Morphological effects of degranulation upon me-senteric mast cells of albino rats (SPrague-Dawley strain) by means of lipid administration were studied. An evident degranulation of metachromatic granules from mesenteric tissue mast cells was observed in more than half of experimental rats which were intraperitoneally given 10cc of stearic monoglyceride suspension in warm Tyrode solution (5Omg. of stearic monoglyceride in 10cc of Tyrode solution). A fairly light degranulation of metachro-matic granules from mesenteric mast cells was also displayed by the rats fed ad libitum with butter for 6 hours after being deprived of food for 24 hours.
Animals ; Cytoplasmic Granules/*drug effects ; Lipids/*pharmacology ; Mast Cells/*drug effects ; Mesentery/cytology ; Rats

Degranulation of the mast cell has been reported by the injection of histamine liberators and other chemical agents. Chlorpheniramine maleate (1.2mg./kg. and 0.3mg./kg. comprising 1/74and 1/290 of LD50 respectively), which is an antihistamine agent, in physiological saline solution for intravenous injection and in Tyrode solution for intraperitoneal injection were given in single dose. The mesenteric mast cells stained in Pugh solution, as applied by Lee (1968), were counted according to the classification of An (1964) in 4 types; the typical normal mast cell, the Grade I type of mast cell, the Grade II type of mast cell and the Grade III type of mast cell. In the experimental rats given 1.2mg./kg. of chlorpheniramine intravenously, more mesenteric mast cells were s1ightly degranulated than those cells of the rats given 0.3mg./kg. of chlorpheniramine and the control rats. In the experimental rats given 1.2mg./kg. and 0.3 mg./kg. of chlorpheniramine intraperitoneally, more mesenteric mast cells were slightly degranulated than those cells of the control rats. However, in this intraperitoneal study the degree, or severity, of degranulation of the mesenteric mast cell was not in direct proportion to the dosage of this antihistamine. Consequently it is deduced that the experimental dosage of the antihistamine chlorpheniramine maleate, applied 1/74 and l/290 of LD50, caused an evient degranulation of mesenteric mast cells of the albino rats associated with probable histamine liberation.
Animal ; Chlorpheniramine/pharmacology ; Cytoplasmic Granules* ; Female ; Histamine H1 Antagonists/pharmacology* ; Male ; Mast Cells/drug effects* ; Rats

The effects of morphine HCI on the rat mesenteric mast cells were studied with the electron microscopy. The materials were prepared for electron microscopy by osmium tetroxide fixation and embedding in Epon. The rat mesenteric mast cells showed no distinct morphological changes due to morphine HCl, but the mast cell granlues were changed in various ways. For instance, they formed dusters, showed granular lysis, and an appearance of electron transparency. Frequently, some granules appeared in the extracellular space and the boundary of the granules was not evident. From the results mentioned above, it was suggested that rat mesenteric mast cell granules were affected by morphine HCl in the shape, the granular matrix, and the granular boundaries.
Animal ; Cell Nucleus/ultrastructure ; Cytoplasm/ultrastructure ; Cytoplasmic Granules/drug effects ; Cytoplasmic Granules/ultrastructure ; Golgi Apparatus/ultrastructure ; Male ; Mast Cells/drug effects ; Mast Cells/ultrastructure* ; Mesentery/drug effects ; Mesentery/ultrastructure* ; Microscopy, Electron ; Mitochondria, Muscle/ultrastructure ; Morphine/pharmacology* ; Rats

The authors have demonstrated the effect of sodium selenite on the hepatotoxicity due to carbon tetrachloride, by observing the distribution and disaggregation of the pyroninophilic granules in the hepatic cell of the mature male albino mice. Each experimental mouse of the selenite and the selenite plus carbon tetrachloride groups was given a single dose of 4 ug. of sodium selenite per kilogram of body weight and that of the control and the carbon tetrachloride groups was given 0.1 ml. of distilled water alone. Six hours after the first administration of distilled water or sodium selenite, the experimental mice of the carbon tetrachloride and the selenite plus carbon tetrachloride groups were given a single dose of l.0 ml. of carbon tetrachloride per kilogram of body weight and those of the selenite groups were given 0.l ml. of paraffin oil alone. Following the 1ast administration of carbon tetrachloride or paraffin oil, the mice were sacrificed by bleeding (cutting the common carotid artery) at the intervals of 2,3,4,6,8, and 12 hours respectively. Histochemical preparations were stained by the methyl-green and pyronin method and oil red 0 method. The hepatotoxicity due to the administration of carbon tetrachoride was evident in the hepatic cells; the pyroninophilic granlues were partly reduced in volume in the hepatic cells of the centrilobular and the intermediate zones as early as the 3 hour-period, and markedly reduced or disappeared in the centrilobular and some part of the intermediate zones associated with hydropic degeneration as well as in the 6 hour-period. Thereafter marked reduction or dissolution of the pyroninophilic granules was found and extended as the periportal zone at the 12 hour-period. However, the pyroninophilic granules in the hepatic cells of selenite plus carbon tetrachbride group showed no significant changes in the hepatic cells of these zones, compared to the histochemical feature of the granules in the hepatic cells of the control and the selenite groups. Consequently it is suggested that the lipid peroxidative decomposition of the microsomal membranes, which is induced with carbon tetrachloride, would be prevented by a previous administration of sodium selenite.
Animal ; Carbon Tetrachloride Poisoning*/pathology ; Cell Nucleus/drug effects ; Cytoplasm/drug effects ; Cytoplasmic Granules ; Lipids ; Liver/drug effects* ; Liver/pathology ; Male ; Mice ; Selenium/pharmacology* ; Vacuoles/drug effects

OBJECTIVEThe present study was designed to investigate whether Tumor necrosis factor (TNF)-alpha stimulates release of endothelial microparticles (EMPs) by human endothelial cells, and whether EMPs may serve as a promising marker for endothelial injury and dysfunction.

METHODSHuman umbilical venous endothelial cells (HUVEC) were incubated with or without TNF-alpha for 24 hours at 37 degrees C. EMPs generated on the surface of HUVEC were observed with a scanning electron microscopy. The CD31 and CD51 positive EMPs in culture supernatants were measured by flow cytometer.

RESULTSFewer vesicles were observed on cell surface of control group, in TNF-alpha-stimulated one, however, cells manifested a blebby surface (eruption phenomenon) and more vesicles on surface were observed. The levels of EMPs were significantly increased in TNF-alpha stimulated cells compared with controls [CD31 + EMP, (164 +/- 63)/1000 cells vs. (42 +/- 10)/1000 cells, P < 0.05; CD51 + EMP, (260 +/- 108)/1000 cells vs. (19 +/- 4)/1000 cells, P < 0.05].

CONCLUSIONTNF-alpha can stimulate HUVEC to release EMPs which may serve as a surrogate marker for endothelial injury and dysfunction.

Cells, Cultured ; Cytoplasmic Granules ; metabolism ; Endothelial Cells ; drug effects ; metabolism ; Endothelium, Vascular ; cytology ; Flow Cytometry ; Humans ; Tumor Necrosis Factor-alpha ; metabolism ; pharmacology ; Umbilical Veins ; cytology

OBJECTIVE: To investigate the protective effect of epigallocatechin-3 -gallate (EGCG) on apoptosis of cerebellar granule neurons (CGNs) induced by acrylamide (ACR). METHODS: CGNs were cultured with the addition of 5 mmol/L ACR for 24 hours to set up a cell injury model. Prior to ACR treatment, CGNs were treated with different concentrations of EGCG (0, 5, 10, 25, 50, 100 μmol/L) for 48 hours. Neuronal viability was measured with metylthiazdyltetrazolium (MTT). The activity of SOD and the content of MDA were assayed. Hoechst33342 staining was employed to observe morphological changes of the cell nucleus. Reverse transcription-polymerase chain reaction (RT-PCR) was used to measure expression of bcl- 2 mRNA and bax mRNA. RESULTS: At the concentrations of 10, 25 or 50 μmol/L, EGCG played a protective role against ACRinduced CGN injury. Compared with ACR injured group (no EGCG), EGCG improved the cell viability, enhanced SOD activity, decreased the level of MDA as well as the cell apoptosis ratio (P<0.05). Bcl-2 mRNA expression was increased and bax mRNA expression was reduced (P<0.05). 25 μmol/L EGCG had the largest effect. However, 100 μmol/L EGCG did not have a significantly protective effect. CONCLUSION EGCG at appropriate concentration has protective effect against the CGNs on apoptosis induced by ACR.
Acrylamide ; toxicity ; Animals ; Apoptosis ; drug effects ; Catechin ; analogs & derivatives ; pharmacology ; Cells, Cultured ; Cerebellum ; cytology ; drug effects ; Cytoplasmic Granules ; Female ; Male ; Neurons ; cytology ; drug effects ; Neuroprotective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study the pathological and clinical characteristics of a patient with spontaneous platelet aggregation of his giant and morphologically abnormal platelets.

METHODSPlatelet size and structure were observed under light microscope and electron microscope. Platelet aggregation was measured turbidometrically. Platelet glycoproteins (GP) were analyzed using flow cytometry. PCR and DNA sequencing were performed to identify the gene abnormality.

RESULTSThe patient had spontaneous platelet aggregation of giant platelets with thickened plasma membrane and increased number of granules in various shapes. Aspirin and ticlopidine did not affect the spontaneous aggregation. The expression of GP I b, GP II b, GP III a and P-selectin in the platelet membrane were in normal range. Results of gene analyses for GP I balpha, GP I bbeta and GPIX were also normal.

CONCLUSIONBoth morphological and functional abnormalities of the platelets from the patient were clearly distinguishable from that of other hereditary giant platelet disorders. It would probably represent a novel platelet disorder which had not been reported to date.

Aspirin ; pharmacology ; Bernard-Soulier Syndrome ; metabolism ; pathology ; Blood Platelet Disorders ; metabolism ; pathology ; Cell Size ; physiology ; Child ; Cytoplasmic Granules ; pathology ; ultrastructure ; Female ; Humans ; Platelet Aggregation ; drug effects ; physiology ; Platelet Aggregation Inhibitors ; pharmacology ; Platelet Membrane Glycoproteins ; genetics ; metabolism ; Ticlopidine ; pharmacology