concentration-dependent toxicity of iron oxide nanoparticles mediated by increased oxidative stress

Naqvi¹,

Samim²,

Abdin³

et al. 2010

IJN

Self Cite

430

262

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Iron oxide nanoparticles with unique magnetic properties have a high potential for use in several biomedical, bioengineering and in vivo applications, including tissue repair, magnetic resonance imaging, immunoassay, drug delivery, detoxification of biologic fluids, cell sorting, and hyperthermia. Although various surface modifications are being done for making these nonbiodegradable nanoparticles more biocompatible, their toxic potential is still a major concern. The current in vitro study of the interaction of superparamagnetic iron oxide nanoparticles of mean diameter 30 nm coated with Tween 80 and murine macrophage (J774) cells was undertaken to evaluate the dose-and time-dependent toxic potential, as well as investigate the role of oxidative stress in the toxicity. A 15-30 nm size range of spherical nanoparticles were characterized by transmission electron microscopy and zeta sizer. MTT assay showed .95% viability of cells in lower concentrations (25-200 µg/mL) and up to three hours of exposure, whereas at higher concentrations (300-500 µg/mL) and prolonged (six hours) exposure viability reduced to 55%-65%. Necrosis-apoptosis assay by propidium iodide and Hoechst-33342 staining revealed loss of the majority of the cells by apoptosis. H 2 DCFDDA assay to quantify generation of intracellular reactive oxygen species (ROS) indicated that exposure to a higher concentration of nanoparticles resulted in enhanced ROS generation, leading to cell injury and death. The cell membrane injury induced by nanoparticles studied using the lactate dehydrogenase assay, showed both concentration-and time-dependent damage. Thus, this study concluded that use of a low optimum concentration of superparamagnetic iron oxide nanoparticles is important for avoidance of oxidative stress-induced cell injury and death.

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Section: Apoptotic Assaymentioning

confidence: 99%

Concentration-dependent toxicity of iron oxide nanoparticles mediated by increased oxidative stress

Naqvi¹,

Samim²,

Abdin³

et al. 2010

IJN

Self Cite

430

262

View full text Add to dashboard Cite

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“…In fact, several opiates promote neuronal and non-neuronal apoptosis [59][60][61][62] . There is also evidence that morphine produces intestinal injury and breakdown of the host defense mechanism by generating nitric oxide [63] . Moreover, because intrinsic opiate signaling regulates certain types of neurogenesis, there is a suggestion that perinatal opiate exposure may disrupt normal neuronal development [64] .…”

Section: Discussionmentioning

confidence: 99%

Neonatal Stress or Morphine Treatment Alters Adult Mouse Conditioned Place Preference

et al. 2008

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Background: Hospitalized preterm infants may experience pain and stress, and narcotics are often administered to lessen their suffering. However, prolonged narcotic therapy may be detrimental during neonatal brain development. Using a rat model combining neonatal stress and morphine, we found that neonatal morphine impaired adult learning. Here we describe a new mouse model examining lasting effects of neonatal stress and morphine. Objective: We tested whether repeated neonatal stress and/or morphine exposure affects early neurodevelopmental or adult behaviors. Methods: Five groups of C57/BL6 mice (1: untreated; 2: morphine (2 mg/kg s.c., b.i.d.); 3: saline, 4: stress + morphine; 5: stress + saline) were treated from postnatal day (P) 5 to P9. Stress consisted of daily maternal separation/isolation (08:00–15:00 h) with gavage feedings and twice daily exposure to brief hypoxia/hyperoxia. Developmental behaviors included righting (P5) and negative geotaxis (P9). Adult behaviors included elevated plus maze, morphine place-preference conditioning, and forced-swimming. Plasma con- centrations of morphine (P7) and corticosterone (P9 and adult) were measured. Results: Neonatal stress or neonatal morphine alone impaired adult place-preference conditioning, but the combination did not (interaction p < 0.01). Adult basal corticosterones were reduced by neonatal morphine treatment. There were no substantial differences in elevated plus maze or forced-swimming times. Conclusions: Neonatal stress and morphine treatment produced long-lasting behavioral and hormonal effects which suggest that neonatal morphine reduces adult arousal and neonatal stress exaggerates adult arousal, each to a degree sufficient to alter learning, while the combined impact of these neonatal treatments does not alter adult learning.

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“…Morphine induces intestinal injury through nitric oxide (NO) generation. The degradation of the host defense barrier correlates with macrophage injury, but not intestinal injury [25]. However, the specific cellular and molecular mechanisms underlying morphine's effects on the epithelial barrier still need to be elucidated.…”

Section: Physical Barriers: Epitheliamentioning

confidence: 99%

Opiate abuse, innate immunity, and bacterial infectious diseases

Wang

Barke

et al. 2008

Arch. Immunol. Ther. Exp.

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The first line of defense against invading bacteria is provided by the innate immune system. Morphine and other opiates can immediately disrupt the body's first line of defense against harmful external bacteria. Opiate, for example morphine, abuse degrades physical and physiologic barriers, and modulates phagocytic cells (macrophages, neutrophils) and, nonspecific cytotoxic T cells (gammadelta T), natural killer cells, and dendritic cells, that are functionally important for carrying out a rapid immune reaction to invading pathogens. In vitro studies with innate immune cells from experimental animals and humans and in vivo studies with animal models have shown that opiate abuse impairs innate immunity and is responsible for increased susceptibility to bacterial infection. However, to better understand the complex interactions between opiates, innate immunity, and bacterial infection and develop novel approaches to treat and even prevent bacterial infection in the opiate-abuse population, there is an urgent need to fill the numerous gaps in our understanding of the cellular and molecular mechanisms by which opiate abuse increases susceptibility to bacterial infection.

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Morphine-Induced Degradation of the Host Defense Barrier

Cited by 19 publications

References 18 publications

Concentration-dependent toxicity of iron oxide nanoparticles mediated by increased oxidative stress

Concentration-dependent toxicity of iron oxide nanoparticles mediated by increased oxidative stress

Neonatal Stress or Morphine Treatment Alters Adult Mouse Conditioned Place Preference

Opiate abuse, innate immunity, and bacterial infectious diseases

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