Morphological changes induced by phalloidin in the rat liver

Agostini, Bruno; Govindan, V. M.; Hofmann, Walter

doi:10.1007/978-94-011-6618-8_16

Cited by 15 publications

(6 citation statements)

References 25 publications

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“…These cells possess a thin parietal layer of cytoplasm and several transvacuolar strands, one or more of which usually intersects the nucleus (Figs. 1,8). Although strands are also present in guard cells (GC) and directional movement of particles is pronounced, bulk cytoplasmic flow is not as evident in these cells.…”

Section: Cytochalasirz Bmentioning

confidence: 98%

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Comparative effects of phalloidin and cytochalasin B on motility and morphogenesis in Allium

Palevitz¹

1980

Can. J. Bot.

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Cytochalasin B (CB), thought to disaggregate F-actin in animal cells, and phalloidin (Phal), known to stabilize F-actin in vivo and in vitro, have nearly identical effects on cotyledon epidermal cells of Allium cepa. Both drugs rapidly induce cessation of streaming and both, by preventing normal telophase reorientation movement, lead to abnormal division planes in dividing guard mother cells. Neither, however, prevents normal microtubule deposition, wall thickening, and cellulose orientation during guard cell differentiation. Furthermore, both drugs have no effect on spindle formation and anaphase chromosome motion. Examination of Nitella and Chara cells, in which streaming had been stopped by either agent, shows that microfilament cables are still present. With both drugs, the minimum effective concentrations were routinely used (CB, 2 μM; Phal, 100–200 μM). Our results are discussed in terms of the mode of action of these drugs and their possible role in host-fungus interactions. Implications for the mechanisms underlying cell plate alignment, cellulose orientation, and cytoplasmic streaming are discussed.

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Section: Cytochalasirz Bmentioning

confidence: 98%

“…These changes are linked to the abnormal accumulation of actin-containing microfilaments in the treated cells (1,55). In uitro, Phal has been convincingly shown to bind to F-actin and stabilize it against a plethora of disruptive agents including CB (29,55).…”

Section: Introductionmentioning

confidence: 98%

Comparative effects of phalloidin and cytochalasin B on motility and morphogenesis in Allium

Palevitz¹

1980

Can. J. Bot.

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“…Phalloidin increases the quantity of F-actin when added to isolated hepatocytes (4) or to isolated liver plasma membranes (2,5,6) and produces a marked increase in microfilaments in the pericanalicular region of hepatocytes when the alkaloid is administered chronically in low doses to rats (7). In the intact rat, chronic phalloidin administration, like other microfilament poisons, is associated with a diminution in bile production (7)(8)(9) and an extensive rearrangement of hepatocyte junctional elements observed by freeze-fracture electron microscopy (10).…”

mentioning

confidence: 99%

Phalloidin-induced cholestasis: a microfilament-mediated change in junctional complex permeability.

Elias¹,

Hruban²,

Wade³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

105

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Phalloidin, administered to male rats for 7 days (500 ,sg per kg/day), increased the mean hepatic content of filamentous actin. Both bile flow and bile acid excretion diminished proportionally, whereas the bile-to-plasma ratios of Phalloidin, a cyclic peptide derived from the poisonous mushroom Amanita phalloides, specifically binds to purified muscle F-actin and prevents its depolymerization (1-3). Phalloidin increases the quantity of F-actin when added to isolated hepatocytes (4) or to isolated liver plasma membranes (2, 5, 6) and produces a marked increase in microfilaments in the pericanalicular region of hepatocytes when the alkaloid is administered chronically in low doses to rats (7). In the intact rat, chronic phalloidin administration, like other microfilament poisons, is associated with a diminution in bile production (7-9) and an extensive rearrangement of hepatocyte junctional elements observed by freeze-fracture electron microscopy (10).These changes in junctional structure suggest that microfilaments help regulate junctional development and support the notion that the junctional barrier may in turn influence the formation of bile. Because accumulating evidence suggests that the paracellular pathway is an important site for water, electrolyte, and solute entry into bile (11-14), the phalloidin-treated rat provides a useful experimental model to examine more closely the relationship among microfilament function, junctional structure, and bile secretion. In this study, we measure the effects of phalloidin on bile formation and biliary permeability to inulin and sucrose, two large molecular weight solutes that rapidly reach equilibrium between plasma and bile before liver water, suggesting that their entry into bile is via a paracellular route. Junctional structure and permeability were also examined by freezefracture studies and by the infusion of ionic lanthanum chloride at a time when increases in hepatic content of polymerized actin were also observed. METHODSMale Sprague-Dawley rats (Charles River), initially weighing 175-225 g, were treated for 7 days with either phalloidin at 500 ug kg-' day-' in saline (16 animals) or saline alone as a control (16 animals) by intraperitoneal injection as described by Gabbiani et al. (7). Phalloidin was obtained from Boehringer Mannheim. On the eighth day, the rats were anesthetized by intraperitoneal injection of sodium phenobarbital at 50 mg (kg of body weight)-I, and the bile duct was cannulated with polyethylene tubing (PE10, Clay Adams). Body temperature was monitored by rectal probe and maintained at 370C by a heating lamp regulated by a constant temperature regulator (Yellow Springs Instrument). After 60-80 min, the abdomen was reopened and heparin (10,000 units kg-') was injected into the inferior vena cava before fixation of the liver by portal vein perfusion.Bile Flow and Bile Acid Excretion. Bile was collected for 80 min at 20-min intervals and expressed as !ul mind (g of body weight)-l and as gl min-1 (g of liver)-l. Bile acids were analyzed ...

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“…Phalloidin is a toxic bicyclic heptapeptide isolated from the mushroom Amanita phalloides (16,17). Treated animals die within a few hours with a hemorrhagic necrosis of the liver characterized by numerous nonfatty vacuoles (18). Phalloidin is active on rat hepatocytes in uitro, where it produces easily observed deformations of the cell surface that accompany the death of the cells (14,15).…”

mentioning

confidence: 99%

“…Phalloidin is active on rat hepatocytes in uitro, where it produces easily observed deformations of the cell surface that accompany the death of the cells (14,15). The protrusions or evaginations of the plasma membrane seen by scanning electron microscopy are felt to correspond to the invaginations of the plasma membrane and subsequent vacuolization of the cells in the intact liver as seen by transmission electron microscopy (14,15,18). The molecular basis of this injury most likely lies in the interaction of phalloidin with actin filaments intimately associated with the plasma membrane (19)(20)(21).…”

mentioning

confidence: 99%