There is considerable interests in the effect of regular, vigorous exercise, in particular weight training as a possible measure in improving myocardial function. The present investigation aimed to examine possible effect of a long-term weight training program on the heart in aging rats. Male rats aged 3-,10-, and 20-month-old were divided at random into a control (sedentary) and the exercise group. The training group was exercised for 5 days a week by 1 RM of ten times with weight training apparatus. This investigation examined the changes of the heart muscle relative to histological, ultrastructural, cytochemical, and stereological studies in rats. Quantity of lipofuscin pigments was clearly increased in the weight training group of 15-month-old rats, and mitochondrial degeneration, vacuolization, and interstitial proliferation were observed as well. In the weight training group of 25-month-old rats the frequency as separated intercalated discs, fraying myofibrils and hypercontraction band increased in number compared with the same 15-mon1h-old group. From the experimental result of glucose-6-phosphatase activity, the enzyme activities decreased in the weight training group of 15-month-old rats, and more decreased in the same 25-month-old group. In stereological study, both 15- and 25-month-old training groups, mitochondrial and myofibrilar volume densities significantly decreased, whereas interstitial volume density significantly increased. From the experimental results obtained in the present study, it is suggested that long-term weight training exercise do not cause any significantly qualitative and quantitative ultrastructural change of the heart muscle in the young. On the contrary, long-term weight training exercise stress may actually induce degenerative changes in the heart muscle in the old age.
It has been well known that ischemia and reperfusion injury to skeletal muscle following an acute arterial occlusion causes significant morbidity and mortality. The skeletal muscle, which contains high energy phosphate compounds, has ischemic tolerance. During the ischemia, the ATP is catalyzed to hypoxanthine anaerobically and hypoxanthine dehydrogenase is converted to xanthine oxidase. During reperfusion, the hypoxanthine is catalyzed to xanthine by xanthine oxidase under $O_2$, presence and that results in production of cytotoxic oxygen free radicals. These cytotoxic free radicals, $O_2^-,\;H_{2}O_2,\;OH^-$, are toxic and make lesions in skeletal muscle during reperfusion. The authors perform the present study to investigate the effects of allopurinol, the inhibitor of xanthine oxidase, on reperfused ischemic skeletal muscles by observing the ultrastructural changes of the muscle fibers. A total of 48 healthy Sprague-Dawley rats weighing from 200 g to 250 g were used as experimental animals. Under urethane(3.0mg/kg., IP) anesthesia, lower abdominal incision was done and the left common iliac artery were ligated by using vascular clamp for 1, 2 and 6 hours. The left rectus femoris muscles were obtained at 6 hours after the removal of vascular clamp. In the allopurinol pretreated group, 50mg/kg of allopurinol was administered once a day for 2 days and before 2 hours of ischemia. The specimens were sliced into $1mm^3$ and prepared by routine methods for electron microscopic observations. All preparations were stained with uranyl acetate and lead citrate, and then observed with Hitachi -600 transmission electron microscope. The results were as follows: 1. In 1 hour ischemia/6 hours reperfused rectus femoris muscles of rats, decreased glycogen particles and electron density of mitochondrial matrix and dilated terminal cisternae are seen. In 2 hours ischemia/6 hours repersed rectus femoris muscles of rats, mitochondria with electron lucent matrix, irregularly dilated triad and spheromembranous bodies are observed. In 6 hours ischemia/6 hours reperfused rectus femoris muscles of rats, irregularly arranged myofibrils, and many spheromembranous bodies, fat droplets and lysosome are seen. 2. In 1 hour ischemia/6 hours reperfused rectus femoris muscles of rats pretreated with allopurinol, decreased glycogen particle and dilated cisternae of sarcoplasmic reticulum and triad are observed. In 2 hours ischemia/6 hours reperfused rectus femoris muscles of rats pretreated with allopurinol decreased electron density of mitochondrial matrix and spheromembranous bodies are seen. In 6 hours ischemia/6 hours reperfused rectus femoris muscles of rats pretreated with allopurinol, mitochondria with electron lucent matrix, spheromembranous bodies and dilated cisternae of sarcoplasmic reticulum and terminal cistern are observed. The results suggest that the allopurinol attenuates the damages of the skeletal muscles of rats during ischemia and reperfusion.
Chick embryos which have received a single injection of the organophosphate compound,malathion (0.1 mg, 0.5 mg, 1.0 mg or 2.0 mg in 0.05 ml of corn oil) via the yolk sac at certain times (2 daya, 4 days or 6 days after incubation) have been investigated. After 9 days of incubation, chick embryos were harvested to investigate the effects of malathion on the development of cerebrum morphologically and biochemically. The effects of simultaneous injection of malathion and nicotinamide were also compared. On ultrastructural examination, neurons in cerebral cortex showed to be inhibited in their differentiation by malathion; nuclear irregularity, swelling of endoplasmic reticulum, and cytoplasmic vacuoles were observed. On cytochemical study of acetylcholinesterase(AChE) by electron microscope, the positive reaction products of this enryme were localized at the membrane of nucleus and endoplasmic reticulum of neurons. Inhibition of AChE activty was severe in groups treated with relatively low doses, which was consistent with the results of spectrophotometric analysis. The activity of lactate dehydrogenase(LDH) of cerebrum in groups treated with malathion was higher than that of the control group. The nicotinamide adenine dinucleotide(NAD) content of chick embruo treated with malathioti decreased significantly, and nicotinamide coinjection raised the NAD level as compared with the control group, thus preventing malathion-induced momhological alteration. In conclusion, it is suggested that malathion changes the ultrastructure of differentiating neurons and alters some enzyme activities in chick embryo cerebrum, and the severity of which is consistently dose-or age-dependent.
The effects of diclazuril on the bursa of Fabricius (BF) structure and secretory IgA (SIgA) expression in chickens infected with Eimeria tenella were examined. The morphology of the BF was observed by hematoxylin and eosin staining, while ultrastructural changes were monitored by transmission electron microscopy. E. tenella infection caused the BF cell volumes to decrease, irregularly arranged, as well as, enlargement of the intercellular space. Diclazuril treatment alleviated the physical signs of damages associated with E. tenella infection. The SIgA expression in BF was analyzed by immunohistochemistry technique. The SIgA expression increased significantly by 350.4% (P<0.01) after E. tenella infection compared to the normal control group. With the treatment of diclazuril, the SIgA was relatively fewer in the cortex, and the expression level was significantly decreased by 46.7% (P<0.01) compared with the infected and untreated group. In conclusion, E. tenella infection in chickens induced obvious harmful changes in BF morphological structure and stimulated the expression of SIgA in the BF. Diclazuril treatment effectively alleviated the morphological changes. This result demonstrates a method to develop an immunological strategy in coccidiosis control.
A new sudden death in rabbits appeared in China and Korea in 1984 and 1985, respectively, and was recognized to be an acute infectious disease caused by a virus. The disease was reported as a "new viral disease," and thereafter, a tentative name of "viral hemorrhagic disease", "hemorrhagic pneumonia" or "viral hemorrhagic pneumonia" has been described in the case reports. But authors had called the viral disease "rabbit viral hepatitis" due to picornavirus infection, because the principal lesion of the disease was an acute hepatitis. The purpose of this report is to describe the electron microscopic findings on the livers in experimentally infected rabbits. All the livers of the affected rabbits were shown to have degenerative changes of a type that is characteristic of acute hepatitis. In the liver cells, there were dilation of rER and mitochondria, vacuole formation of various sizes, and appearances of many virus-like particles in the vicinity of rER, granular bodies and crystalline arrays of viral particles in the cytoplasm with necrotic changes of the nucleus. Clusters of virus-like particles and viral crystals appeared in the cytoplasm of sinusoid endothelial cells and Kupffer's cells with morphological changes of organelles. Also viral crystals were demonstrated in the cytoplasm of macrophages among the liver cells. On the whole, the liver cells had many virus-like particles and a few crystalline arrays of viral particles. Therefore, this implies that the liver cells are the main site of the viral replication in inducing the viremia. It was concluded that the liver was the primary target organ of this viral disease, and the pathological and the ultrastructural evidence suggest that the virus may be belong to genus enterovirus.
Distraction osteogenesis (DO) is frequently used technique in reconstruction of bony defects resulted from tumor resection, congenital deformity, and trauma in the maxillofacial region. Although the histologic and ultrastructural changes associated with distraction osteogenesis have been extensively described, the exact changing of the surrounding tissues, such as nerve tissues, were still unclear. This study observed the histological changes and the expression of nerve growth factor (NGF) in the inferior alveolar nerve (IAN) after distraction osteogenesis. Unilateral mandibular distraction (0.5 mm twice per day for 10 days) was performed in eight mongrel dogs. Two animals were sacrificed at 7, 14, 28 and 56 days after completion of distraction, respectively. The distracted IAN and contralateral control nerve were harvested and processed for histological and innunohistochemical examinations. The signs of acute nerve injuries, such as demyelination and partial discontinuation of nerver fiber, were observed in the distracted IAN on 7 and 14 days after distraction. The initial remyelination and regeneration of distracted IAN were showed at 14 days after completion of distraction. At 56 days later, the histologic features of distracted IAN was similar to those of the normal control IAN. The expression of NGF was significantly increased in most distracted nerve tissues on 7, 14 and 28 days after distraction. On 56 days after distraction, the expression of NGF returned to the normal level. This study suggested that the acute IAN injury caused by mandibular distraction were mostly recovered during consolidation period. The NGF was seemed to be induced from Schwann cell and damaged nerve tissues, and it may have important roles in the initial healing of damaged nerves.
The morphological changes of Sertoli cells of the Korean native pheasant were studied in the active and inactive spermatogenic phases. Twenty-four male of the pheasants were studied in the active (April~June) and inactive(August~March) phase. These data are useful in studying the male genital organs of the Korean native pheasant. Light microscopic morphological changes of the Sertoli cells were studied on paraffin-embedded sections stained with hematoxylin-eosin stain. Ultrastructural changes of Sertoli cells were investigated of ultrathin section using electron microscope. Results are summarized as follows: During the active phase, the average diameter of seminiferous tubule was $245.33{\pm}29.93{\mu}m$ and was largely decreased by $94.50{\pm}14.10{\mu}m$, and the thickness of interstitial tissue was comparatively increased during the inactive phase. During the active phase, in the cytoplasmic process of Sertoli cell and lipid droplets appeared disperse. Well-developed smooth Endoplasmic Reticulum and microtuble were observed in the cytoplasmic process. The nuclei of Sertoli cells were adjacent to the basement membrane. The size of nuclei was reduced and nuclei of Sertoli cells were densely packed within the tubule. Few collagen fibers, fibroblast and various sizes of lipid droplets were observed in the interstitial cell of the seminiferous tubule.
This study was made to investigate the ultrastructural changes of the hepatocyte of the maternal liver, and fetal liver by Actinomycin D in Wistar rats at the stage of pregnancy. Peritoneal injection of Actinomycin D to rats carried out gestation day 7 to 9 at the level of $15{\mu}g(11.5{\mu}g/100g$ body wt.), $20{\mu}g(15.8{\mu}g/100g$ body wt.) on each day. Treated animals with saline only were used for controls. Animals were sacrificed on day 15 of gestation. On electron microscopic examination, the hepatocytes of maternal liver given Actinomycin D $15{\mu}g$/ml had evidence of serious cellular damage, for example, hypertrophy of rough endoplasmic reticulum, loss in nucleolar osmiophilia, swelling of Golgi apparatus and change of mitochondrial structure. Maternal liver given Actinomycin D $20{\mu}g/ml$ shown similar changes to that of the $15{\mu}g/ml$ treated animals. But mitochondria of this group were not changed than that of $15{\mu}g/ml$ treated group. In the hepatocytes of fetal liver, changes were more pronounced. The drug produced alteration in nuclei and cytoplasm. The rough endoplasmic reticulum was swollen and there were ribosomes detachement. In addition, damages of mitochondria, Golgi apparatus were detected.
The unwanted artificial oil-spill has severely contaminated the coastal environment in the world. Level of contamination has so far been monitered by various indicator species including mussel, oysters, flounder, and cockle. In this study, we decided to use the oyster as a model organism to observe the morphological changes being exposed to the artificial oil-spill in the coastal areas in Taean, Korea. The oysters were collected from four local sites (Sindu-ri, Uiwang-ri, Jonghyeon-dong, Ansan and Uihang-ri) exposed to various levels of pollution after an oil spill in Taean. Microscopic analysis of the hepatopancreatic microstructure in the digestive gland from the collected oysters show that the swelling, whorl, and destruction phenomenon of the nuclear membrane, a well-known microstructure induced by heavy metal exposure, was observed. Nuclear body (Nb), another typical characteristic of contamination or infection were also observed in some samples. Necrosis was observed in tissue samples collected from the area with a high degree of oil pollution. In addition, parasite-like particles (virus, perkinsus) were observed in most samples. Taken together, these results suggest that oil contamination in the oyster habitats influences the cytopathological changes in Crassostrea gigas.
Ultrastmctura changes of multivesicular bodies and mitochondria of oocytes of PseudopotamU- Ia occelata Moore were examined with transmission electron microscope in order to follow the process of yolk formation. Yolk granules begin to form at the previtellogenic stages of 50 $\mu$m diameter from multivesicular bodies. Small vesicles and membranous structures within the multivesicular bodies are fused to form the precursors of core bodies of yolk granules. Some vesicles from cytoplasm are also coalesced into the multivesicular bodies. Mature yolk granules are composed of electron-dense core bodies which are seperated from each other by electronopaque small vesicle-like structures. Structural changes of cristae into vesicular shapes and increase in electron density of matrix in mitochondria strongly suggested that mitochondria are in the process of transformation. The transformed mitochondria appear to be basic structures which later become multivesicular bodies.
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