Cell membrane‐related toxic responses and disruption of intercellular communication in PCB mechanisms of toxicity: A review

2020 ◽  
Vol 40 (12) ◽  
pp. 1592-1601
Author(s):  
Teuta Murati ◽  
Marina Miletić ◽  
Jelka Pleadin ◽  
Branimir Šimić ◽  
Ivana Kmetič
Keyword(s):  
Cell Membrane ◽  
Intercellular Communication ◽  
Mechanisms Of Toxicity ◽  
Toxic Responses

Vanadium accumulation in alveolar macrophages studied with the Zeiss CEM902

1992 ◽  
Vol 50 (1) ◽  
pp. 638-639
Author(s):  
John J. Godleski ◽  
Rebecca C. Stearns ◽  
Marshall Katler
Keyword(s):  
Cell Membrane ◽  
Energy Loss ◽  
Respiratory System ◽  
Alveolar Macrophages ◽  
Electron Spectroscopic Imaging ◽  
Vanadium Compounds ◽  
Primary Target ◽  
Mechanisms Of Toxicity ◽  
Vanadium Accumulation ◽  
Electron Energy Loss

Vanadium compounds are known to cause irritation of the respiratory system. Mechanisms of toxicity include actions at the cell membrane and mitochondria. However, the primary target of toxicity has not been delineated. Alveolar macrophages are the primary defensive cells of the lung and likely to interact with inhaled vanadium compounds. The purpose of this study was to identify sites of vanadium accumulation in alveolar macrophages. The Zeiss CEM902 with capabilities to detect vanadium within the ultrastructural context of the cell by Electron Spectroscopic Imaging (ESI) and by Electron Energy Loss Spectral (EELS) analysis was used for this investigation.

Toxicity Mechanism of Gadolinium Oxide Nanoparticles and Gadolinium Ions in Human Breast Cancer Cells

2019 ◽  
Vol 20 (11) ◽  
pp. 907-917 ◽  
Author(s):  
Mohd Javed Akhtar ◽  
Maqusood Ahamed ◽  
Hisham Alhadlaq ◽  
Salman Alrokayan
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cell Membrane ◽  
Oxidative Damage ◽  
Human Breast Cancer ◽  
Membrane Damage ◽  
Gadolinium Oxide ◽  
Human Breast ◽  
Mechanisms Of Toxicity

Background: Due to the potential advantages of Gadolinium Nanoparticles (NPs) over gadolinium elements, gadolinium based NPs are currently being explored in the field of MRI. Either in elemental form or nanoparticulate form, gadolinium toxicity is believed to occur due to the deposition of gadolinium ion (designated as Gd3+ ion or simply G ion). Objective: There is a serious lack of literature on the mechanisms of toxicity caused by either gadolinium-based NPs or ions. Breast cancer tumors are often subjected to MRIs, therefore, human breast cancer (MCF-7) cells could serve as an appropriate in vitro model for the study of Gadolinium Oxide (GO) NP and G ion. Methods: Cytotoxicity and oxidative damage was determined by quantifying cell viability, cell membrane damage, and Reactive Oxygen Species (ROS). Intracellular Glutathione (GSH) was measured along with cellular Total Antioxidant Capacity (TAC). Autophagy was determined by using Monodansylcadaverine (MDC) and Lysotracker Red (LTR) dyes in tandem. Mitochondrial Membrane Potential (MMP) was measured by JC-1 fluorescence. Physicochemical properties of GO NPs were characterized by field emission transmission electron microscopy, X-ray diffraction, and energy dispersive spectrum. Results: A time- and concentration-dependent toxicity and oxidative damage was observed due to GO NPs and G ions. Bax/Bcl2 ratios, FITC-7AAD double staining, and cell membrane blebbing in phase-contrast images all suggested different modes of cell death induced by NPs and ions. Conclusion: In summary, cell death induced by GO NPs with high aspect ratio favored apoptosis-independent cell death, whereas G ions favored apoptosis-dependent cell death.

scholarly journals The Research Progress of Exosomes in Osteoarthritis, With Particular Emphasis on the Mediating Roles of miRNAs and lncRNAs

2021 ◽  
Vol 12 ◽  
Author(s):  
Chenggui Miao ◽  
Wanwan Zhou ◽  
Xiao Wang ◽  
Jihong Fang
Keyword(s):  
Extracellular Matrix ◽  
Biological Activity ◽  
Cell Membrane ◽  
Intercellular Communication ◽  
Noncoding Rnas ◽  
Regulatory Mechanisms ◽  
Research Progress ◽  
Diagnostic Biomarkers ◽  
Receptor Cells ◽  
Non Coding Rna

Osteoarthritis (OA) is a kind of degenerative disease, which is caused by many factors such as aging, obesity, strain, trauma, congenital joint abnormalities, joint deformities. Exosomes are mainly derived from the invagination of intracellular lysosomes, which are released into the extracellular matrix after fusion of the outer membrane of multi vesicles with the cell membrane. Exosomes mediate intercellular communication and regulate the biological activity of receptor cells by carrying non-coding RNA, long noncoding RNAs (lncRNAs), microRNAs (miRNAs), proteins and lipids. Evidences show that exosomes are involved in the pathogenesis of OA. In view of the important roles of exosomes in OA, this paper systematically reviewed the roles of exosomes in the pathogenesis of OA, including the roles of exosomes in OA diagnosis, the regulatory mechanisms of exosomes in the pathogenesis, and the intervention roles of exosomes in the treatment of OA. Reviewing the roles of exosomes in OA will help to clarify the pathogenesis of OA and explore new diagnostic biomarkers and therapeutic targets.

scholarly journals Mechanisms of Toxicity of Industrially Relevant Silicomanganese Dust on Human 1321N1 Astrocytoma Cells: An In Vitro Study

2019 ◽  
Vol 20 (3) ◽  
pp. 740
Author(s):  
Yke Arnoldussen ◽  
Torunn Kringlen Ervik ◽  
Johanna Samulin Erdem ◽  
Ida Kero ◽  
Mina Baarnes Eriksen ◽  
...  
Keyword(s):  
Intercellular Communication ◽  
Biological Effects ◽  
In Vitro Study ◽  
Dust Particles ◽  
Gap Junctional Intercellular Communication ◽  
Cellular Mechanisms ◽  
Mechanisms Of Toxicity ◽  
Time Dependent Effect ◽  
Gap Junctional

Tremendous efforts are applied in the ferroalloy industry to control and reduce exposure to dust generated during the production process, as inhalable Mn-containing particulate matter has been linked to neurodegenerative diseases. This study aimed to investigate the toxicity and biological effects of dust particles from laboratory-scale processes where molten silicomanganese (SiMn) was exposed to air, using a human astrocytoma cell line, 1321N1, as model system. Characterization of the dust indicated presence of both nano-sized and larger particles averaging between 100 and 300 nm. The dust consisted mainly of Si, Mn and O. Investigation of cellular mechanisms showed a dose- and time-dependent effect on cell viability, with only minor changes in the expression of proteins involved in apoptosis. Moreover, gene expression of the neurotoxic biomarker amyloid precursor protein (APP) increased, whereas APP protein expression decreased. Finally, induction of gap junctional intercellular communication (GJIC) increased with higher doses and correlated with the other endpoints. Thus, the effects of SiMn dust on 1321N1 cells are highly dependent on the dose of exposure and involves changes in APP, apoptosis-related proteins and intercellular communication.

Sarcolemmal permeability changes during early myocardial anoxia

1978 ◽  
Vol 36 (2) ◽  
pp. 642-643
Author(s):  
M. Ashraf ◽  
L. Landa ◽  
L. Nimmo ◽  
C. M. Bloor
Keyword(s):  
Cell Membrane ◽  
Membrane Permeability ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Cell Membrane Permeability ◽  
Enzyme Release ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Sarcolemmal Permeability ◽  
Membrane Changes

Following coronary artery occlusion, the myocardial cells lose intracellular enzymes that appear in the serum 3 hrs later. By this time the cells in the ischemic zone have already undergone irreversible changes, and the cell membrane permeability is variably altered in the ischemic cells. At certain stages or intervals the cell membrane changes, allowing release of cytoplasmic enzymes. To correlate the changes in cell membrane permeability with the enzyme release, we used colloidal lanthanum (La+++) as a histological permeability marker in the isolated perfused hearts. The hearts removed from sprague-Dawley rats were perfused with standard Krebs-Henseleit medium gassed with 95% O2 + 5% CO2. The hypoxic medium contained mannitol instead of dextrose and was bubbled with 95% N2 + 5% CO2. The final osmolarity of the medium was 295 M osmol, pH 7. 4.

Flagellar Attachment in Selected Trypanosomes

1973 ◽  
Vol 31 ◽  
pp. 496-497
Author(s):  
J. J. Paulin
Keyword(s):  
Cell Membrane ◽  
Lateral Surface ◽  
The Body ◽  
Flagellar Pocket ◽  
Integral Component ◽  
Free Flagellum ◽  
Flagellar Axoneme

Movement in epimastigote and trypomastigote stages of trypanosomes is accomplished by planar sinusoidal beating of the anteriorly directed flagellum and associated undulating membrane. The flagellum emerges from a bottle-shaped depression, the flagellar pocket, opening on the lateral surface of the cell. The limiting cell membrane envelopes not only the body of the trypanosome but is continuous with and insheathes the flagellar axoneme forming the undulating membrane. In some species a paraxial rod parallels the axoneme from its point of emergence at the flagellar pocket and is an integral component of the undulating membrane. A portion of the flagellum may extend beyond the anterior apex of the cell as a free flagellum; the length is variable in different species of trypanosomes.

Trophoblast Cell Membrane Interactions at Implantation

1970 ◽  
Vol 28 ◽  
pp. 310-311
Author(s):  
A. C. Enders
Keyword(s):  
Epithelial Cells ◽  
Cell Membrane ◽  
Membrane Fusion ◽  
Trophoblast Cell ◽  
Membrane Interactions ◽  
Uterine Epithelial Cells ◽  
Functional Complex ◽  
Cytotrophoblast Cells ◽  
Complex Relationships ◽  
Syncytial Trophoblast

The alteration in membrane relationships seen at implantation include 1) interaction between cytotrophoblast cells to form syncytial trophoblast and addition to the syncytium by subsequent fusion of cytotrophoblast cells, 2) formation of a wide variety of functional complex relationships by trophoblast with uterine epithelial cells in the process of invasion of the endometrium, and 3) in the case of the rabbit, fusion of some uterine epithelial cells with the trophoblast.Formation of syncytium is apparently a membrane fusion phenomenon in which rapid confluence of cytoplasm often results in isolation of residual membrane within masses of syncytial trophoblast. Often the last areas of membrane to disappear are those including a desmosome where the cell membranes are apparently held apart from fusion.

Some Conditions Necessary for Pinocytosis

1968 ◽  
Vol 26 ◽  
pp. 142-143
Author(s):  
M. W. Brightman
Keyword(s):  
Smooth Muscle ◽  
Cell Membrane ◽  
Toxic Effects ◽  
Cytological Evidence ◽  
Cell Processes

The cytological evidence for pinocytosis is the focal infolding of the cell membrane to form surface pits that eventually pinch off and move into the cytoplasm. This activity, which can be inhibited by oxidative and glycolytic poisons, is performed only by cell processes that are at least 300A wide. However, the interpretation of such toxic effects becomes equivocal if the membrane invaginations do not normally lead to the formation of migratory vesicles, as in some endothelia and in smooth muscle. The present study is an attempt to set forth some conditions under which pinocytosis, as distinct from the mere inclusion of material in surface invaginations, can take place.

Electron microscopic radioautographic studies on the incorporation of 3H proline in the glomerular basement membrane (GBM) in antistreptococcal-cell-membrane (SCM) injected mice

1984 ◽  
Vol 42 ◽  
pp. 188-189
Author(s):  
R.P. Nayyar ◽  
C.F. Lange ◽  
J. L. Borke
Keyword(s):  
Body Weight ◽  
Cell Membrane ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Mesangial Matrix ◽  
Electron Microscopic ◽  
Group A ◽  
Injection Protocol

Streptococcal cell membrane (SCM) antiserum injected mice show a significant thickening of glomerular basement membrane (GBM) and an increase in mesangial matrix within 4 to 24 hours of antiserum administration (1,2,3). This study was undertaken to evaluate the incorporation of 3H proline into glomerular cells and GBM under normal and anti-SCM induced conditions. Mice were administered, intraperitoneally, 0.1 ml of normal or anti-SCM serum followed by a 10 µC/g body weight injection of 3H proline. Details of the preparation of anti-SCM (Group A type 12 streptococcal pyogenes) and other sera and injection protocol have been described elsewhere (2). After 15 minutes of isotope injection a chase of cold proline was given and animal sacrificed at 20 minutes, 1,2,4,8,24 and 48 hours. One of the removed kidneys was processed for immunofluorescence, light and electron microscopic radioautographic studies; second kidney was used for GBM isolation and aminoacid analysis.

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