• Proceedings of the Zoological Society Korea Conference
• /
• 1997.04a
• /
• pp.64.2-64
• /
• 1997

No Abstract, See Full Text

• Applied Microscopy
• /
• v.17 no.1
• /
• pp.115-130
• /
• 1987

The present experiment was performed to investigate the acute effects of cadmium on ultrastructural and biochemical changes in mouse kidney and compare these changes with liver damage. Mouse were injected with cadmium chloride at a dose of 5 mg/kg body weight. After treatment, mouse were sacrificed at time intervals of 6, 12, 24 and 48 hours. It was observed that ultrastructural changes in mouse kidney were composed of swelling of mitochondria, dilation in endoplasmic reticulum, wrinkling at basal infolded membrane, formation of autophagosome and partial loss of microvilli in brush. border, and that ultrastructural changes in liver were mitochondrial change, dilation and deterioration of rough endoplasmic reticulum and proliferation of smooth endoplasmic reticulum. Biochemical effects of cadmium were more severe on liver than kidney. Therefore, acutely injected cadmium caused not only liver damage, but also kidney damage.

• Applied Microscopy
• /
• v.8 no.1
• /
• pp.1-8
• /
• 1978

The aim of this research was to discover the action mechanism of various antituberculosis agents (isoniazid, paraaminosalicylic acid and streptomycin) which act on Mycobacteria tuberculosis hominis $H_{37}R_v$ and also to study the relationship of ultrastructural changes and the growth pattern in Mycobacterium tuberculosis hominis. The ultrastructural change was observed with an electron microscope while the growth pattern was studied through in vitro culture. The results are summarized as follows: 1. The ultrastructural changes found in the group treated only with isoniazid were the loss of nuclear materials and the appearence of electron dense granules. 2. In the group treated with paraaminosalicylic acid, thickening of nuclear filaments and meso some arrangement disorders were observed. 3. In the group treated with streptomycin, the ribosome particles appeared indistinct and the cytoplasm was denaturalized. 4. In the group cross treated with all three agents, all the ultrastructural changes mentioned above could be observed in the cell just as they appeared in the single treated groups. 5. In all of the single and in the crossly treated group, there were no significant changes note in the cell wall or cytoplasmic membranes of any of the cells observed. 6. In the cultural data in vitro, through the crossly treated group and single treated group. growth was observed in 3-5 weeks of culture.

• Korean Journal of Bronchoesophagology
• /
• v.4 no.2
• /
• pp.182-187
• /
• 1998

Platelet activating factor (PAP) has been known as implicating as one of potent inflammatory mediators and reported 0 be involved in inflammation and allergy. PAF induces ciliary dysfunction and epithelial damage of human paranasal sinus mucosa in vitro. However, several recent papers have reported that PAF may not readily damage the airway epithelium. The aim of this study was to investigate the ultrastructural evidence to elucidate the pathogenesis of epithelial damage induced by PAF. Sixteen $\mu\textrm{g}$ g of PAF was applied into the maxillary sinuses of 6 rabbits. Rabbits were divided into 2 subgroups along with time interval at 1st and 3rd experimental day, and sinus mucosae were taken for the histopathologic study using electron microscopy. At 1st day, epithelial cells showed no ultrastructural change. Ultrastructures of the cilia were well preserved. Subepithelial space showed no evidence of the infiltration of inflammatory cells. Intravascular platelet aggregation and swelling of endothelial cells were evident. At 3rd day, epithelial cells showed vacuolar degeneration. Fusion of cilia forming giant cilia and focal loss of cilia were evident. Eosinophils were infiltrated in subepithelial and intraepithelial space. Swelling of endothelial cells, and migration of inflammatory cells into the connective tissue were evident. This study implies that epithelial damage induced by PAF may be secondary to the cytotoxicity of mobilized eosinophils rather than direct cytotoxicity of PAF.

• Journal of fish pathology
• /
• v.26 no.1
• /
• pp.1-9
• /
• 2013

The acute toxicity and sublethal effects of nitrite on the dark-banded rockfish, Sebastes inermis (mean body weight: $83.3{\pm}7.2$ g), were studied under static conditions for a period of 96 h. The acute toxicity of nitrite was at the 50% lethal concentration ($LC_{50}$) of 700 mg/L. The sublethal effects on selected hematological parameters of the dark-banded rockfish, such as its osmolality, hematocrit, cortisol, alanine aminotransferase (ALT), and aspartate aminotransferase (AST), were measured after 0, 6, 12, 24, 48, 72, and 96 h of exposure to 0, 50, 100, 200, 400, or 700 mg/L nitrite. Sublethal nitrite caused a progressive reduction in the hematocrit of the fish, depending on the nitrite concentration and the exposure period. Exposure to 100-700 mg/L nitrite for 96 h caused a reduction in the hematocrit and an increase in cortisol, ALT, and AST compared with the control levels. Abnormal ultrastructural changes in the gills and liver tissues were observed in fish exposed to 700 mg/L nitrite for up to 96 h compared with the control tissues. Ultrastructural changes included atrophic gill mitochondria and hepatocytes that developed smooth endoplasmic reticulum and atrophic mitochondria. Although no rockfish mortality occurred at 500 mg/L nitrite, all the hematological parameters examined responded adversely to a nitrite dose of 200 mg/L for 96 h. These results show that although the acute toxic concentration of nitrite for the dark-banded rockfish is > 700 mg/L, sublethal concentrations of nitrite also negatively affect its hematological parameters.

• Preventive Nutrition and Food Science
• /
• v.3 no.1
• /
• pp.56-61
• /
• 1998

This study was conducted to investigate the effect of dietary supplementation of vitamin A on the membrane property and ultrastructure in ethanol-administered rat livers. Male Sprague-Dawley rats weighing of 130 ~150g were fed with experimental diets for 7 weeks. The diets contained different types of vitamin A which were $\beta$-carotene, retinyl acetate and retinoic acid. After feeding theexperimental diets for 7 weeks, a dose of 3.0g ethanol (30%, W/V)/kg B.W was injected to rats intraperitoneally. Control rats received 0.9% saline containing isocaloric sucrose instead of ethanol. Plasma membrane fluidity of liver decreased in rats fed with vitamin a -Deficient diet with ethanol as compared to that of control rats. Fluidity change of liver plasma membrane that ethanol had induced was influenced by dietary supplementation of vitamin A, but not influenced by the type of supplemented vitamin. A . The ultrastructural changed of hepatic mitrochondria were observed in some rats such as vitamin A-deficient rats with ethanol. Inadequate consumptionof vitamin A contributed to ultrastructural changes such as swelled mitochondria occurred by ethanol-induced hepatotoxicity. Although accurate mechanism involved in the plasma membrane-stabilizing effect of vitamin A is still unclear, dietary supplementation of vitamin A such as retinyl acetate is neede to modulate this change. The direct involvement of membrane property on the cell damage caused by ethanol treatment remains to be established.

• Applied Microscopy
• /
• v.28 no.4
• /
• pp.551-561
• /
• 1998

The autometallographic method was used to demonstrate the localization of mercury deposits in spleen of mouse. The mercury deposits were identified with the light and electron mocroscope. Mice were treated with methylmercuric chloride in the drinking water (demineralized water) for 40 days. Control and mercury treated groups showed no significant differences in mean body weight and spleen weight per one mouse. Mercury grains were appeared in the germinal center of white pulp consist of a preponderancing lymphocytes, not in red pulp and capsule. At the ultrastructural level, mercury deposits were restricted to lysosomes of macrophage and lymphocyte. Specially, volume in lysosomes of the macrophage was increased. These results suggest that mercury localization in lysosomes is associated with the change of immune activity.

• Applied Microscopy
• /
• v.28 no.1
• /
• pp.21-38
• /
• 1998

The present study was performed to determine the effect of cold stress on myocardium of aging rat. Control groups, which aged 6, 12 and 24 months, were compared with age-matched experimental groups that were exposed to moderate cold stress for a hours daily in a week at laboratory cold room $(4{\pm}1^{\circ}C)$. The histological, histochemical and ultrastructural changes of myocardium were observed. The results were summarized as follow: 1. Age-dependent histological change of control groups was observed the formation of contraction band in 24months aged group. The experimental groups submitted to cold stress showed a similar change pattern as seen in control groups. However, the degree of change in the experimental groups was significantly larger than that of control groups. In the 34 months aged group the formation of hypercontraction band was observed. 2. Regarding age-dependent histochemical changes of control groups, we observed the increase activities of PAS and Masson's trichrome. In experimental groups the activities of PAS and Masson's trichrome were also increased with age. Compare with control group, the activities of PAS was increased but the activities of Masson's trichrome was decreased. 3. Age-dependent ultrastructural changes on vacuolization, lysosome were observed. In control groups the structural changes occur at 12 months. The accumulation of lipofuscin, contraction band, hypercontraction band and a component of connective tissue were observed in 24 months. However, the degree of change in the experimental groups was significantly larger than that of control groups. In contract, the myelin body in intercalated discs was observed in 24 months of experimental groups.

• Applied Microscopy
• /
• v.27 no.3
• /
• pp.333-346
• /
• 1997

The ischemia and reperfusion injury of the skeletal muscles is caused by generation of reactive oxygen during ischemia and reperfusion. It is well known that over 4 hours of ischemia injures the skeletal muscles irreversibly. The author has demonstrated the effects of SOD (superoxide dismutase), DMTU (dimethyl thiourea) and ischemic preconditioning on ultrastructural changes of the muscle fibers in the rectus femoris muscles after 4 hours of ischemia and 1 day and 3 days of reperfusion. A total of 72 healthy Sprague-Dawley rats weighing from 200 gm to 250 gm were used as experimental animals. Under urethane(1.15 g/kg, IP, 2 times) anesthesia, lower abdominal incision was done and the left common iliac artery was occluded by using vascular clamp for 4 hours. The left rectus femoris muscles were obtained at 1 and 3 days after the removal of vascular clamp. The SOD (15,000 unit/kg) or DMTU (500 mg/kg) were administered intraperitoneally at 1 hour before induction of ischemia. The ischemic preconditioned group underwent three episodes of 5 minutes occlusion and 5 minutes reperfusion followed by 4 hours of ischemia and 1 day and 3 days of reperfusion. The specimens were sliced into $1mm^3$ and prepared by routine methods for electron microscopic observation. All specimens were stained with uranyl acetate and lead citrate and then observed with Hitachi-600 transmission electron microscope. The results were as follows: 1. SOD or DMTU alone did not affect the ultrastructure of muscle fibers in the rectus femoris muscles. The electron density of mitochondrial matrix was decreased by ischemic preconditioning. 2. Dilated cisternae of sarcoplasmic reticulum, triad, mitochondria and the loss of myofilament in the sarcomere were observed in the 4 hours ischemia and 1 day reperfused rectus femoris muscles. Markedly changed sarcoplasmic reticulum, triad, disordered or loss of myofilament, indistinct A-band and I-band, and irregular electron lucent M -line and Z-line are seen in the 4 hours ischemia and 3 days reperfused rectus femoris muscles. 3. SOD reduced the changes of organelles in the muscle fibers of the 4 hours ischemia and 1 day reperfused rectus femoris muscles of the rats, but SOD did not affect the changes of muscle fibers in the 4 hours ischemia and 3 days reperfused muscles. On the other hand, DMTU markedly attenuated considerably the ultrastructural change of the 4 hours ischemia and 1 day or 3 days reperfused rectus femoris muscles. 4. By the ischemic preconditioning, the change was attenuated remarkably in the 4 hours ischemia and 1 day reperfused rectus femoris muscles. As the ischemic reperfused changes of muscle fibers were regenerated or recovered by ischemic preconditioning, the ultrastructures of them were similar to those of normal control in the 4 hours ischemia and 3 days reperfused rectus formoris muscles. Consequently, it is suggested that DMTU is stronger inhibitor to ischemic reperfused change than SOD. The ischemia and reperfusion-induced muscular damage is remarkably inhibited by ischemic preconditioning.

• Molecules and Cells
• /
• v.40 no.8
• /
• pp.558-566
• /
• 2017

Regular monitoring on experimental animal management found the fluctuation of ART outcome, which showed a necessity to explore whether superovulation treatment is responsible for such unexpected outcome. This study was subsequently conducted to examine whether superovulation treatment can preserve ultrastructural integrity and developmental competence of oocytes following oocyte activation and embryo culture. A randomized study using mouse model was designed and in vitro development (experiment 1), ultrastructural morphology (experiment 2) and functional integrity of the oocytes (experiment 3) retrieved after PMSG/hCG injection (superovulation group) or not (natural ovulation; control group) were evaluated. In experiment 1, more oocytes were retrieved following superovulation than following natural ovulation, but natural ovulation yielded higher (p < 0.0563) maturation rate than superovulation. The capacity of mature oocytes to form pronucleus and to develop into blastocysts in vitro was similar. In experiment 2, a notable (p < 0.0186) increase in mitochondrial deformity, characterized by the formation of vacuolated mitochondria, was detected in the superovulation group. Multivesicular body formation was also increased, whereas early endosome formation was significantly decreased. No obvious changes in other microorganelles, however, were detected, which included the formation and distribution of mitochondria, cortical granules, microvilli, and smooth and rough endoplasmic reticulum. In experiment 3, significant decreases in mitochondrial activity, ATP production and dextran uptake were detected in the superovulation group. In conclusion, superovulation treatment may change both maturational status and functional and ultrastuctural integrity of oocytes. Superovulation effect on preimplantation development can be discussed.