Effects of swainsonine on rat liver and kidney: biochemical and morphological studies.

Among the reported effects of the plant toxin swainsonine in animals are a decreased level of Golgi mannosidase II activity, an increase in lysosomal alpha-D-mannosidase activity, oligosaccharide accumulation, vacuolization of cells, and neurological changes. We now find that, in the rat, the alkaloid rapidly induces vacuolization of both liver and kidney cells, but oligosaccharides accumulate only in the latter. We demonstrate by enzyme- and immunocytochemistry that the induced pleomorphic vacuoles are lysosomal in nature. The vacuoles do not appear to be derived from the Golgi apparatus, which retains its typical ultrastructural appearance, but are formed by autophagy. In swainsonine-fed rats, the lysosomal system is highly developed in hepatocytes, Kupffer cells, and cells of the proximal convoluted tubules. The relation of this hypertrophy of the lysosomal system to the known effects of swainsonine on glycoprotein biosynthesis and on Golgi and lysosomal alpha-mannosidases is not clear. In addition, in liver there occurs a marked increase in mitotic figures in the hepatocytes. This occurred in the absence of both cell death and increased liver size as estimated by gross morphology.

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Regucalcin ameliorates Doxorubicin-induced cytotoxicity in Cos-7 kidney cells and translocates from the nucleus to the mitochondria

Bioscience Reports ◽

10.1042/bsr20211464 ◽

2021 ◽

Author(s):

Noor A Mohammed ◽

Israa Hakeem ◽

Nikolas J Hodges ◽

Francesco Michelangeli

Keyword(s):

Cell Death ◽

Cell Model ◽

Cancer Drug ◽

Kidney Cells ◽

Strongly Correlated ◽

Caspase 9 ◽

Membrane Blebbing ◽

Chemically Induced ◽

Anti Cancer ◽

Liver And Kidney

Doxorubicin (DOX) is a potent anti-cancer drug, which can have unwanted side-effects such as cardiac and kidney toxicity. A detailed investigation was undertaken of the acute cytotoxic mechanisms of DOX on kidney cells, using Cos-7 cells as kidney cell model. Cos-7 cells were exposed to DOX for a period of 24 hours over a range of concentrations and the LC50 was determined to be 7µM. Further investigations showed that cell death was mainly via apoptosis involving Ca2+ and caspase 9, in addition to autophagy. Regucalcin (RGN), a cytoprotective protein found mainly in liver and kidney tissues, was overexpressed in Cos-7 cells and shown to protect against DOX-induced cell death. Subcellular localization studies in Cos-7 cells showed RGN to be strongly correlated with the nucleus. However, upon treatment with DOX for 4 hours, which induced membrane blebbing in some cells, the localization appeared to be correlated more with the mitochondria in these cells. It is yet to be determined whether this translocation is part of the cytoprotective mechanism or a consequence of chemically-induced cell stress.

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The effect of different doses levels of silver nanoparticles (AgNPs) on the kidney and liver in Albino male Rat. Histopathological study

Baghdad Science Journal ◽

10.21123/bsj.11.4.1503-1509 ◽

2014 ◽

Vol 11 (4) ◽

pp. 1503-1509

Author(s):

Baghdad Science Journal

Keyword(s):

Silver Nanoparticles ◽

Body Weight ◽

Male Rat ◽

Central Vein ◽

Average Particle ◽

Ag Nps ◽

Hepatic Cells ◽

Liver And Kidney ◽

Collecting Tubules ◽

Convoluted Tubules

Objective: In this study ,the effects of silver nanoparticles (Ag NPs)were investigated on the liver and kidney tissues. Methodology: The produced nanoparticles have an average particle size of about 30 nm. Eighteen male albino rats were used by dividing them into three groups, each group comprise 6 rats. First group(control group) given food and water like other groups by liberty. Second group was tail injected by (AgNPs) at dose of (0.4 mg/kg. body weight/day). Third group was injected by (AgNPs) at dose of (0.6 mg/kg. body weight/day) for 15 days. All animals were sacrified at the end of experiment. The liver and kidney tissues specimens were fixed in 10% formalin and histological preparations were carried out then stained with H&E. Pathological changes in liver and kidney tissues were showed. Results: Histopathological studies revealed the harmful effect of the silver nanoparticles uses on the liver and kidney rats, second group that treated with Ag NPs (0.4 mg/kg.body.weight/day), kidney sections showed enlargement of collecting tubules, increase in interstitial tissue medulla, necrosis and enlargement in proximal and distal convoluted tubules. Liver showed enlargement of the central vein and degeneration of hepatic cells. Third group that treated with Ag NPs (0.6 mg/kg. body weight/day); kidney sections showed hyperplasia of the interstitial connective tissue of renal medulla with hemorrhages, renal cortex showed, degenerative changes and necrosis of proximal and distal convoluted tubules. Liver section showed congestion and necrosis of hepatic cells. Conclusion: Silver nanoparticles cause damage in liver and kidney tissues. Recommendation: Further study is needed for the effect of Ag NPs on the other tissues.

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Programmed cell death during Drosophila embryogenesis

Development ◽

10.1242/dev.117.1.29 ◽

1993 ◽

Vol 117 (1) ◽

pp. 29-43 ◽

Cited By ~ 30

Author(s):

J.M. Abrams ◽

K. White ◽

L.I. Fessler ◽

H. Steller

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Acridine Orange ◽

Nile Blue ◽

Molecular Genetic ◽

Blue Staining ◽

Nuclear Condensation ◽

The Central Nervous System ◽

Ultrastructural Appearance ◽

Dying Cells

The deliberate and orderly removal of cells by programmed cell death is a common phenomenon during the development of metazoan animals. We have examined the distribution and ultrastructural appearance of cell deaths that occur during embryogenesis in Drosophila melanogaster. A large number of cells die during embryonic development in Drosophila. These cells display ultrastructural features that resemble apoptosis observed in vertebrate systems, including nuclear condensation, fragmentation and engulfment by macrophages. Programmed cell deaths can be rapidly and reliably visualized in living wild-type and mutant Drosophila embryos using the vital dyes acridine orange or nile blue. Acridine orange appears to selectively stain apoptotic forms of death in these preparations, since cells undergoing necrotic deaths were not significantly labelled. Likewise, toluidine blue staining of fixed tissues resulted in highly specific labelling of apoptotic cells, indicating that apoptosis leads to specific biochemical changes responsible for the selective affinity to these dyes. Cell death begins at stage 11 (approximately 7 hours) of embryogenesis and thereafter becomes widespread, affecting many different tissues and regions of the embryo. Although the distribution of dying cells changes drastically over time, the overall pattern of cell death is highly reproducible for any given developmental stage. Detailed analysis of cell death in the central nervous system of stage 16 embryos (13-16 hours) revealed asymmetries in the exact number and position of dying cells on either side of the midline, suggesting that the decision to die may not be strictly predetermined at this stage. This work provides the basis for further molecular genetic studies on the control and execution of programmed cell death in Drosophila.

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Apoptosis as the mode of cell death in antibody-dependent lymphocytotoxicity

Journal of Cell Science ◽

10.1242/jcs.74.1.169 ◽

1985 ◽

Vol 74 (1) ◽

pp. 169-179

Author(s):

N.H. Stacey ◽

C.J. Bishop ◽

J.W. Halliday ◽

W.J. Halliday ◽

W.G. Cooksley ◽

...

Keyword(s):

Cell Death ◽

Human Peripheral Blood ◽

Cell Activity ◽

Peripheral Blood Lymphocytes ◽

Cell Killing ◽

Target Cells ◽

Human Antibody ◽

Electron Microscopic ◽

Effector Cells ◽

Morphological Studies

A light and electron microscopic study of antibody-dependent lymphocytotoxicity was carried out with the object of elucidating the mechanisms responsible for the cell killing, the basis for the research being the relationship that has recently been shown to exist between the morphology of cell death and its pathogenesis. Chang liver cells coated with a rabbit anti-human antibody were used as targets and normal human peripheral-blood lymphocytes as effector cells. Cytotoxicity assays using release of 51Cr demonstrated extensive K-cell killing, thus validating the suitability of the model for morphological studies. Cell death displaying the features of apoptosis correlated with K-cell activity. A small amount of cell death by classical necrosis was observed, but its extent appeared to be unrelated to the presence of lymphocytes, to pre-treatment of the target cells with antibody, or to the magnitude of 51Cr release. The results support evidence indicating that lymphocytotoxicity depends on activation of a self-destruct program within the target cell. They do not favour a mechanism involving the production of plasma membrane lesions analogous to those responsible for complement-mediated immune cytolysis.

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F-actin as a functional target for retro-retinoids: a potential role in anhydroretinol-triggered cell death

Journal of Cell Science ◽

10.1242/jcs.112.15.2521 ◽

1999 ◽

Vol 112 (15) ◽

pp. 2521-2528 ◽

Cited By ~ 1

Author(s):

I. Korichneva ◽

U. Hammerling

Keyword(s):

Cell Death ◽

Early Event ◽

Pattern Reversal ◽

Cell Periphery ◽

Growth And Survival ◽

Signalling Molecules ◽

Herbimycin A ◽

Morphological Studies ◽

A Cell ◽

Survival Potential

The retro-retinoids, metabolites of vitamin A (retinol), belong to a family of lipophilic signalling molecules implicated in regulation of cell growth and survival. Growth-promoting properties have been ascribed to 14-hydroxy-retro-retinol (14HRR), while anhydroretinol (AR) was discovered to act as a natural antagonist triggering growth arrest and death by apoptosis. Based on morphological studies and inhibition of apoptosis by the kinase blocker, herbimycin A, it has been suggested that retro-retinoids exhibit their function in the cytosolic compartment. F-actin emerged as a functional target for retro-retinoid action. By FACS analysis and fluorescence microscopy of phalloidin-FITC labeled cells we demonstrated that F-actin reorganization was an early event in AR-triggered apoptosis. Fluorescence images of AR-treated fibroblasts displayed short, thick, stick-like and punctate structures, and membrane ruffles at the cell periphery along with an increased diffuse staining pattern. Reversal of the AR effect by 14HRR or retinol indicates that F-actin is a common site for regulation by retro-retinoids. Inhibition of both cell death and actin depolymerisation by bcl-2 implies that cytoskeleton reorganization is downstream of bcl-2-related processes. Furthermore, stabilization of microfilaments by jasplakinolide increased the survival potential of AR treated cells, while weakening the cytoskeleton by cytochalasin B abetted apoptosis. Thus the cytoskeleton is an important way station in a communication network that decides whether a cell should live or die.

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Glutathione and Glutathione Conjugate Metabolism in Isolated Liver and Kidney Cells

Proceedings in Life Sciences - Functions of Glutathione in Liver and Kidney ◽

10.1007/978-3-642-67132-6_24 ◽

1978 ◽

pp. 194-200 ◽

Cited By ~ 9

Author(s):

D. P. Jones ◽

A. H. Stead ◽

P. Moldéus ◽

S. Orrenius

Keyword(s):

Kidney Cells ◽

Glutathione Conjugate ◽

Liver And Kidney ◽

Isolated Liver

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Acaricidal activity of the aqueous and hydroethanolic extracts of 15 South African plants against Rhipicephalus turanicus and their toxicity on human liver and kidney cells

Onderstepoort Journal of Veterinary Research ◽

10.4102/ojvr.v86i1.1665 ◽

2019 ◽

Vol 86 (1) ◽

Cited By ~ 2

Author(s):

Gerda Fouche ◽

Olubukola T. Adenubi ◽

Tlabo Leboho ◽

Lyndy J. McGaw ◽

Vinny Naidoo ◽

...

Keyword(s):

South African ◽

Human Liver ◽

Acaricidal Activity ◽

Kidney Cells ◽

Liver And Kidney ◽

South African Plants ◽

African Plants

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Kidney Inflammation, Injury and Regeneration

International Journal of Molecular Sciences ◽

10.3390/ijms21031164 ◽

2020 ◽

Vol 21 (3) ◽

pp. 1164 ◽

Cited By ~ 4

Author(s):

Baer ◽

Koch ◽

Geiger

Keyword(s):

Acute Kidney Injury ◽

Cell Death ◽

Kidney Injury ◽

Kidney Cells

Damage to kidney cells can occur due to a variety of ischemic and toxic insults and leads to inflammation and cell death, which can result in acute kidney injury (AKI) [...]

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