Cell Membrane Lysis Research Articles

Selective labelling of melittin with a fluorescent dansylcadaverine probe using guinea-pig liver transglutaminase

Melittin, a C-terminal peptide, incorporated the fluorescent probe monodansylcadaverine (DNC) when catalysed by guinea-pig liver transglutaminase and Ca 2+, as determined by thin-layer chromatography (TLC) and high-performance liquid chromatography (HPLC). A 1:1 adduct DNC-melittin was identified in which a single glutamine residue out of two, i.e. Gln 25, acts as acyl donor. Incubation of melittin with transglutaminase in the absence of DNC originated high molecular mass complexes indicative that the peptide lysine residue can act as an acyl acceptor. The DNC-melittin was about 3 times more active in the lysis of red cell membranes than native melittin. Fluorescence study of the labelled melittin in the submicromolar range where it is active on cells showed that while totally exposed to solvent in methanol solution, both Trp and dansyl groups are buried in buffer solution. This strongly suggests that DNC-melittin is self-associated and indeed more active than the native melittin groups are buried in buffer solution. This strongly suggests that DNC-melittin is self-associated and indeed more active than the native melittin in the same conditions.

Effects of Cell Membrane Disruption on the Relaxation Rates of Blood and Clot with Various Methemoglobin Concentrations

The magnetic resonance imaging (MRI) characteristics of hemorrhage and clotted blood change with age. The effects of methemoglobin and cell membrane lysis, factors which in part may underlie this evolution of imaging characteristics, were studied using clotted and heparinized dog blood at various methemoglobin concentrations. Cell lysis did not alter the longitudinal relaxation rate (1/T1) in clotted or unclotted samples. Membrane lysis altered significantly the transverse relaxation rate (1/T2) in both clotted and unclotted samples. Lysed samples of oxygenated blood at 0% methemoglobin had significantly higher T2 values than intact samples. At 0% methemoglobin, clotted samples had slightly but significantly shorter relaxation times than unclotted samples. Within the samples studied, large changes in the state of oxygenation and methemoglobin content were observed in less than 24 h. Such changes necessitate frequent monitoring of these parameters if serial studies are to be done.

Cytochalasin B induces cellular DNA fragmentation

Cellular DNA fragmentation can be induced in many biological instances without plasma membrane damage. The fungal metabolite, cytochalasin B, is capable of modifying numerous cellular functions related to DNA synthesis. In this work it is demonstrated that cytochalasin B is capable of inducing DNA fragmentation in a number of cells lines. This DNA fragmentation occurs before plasma membrane lysis and over a period of hours. Cytochalasin E and villin, agents that act on the microfilaments, also induce DNA fragmentation. Phorbol dibutyrate, a diacylglyceral analog, is able to inhibit cytochalasin B-induced DNA fragmentation in a dose-dependent fashion. These findings support the interpretation that cytochalasin B is inducing DNA fragmentation via its effect on the actin filaments.

Nuclear magnetic resonance studies of lithium transport in erythrocyte suspensions of hypertensives

We have applied a nuclear magnetic resonance (NMR) method, based on the 7Li nucleus, to discriminate between intracellular and extracellular lithium ions (Li +) in red blood cell (RBC) suspensions. The NMR method was compared with atomic absorption, a technique that requires physical separation of intra- and extracellular Li + prior to chemical analysis. The rates and rate constants of RBC Na +-Li + countertransport measured by the 7Li NMR method correlated significantly with the measurements made by atomic absorption for both the hypertensive ( r = 0.964) and control ( r = 0.961) groups. The rates of RBC Na +-Li + countertransport measured by NMR were significantly higher for hypertensive patients than for normotensive controls. The fact that the NMR method does not require cell membrane lysis, and its potential to reveal structural and mechanistic information on Li + binding and transport in cellular systems, makes it promising for understanding the basis of Li + transport variations in RBCs, and possibly other tissues, from hypertensive patients.

Bile Salts against Ehrlich Ascites Carcinoma Cells

Surfactants, which are generally good lytic agents for biological membrane have a brilliant possibility to be useful either as a drug or as agent which may help transport of another drug across the cell membrane by changing membrane fluidity. Here we have studied the whole cell lysis with bile salts using Enrlich Ascites Carcinoma (EAC) cells. This investigation is important since bile salts should be less toxic to the normal organ than synthetic detergents. Na-cheno and Na-deoxycholate are more effective lytic agents than Na-cholate for EAC cell membrane lysis while Na-dehydrocholate did not cause any lysis of EAC cells. Specific role of hydroxyl group in the bile salts is apparent EAC cell membrane is more sensitive to the bile salts during the stationary phase of growth than the log phase. Studies under polarizing microscope show that cell lysis is time dependent Preliminary in vivo study indicates that chenodeoxycholate is toxic to the host. Na-cholate treatment with 45 mg/kg shows increase of life span over the control. In vivo studies for the effect of treatment of Na-cholate on the blood of normal healthy male Swiss A mice indicated initial damage of the blood parameters which were found to be recovered with time and the dose was not found to be lethal to the animals.

In vitro effects of fibrous and nonfibrous silicon nitride on bovine pulmonary macrophages

Bovine pulmonary macrophages were exposed in vitro to 0.3, 0.1, 0.03, or 0.01 mg/ml of a fibrous silicon nitride, nonfibrous (milled) silicon nitride comminuted from the fibrous powder, alpha-quartz (an active control), or glass beads (an inert control). Functional evaluation of the exposed cells indicated that the fibrous silicon nitride was as cytotoxic as quartz, while the nonfibrous silicon nitride was relatively inert. To further evaluate the mechanisms of cytotoxicity, the cells were exposed to 1 mg/ml of the control and test materials and biochemical studies were performed. Quartz increased release of both the cytoplasmic enzyme, lactate dehydrogenase (LDH), and the lysosomal enzyme, acid phosphatase (AP), consistent with both cell membrane and lysosome lysis. In addition, total protein levels were significantly depressed, suggesting significant impairment of cellular synthetic processes. LDH, but not AP, values were increased with fibrous silicon nitride treatment, but not with the nonfibrous silicon nitride. In contrast to quartz, which increased LDH levels by 65%, the fibrous silicon nitride only increased LDH levels by 11%. Scanning electron micrographs further indicated that the fibrous silicon is cytotoxic and poorly tolerated by macrophages. These studies provide further evidence of morphology as a primary determinant of cytotoxicity since the milled powder test article was comminuted from the fibrous material.

Acute arthropod envenomation. Incidence, clinical features and management.

Black widow spider (Latrodectus mactans) envenomation is found throughout both the temperate and tropical latitudes, and is one of the leading causes of death from arthropod envenomations worldwide. The venom is highly neurotoxic, affecting the presynaptic motor endplate to allow massive noradrenaline (norepinephrine) and acetylcholine release into synapses causing excessive stimulation and fatigue of the motor end plate and muscle. Clinically, patients develop a bite site lesion and pain, abdominal pain and tenderness, and lower extremity pain and weakness within minutes to hours of envenomation. Symptoms progress over several hours, then subside over 2 to 3 days. The recommended treatment of 'common' envenomation is calcium gluconate 10% intravenously, titrated to relief of symptoms; antivenin, although effective, may cause hypersensitivity and serum sickness reactions, and should be restricted to life-threatening envenomations only. Brown recluse spider (Loxosceles reclusa) envenomations are seen in the Americas and in Europe, and are endemic to the south and central United States. The venom contains at least 8 enzymes, consisting of various lysins (facilitating venom spread) and sphingomyelinase D, which causes cell membrane injury and lysis, thrombosis, local ischaemia, and chemotaxis. Local envenomations begin as pain and itching that progresses to vesiculation with violaceous necrosis and surrounding erythema, and ultimately ulcer formation. Systemic envenomations may be life threatening, and present with fever, constitutional symptoms, petechial eruptions, thrombocytopenia, and haemolysis with haemoglobinuric renal failure. Treatment of local envenomations is conservative (local wound care, cryotherapy, elevation, tetanus prophylaxis, and close follow-up); systemic envenomation requires supportive care and treatment of arising complications, corticosteroids to stabilise red blood cell membranes, and support of renal function. Dapsone 100mg daily has emerged as a promising therapeutic agent in both animal studies and clinical trials. Over 650 species of scorpions are known to cause envenomation (mostly in children under 10 years); they are endemic mostly in arid and tropical areas. Different venoms and clinical presentations are seen across the different species. Most commonly, an inflammatory local reaction occurs with envenomation, which is treated with wound debridement and cleaning, tetanus prophylaxis, and antihistamines. Occasionally the venom is allergenic, and the resultant allergic reaction is treated in a standard fashion.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiotoxicity of kenyan green mamba (dendroaspis angusticeps) venom and its fractionated components in primary cultures of rat myocardial cells

The cardiotoxic actions of Kenyan green mamba ( Dendroaspis angusticeps) venom have been investigated using primary myocardial cell cultures isolated from neonatal rat hearts. The cardiotoxic actions of the whole venom and its fractionated components were evaluated on the basis of leakage of lactate dehydrogenase (LDH), changes in morphology, cell membrane lysis, decreases in viability and inhibition of spontaneous beating activity. The whole venom caused time- and concentration-dependent arrest of myocardial contraction, leakage of LDH, extensive disruption of cell monolayer, and decreases in viability. The venom was separated into 6 (DaI to DaVI) fractions by gel permeation chromatography on Sephadex G-50. Spontaneous beating activity was abolished by DaI to DaVI at high concentrations, while at lower doses they induced progressive depression of beating frequency after a 3-h treatment period. DaI to DaIV caused significant leakage of LDH, morphological damage, and decreases in viability after a 6-h incubation period. The most cardiotoxic fraction (DaIV), which also contains about 54% of the total protein of the whole venom, was fractionated into 18 polypeptides (Da1 to Da18) by ion exchange chromatography on Bio-Rex 70. On the basis of their ability to abolish myocardial contractility, release LDH, alter cellular structure, lyse cell membranes and reduce viability, the 18 fractions have been divided into 4 arbitrary subgroups of cytotoxins: cardiotoxins, Da1 to Da3; cardiotoxin-like polypeptides, Da4 to Da12, Da14; less active membrane lytic polypeptides, Da13, Da15 to Da17; and membrane lytic polypeptide, Da18. Marked synergistic cell membrane lysis occurred in myocardial cell cultures treated simultaneously with 2 cardiotoxin-like polypeptides, Da7 and Da11. It is suggested that the additive and synergistic cardiotoxic effects of high molecular weight cytotoxic proteins (DaI to DaIII), very low molecular weight cholinomimetic substances (DaV to DaVI) and the 4 subgroups of cardiotoxins may directly contribute to the pronounced cardiovascular problems observed in victims of green mamba bites.

Cardiotoxicity of Jamesoni's mamba (Dendroaspis jamesoni) venom and its fractionated components in primary cultures of rat myocardial cells.

Primary cultures of spontaneously beating myocardial cells isolated from neonatal rat hearts were used to screen the cardiotoxic effects of Jamesoni's mamba (Dendroaspis jamesoni) venom and components isolated from the venom by gel filtration and ion exchange chromatography. Cardiotoxicity was evaluated on the basis of leakage of lactate dehydrogenase (LDH), changes in morphology, cell membrane lysis, cellular viability, and alterations in spontaneous beating activity. The whole venom caused dose- and time-dependent leakage of LDH, disruption of the cell monolayer, decreases in viability, and inhibition of beating activity. Gel filtration of the venom yielded eight fractions (DjI to DjVIII). DjI (30 micrograms/ml), DjII (20 micrograms/ml), and DjV (20 micrograms/ml) caused significant (P less than 0.001) leakage of LDH, extensive morphologic damage, and decreases in viability. At lower concentrations DjI to DjVIII caused progressive inhibition of spontaneous beating activity. The main fraction (DjV), which was the most toxic, was further separated into 14 polypeptides (Dj1 to Dj14) by ion-exchange chromatography using Bio-Rex 70. Based on the ability to induce LDH leakage, produce morphologic damage, lyse cell membranes, and arrest beating activity, four categories of polypeptides were identified: cardiotoxins, Dj1 and Dj2; cardiotoxinlike polypeptides, Dj3 to Dj8; less active membrane lytic polypeptides, Dj9 to Dj13; and membrane lytic polypeptide, Dj14.

Suppression of Inhaled Particle Cytotoxicity by Pulmonary Surfactant and Re-Toxification by Phospholipase: Distinguishing Properties of Quartz and Kaolin

Abstract Inhaled particle contact with pulmonary surfactant in the hypophase lining pulmonary alveoli was modelled in vitro by exposing two respirable sized dusts, kaolin and silica quartz, to lecithin, a major component of pulmonary surfactant, emulsified in physiological saline. Lecithin adsorbs to the dusts upon incubation at 37°C and suppresses their cytotoxicity as measured by pulmonary macrophage and erythrocyte assays, suggesting that pulmonary surfactant provides a defence system against prompt cell membrane lysis by inhaled dusts. Subsequent pulmonary macrophage phagocytosis and lysosomal enzyme digestion of the coated dusts was modelled in vitro by incubation with phospholipase A 2 for one hour. With increasing lipase activity, silica haemolytic potential was restored to native silica levels. Kaolin was retoxified to levels far in excess of native kaolin haemolytic potential. Elution, thin layer chromatography and phosphate assay of treated dusts indicate that most lecithin on silica is digested to lysolecithin and desorbed, silica retoxification being due to surface and adherent lysolecithin effects. Most lecithin on kaolin is not digested in the same time; that which is, results in adherent lysolecithin which is responsible for the kaolin retoxification. Digestion with phospholipases A 2 and C together produces only weakly retoxified kaolin. Results suggest that surface adsorption properties which control the adherence of prophylactic surfactant distinguish the pathogenic potentials of quartz, kaolin and mixed dust.

Donor Corneal Endothelial Striae

Excessive traction during excision of donor corneoscleral buttons can result in damage or death to corneal endothelial cells. This damage manifests as multiple peripheral and, less commonly, central striae or stretch marks that correspond to linear opacities at the level of the endothelium. The striae consist of parallel lines of degenerate endothelium, each line three to eight cells wide, and stain readily with trypan blue, which is indicative of cell damage or death. Light and electron microscopy demonstrates cell membrane lysis with abrupt demarcation between abnormal and normal endothelial cells. The number of these striae correlates with the degree of traction or stretch applied during corneoscleral excision. Careful slit-lamp biomicroscopy of corneoscleral buttons discloses endothelial striae in approximately 5% of specimens. Careful excisions of corneoscleral buttons are necessary to decrease the incidence and severity of endothelial striae.

Cytotoxicity of human brain tumors by hematoporphyrin derivative

A number of investigators have successfully applied light activation of hematoporphyrin derivative to treat both animal and human solid tumors [ 1, 2, 4, 111. The biological activity of this treatment modality depends on the selective retention of the HPD by malignant cells, activation by light with the resultant production of singlet oxygen, and the rapid cytotoxicity induced by oxidation-induced cell membrane lysis [9]. Brain tumors would seem to be an ideal system to apply this new treatment modality, since they are lethal by virtue of their local growth [8]. In addition, with new CT scan and fiberoptic technology, a very large area within the brain could be activated by laser-derived light systems. It was the purpose of this study to investigate the in vitro sensitivity of human central nervous system neoplasms to the cytotoxic effects of hematoporphyrin derivative and visible light. The results suggest that there is a relatively uniform cytotoxicity of human brain tumors with hematoporphyrin derivative at dose levels obtainable in clinical practice.

Control of secretion vesicle margination and lysis by glucose, IBMX, and glyburide.

We have attempted to define the effect of glucose, glyburide, and isobutylmethylxanthine (IBMX) upon secretion vesicle margination to the plasma membrane and granule lysis. Margination of secretion vesicles during exocytosis was assessed by measuring the recruitment of somatostatin (SRIF) receptors. Secretion vesicle lysis was studied by measuring insulin release into the incubation media. Our observations suggest that glucose directly affects both secretion vesicle margination and lysis. Both events are rapidly influenced by this secretagogue (within 10 min of incubation). Trifluoperazine (TFP) and removal of Ca2+ from the incubation media significantly reduced glucose-induced margination of secretion vesicles and their lysis (P less than 0.001). IBMX primarily influences the lysis of secretion vesicles and not their margination. IBMX caused a rapid increase in insulin secretion within 10 min without recruitment of SRIF receptors. Neither TFP nor the absence of extracellular Ca2+ affected IBMX-induced insulin release. Late enhancement in margination of secretion vesicles (30 min of incubation with IBMX) is probably related to the initial event of secretion vesicle lysis and is independent of extracellular calcium. Glyburide exerts its action in a manner similar to glucose, affecting both the lysis of secretion vesicles and their margination. However, the action of glyburide is independent of extracellular calcium and partially dependent upon calmodulin.

Differential lysis of plasma membranes and granules of human neutrophilis by digitonin

The effect of the detergent digitonin on lysis of granule and plasma membranes of human neutrophils was studied. Either linear or sigmoid dose-response for release of the cytoplasmic marker lactate dehydrogenase and the granule markers lysozyme, β-glucuronidase. lactoferrin. and myeloperoxidase was noted using digitonin concentrations ranging from 0.001 to 0.1 mM. However, release of the eytosol compartment was far more sensitive to the detergent than the granule compartment, with more release of lactate dehydrogenase than of lysozyme at 0·01–0·08 mM digitonin. Distinction between the two compartments was optimal at 0.025 mM digitonin. By examining in parallel the digitonin-induced release of exogenous fluorescent or luminescent indicators, a granule location was demonstrated for the pH indicator 9-aminoacridine. while the calcium probes aequorin and Ouin 2 were released coincident with release of the cytosolic enzyme lactate dehydrogenase. These findings were employed to validate use of the indicators for monitoring of ion translocation in the intact cell. The differential effect of this detergent on subcellular membranes provides a broadly applicable technique for rapid assessment of the subcellular localization of tracer substances. Rapid monitoring may help to avoid problems of redistribution during cell fractionation.

POLYAMINES, POLYMORPHS AND EXPERIMENTAL RESPIRATORY DISTRESS SYNDROME

The polyamines (PAs) spermine (SPM) and SPM plus spermidine (SPD) produce lesions in B alb C mice as found in Adult Respiratory Distress Syndrome (ARDS). Endocapillary margination of polymorphs (PMNs) was seen 30 min. after i.p. SPM (75 mg/kg bw). At 60 min. endothelial cell vacuolization, RBC engorgement and hemorrhage were observed. Loss of interdigitating cell boundaries suggested edema formation. Seven day PA exposure (SPM 15 mg/kg/d plus SPD 30 mg/kg/d, i.p.) produced severe damage. Leukergy, band-form margination, microatalectasis and hyperplastic type II epithelial cell desquamation in suffused alveoli were noted. Resident PMN swelling included both nuclear chromatin reorganization and cytoplasmic liquifaction. Dissolution of organelles preceded plasma and nuclear membrane lysis. Residual moth-eaten stroma suggested widespread proteolysis. SPM (15 mg/kg/d, i.p.) for 21 days induced fibroblast and type II cell proliferation and fibrotic replacement of parenchyma. Infection, surgery, irradiation, cytoxic drug and collagen-vascular disorders cause increased blood and urinary PA levels and are initial clinical events in ARDS. In our model PAs promote a sustained PMN-endothelial cell membrane association and interstitial edema as the earliest morphological events in the ARDS sequence. This is provisionally attributed to several possible concurrent reactions including poly-electrolyte bridging, endocytotic receptor down-regulation and/or structural surface point charge alteration.

Immunological studies of the embryonic muscle cell surface. Antiserum to the prefusion myoblast.

Xenogeneic antisera raised in rabbits have been used to detect compositional changes at the cell surfaces of differentiating embryonic chick skeletal muscle. In this report, we present the serological characterization of antiserum (Anti-M-24) against muscle tissue and developmental stage-specific cell surface antigens of the prefusion myoblast. Cells from primary cultures of 12-d-old embryonic chick hindlimb muscle were injected into rabbits, and the resulting antisera were selectively absorbed to obtain immunological specificity. Cytotoxicity and immunohistochemical assays were used to test this antiserum. Absorption with embryonic or adult chick heart, brain, retina, liver, erythrocytes, or skeletal muscle fibroblasts failed to remove all reactivity of Anti-M-24 for myogenic cells at all stages of development. After absorption with embryonic myotubes, however, Anti-M-24 no longer reacted with differentiated myofibers, but did react with prefusion myoblasts. The myoblast surface antigens detected with Anti-M-24 are components of the muscle cell membrane: (a) these macromolecules are free to diffuse laterally within the myoblast membrane; (b) Anti-M-24, in the presence of complement, induced lysis of the muscle cell membrane; and (c) intact monolayers of viable myoblasts completely absorbed reactivity of Anti-M-24 for myoblasts. These antigens are not loosely adsorbed culture medium components or an artifact of tissue culture because: (a) absorption of Anti-M-24 with homogenized embryonic muscle removed all antibodies to cultured myoblasts; (b) Anti-M-24 reacted with myoblast surfaces in vivo; and (c) absorption of Anti-M-24 with culture media did not affect the titer of this antiserum for myoblasts. We conclude that myogenic cells at all stages of development possess externally exposed antigens which are undetected on other embryonic and adult chick tissues. In addition, myoblasts exhibit surface antigenic determinants that are either masked, absent, or present in very low concentrations on skeletal muscle fibroblasts, embryonic myotubes, or adult myofibers. These antigens are free to diffuse laterally within the myoblast membrane and may be modulated in response to appropriate environmental cues during myodifferentiation.

Ultrastructural Alterations in Gizzard Smooth Muscle of Selenium-Vitamin-E-Deficient Ducklings

Lesions of gizzard smooth muscle were studied by light and electron microscopy in newly hatched ducklings fed a selenium-vitamin-E-deficient diet for 13-21 days. Histopathologic alterations included initial hyaline change in damaged smooth-muscle cells, subsequent mineralization of sarcoplasmic debris in necrotic smooth-muscle cells, macrophagic invasion and phagocytosis of sarcoplasmic debris, and eventual fibroblastic proliferation and scarring of damaged areas in the gizzard wall. Ultrastructurally, mild damage in smooth-muscle cells was manifested by altered mitochondria with matrical densities and disrupted membranes and dilated elements of sarcoplasmic reticulum. In smooth-muscle cells with severe injury, the alterations of mitochondria and sarcoplasmic reticulum were accompanied by myofibrillar lysis and disruption of plasma membranes and external laminae. Expanding zones of mineralization of sarcoplasmic debris in necrotic smooth muscle cells were present at dense masses of lysed myofilaments that surrounded mineralized and disrupted mitochondria. Numerous macrophages infiltrated the areas of necrosis of smooth muscle and phagocytosed sarcoplasmic debris.

The inhibitors of substrate-incorporation in tumor cells. III. An investigation on the biological activities of renastacarcin.

The purified sample of renastacarcin was tested against various kinds of Gram-positive and -negative bacteria, yeast and fungi. As a result, it was concluded that this compounds was almost devoid of antimicrobial activity even at a concentration of 200 mcg/ml. However, renastacarcin showed a significant antitumor activity both in vitro and in vivo against ascitic type of Ehrlich carcinoma and Sarcoma 180 in mice. When the tumor cells were incubated with renastacarcin, the lysis of cell membrane and subsequent leakage of the cellular contents were observed by means of the optical and microscopical method.The LD50 values of renastacarcin in mice were observed to be 40 mg/kg intraperitoneally, and 23.5 mg/kg intervenously.

Electron microscope studies of experimental Entamoeba histolytica infection in the guinea pig. II. Early cellular and vascular changes accompanying invasion of the lamina propria.

Early cellular and vascular changes in response to invasion of lamina propria by Entamoeba histolytica were studied sequentially, at the ultrastructural level, in germfree guinea pigs inoculated intracecally with amebae and enteric flora derived from patients with acute amebic colitis. Approximately one week post-inoculation the animals developed acute colitis with mucosal invasion by trophic amebae. Although epithelial cells at the sites of amebic invasion showed progressive cytoplasmic changes and desquamation resulting in microerosions, most mesenchymal elements in the lamina propria appeared normal without cytopathic changes even when in direct contact with invading amebae. Only the polymorpho-nuclear leukocytes (PMN) apposed or topographically close to amebae exhibited degenerative changes which were characterized by condensation of nucleoplasm and cytoplasm, extra-cellular release of cytoplasmic components including granules, and, finally, lysis of cell membranes. Capillaries and venules in the lamina propria showed a variety of changes such as swelling and gap formation at the intercellular endothelial junctions and more rarely at the fenestrae. Blood vessels physically close to amebae showed formation of endothelial cytoplasmic blebs which pinched off into the vascular or extravascular space. Platelet and fibrin thromboses were common in the more severely damaged capillaries and venules. Fragments or clumps of fibrin-like material were found also in the extracellular spaces. Amebic invasion of the lamina propria, then, is accompanied by continued epithelial shedding, PMN degeneration, and changes in both capillaries and venules consisting of endothelial damage and occlusive thrombosis. The vascular changes appeared to be closely related to PMN degeneration resulting from interaction of PMN with invading amebae.

Histopathological effects of larval digenea on the digestive epithelia of the marine prosobranch Cerithidea californica: Fine structural changes in the digestive gland

The effects of natural infections by rediae of the heterophyid Euhaplorchis californiensis on the digestive gland cells of Cerithidea californica (Gastropoda: Prosobranchiata) were studied through the use of light and electron microscopy. Pathological changes in secretory and digestive cells, including the disruption of digestive vacuoles and cell-cell junctions, the deformation of lumenal microvilli, the lysis of distal plasma membranes, and nuclear polymorphism, usually accompany the migration of larval trematodes into the digestive gland. Degenerating secretory cells are further characterized by Golgi complexes which assume an inflated appearance and a reduction of rough endoplasmic reticulum in the cell's perinuclear region. Finally, an increase in excretory and autophagic activities in the digestive gland cells of infected snails may be considered possible mechanisms by which the host is able to compensate for adverse metabolic or nutritional stresses of trematode parasitism.