• Journal of Fisheries and Marine Sciences Education
• /
• v.28 no.5
• /
• pp.1231-1243
• /
• 2016

The ultrastructural study on oocyt development and the process of vitellogensis in the oocytes during oogenesis in female Pampus echinogaster were investigated by electron microscope observations. In the previtellogenic phase, in particular, several intermitochondrial cements appear in the cytoplasms of the chromatin nucleleolus oocyte and perinuclear oocyte. The number of intermitochondrial cements are associated with the multiplication of the number of mitochondria in the early developmental stage. In the early vitellogenic phase, the Golgi complex in the cytoplasm of the yolk vesicle oocyte is involved in the formation of yolk vesicles containing carbohydrate yolks. At this time, many pinocytotic vesicles containing yolk precursors (exogenous substances) by pinocytosis are observed in the cytoplasm near the region of initial formation of the zona pellucida. In the late vitellogenic phase, two morphological different bodies, which formed by the modified mitochondria, appeared remarkably in the yolked oocytes. The one is the multivesicular bodies and another is yolk precursors. The multivesicular bodies were transformed into the primary yolk globules, while yolk precursors were connected with exogeneous pinocytotic vesicles near the zona pellucida. After the pinocytotic vesicles were taken into yolk precursors, the yolk precursors were transformed into the primary yolk globules. Thereafter, primary yolk globules mixed with each other, eventually, they developed into secondary and tertiary yolk globules. In this study, vitellogenesis of this species occurred by way of endogenous autosynthesis and exogenous heteogenesis. Vitellogenesis occurred through the processes of endogeneous autosynthesis, involving the combined activity of the Golgi complex, mitochondria and multivesicular bodies formed by modified mitochondria. However, the process of heterosynthesis involved pinocytotic incorporation of extraovarian precursors (such as vitellogenin in the liver) into the zona pellucida (by way of granulosa cells and thecal cells) of vitellogenic oocytes.

• BMB Reports
• /
• v.42 no.11
• /
• pp.719-724
• /
• 2009

Recent studies have revealed that endoplasmic reticulum (ER) disturbance is involved in the pathophysiology of neurodegenerative disorders, contributing to the activation of the ER stress-mediated apoptotic pathway. Therefore, we investigated here the molecular mechanisms underlying the ER-mitochondria axis, focusing on calcium as a potential mediator of cell death signals. Using NT2 cells treated with brefeldin A or tunicamycin, we observed that ER stress induces changes in the mitochondrial function, impairing mitochondrial membrane potential and distressing mitochondrial respiratory chain complex Moreover, stress stimuli at ER level evoked calcium fluxes between ER and mitochondria. Under these conditions, ER stress activated the unfolded protein response by an overexpression of GRP78, and also caspase-4 and-2, both involved upstream of caspase-9. Our findings show that ER and mitochondria interconnection plays a prominent role in the induction of neuronal cell death under particular stress circumstances.

• Journal of Integrative Natural Science
• /
• v.6 no.3
• /
• pp.125-137
• /
• 2013

Promising evidence suggests that amyloid beta peptide ($A{\beta}$), a key mediator in age-dependent neuronal and cerebrovascular degeneration, activates death signalling processes leading to neuronal as well as non-neuronal cell death in the central nervous system. A major cellular event in $A{\beta}$-induced apoptosis of non-neuronal cells, including cerebral endothelial cells, astrocytes and oligodendrocytes, is mitochondrial dysfunction. The apoptosis signalling cascade upstream of mitochondria entails $A{\beta}$ activation of neutral sphingomyelinase, resulting in the release of ceramide from membrane sphingomyelin. Ceramide then activates protein phosphatase 2A (PP2A), a member in the ceramide-activated protein phosphatase (CAPP) family. PP2A dephosphorylation of Akt and FKHRL1 plays a pivotal role in $A{\beta}$-induced Bad translocation to mitochondria and transactivation of Bim. Bad and Bim are pro-apoptotic proteins that cause mitochondrial dysfunction characterized by excessive ROS formation, mitochondrial DNA (mtDNA) damage, and release of mitochondrial apoptotic proteins including cytochrome c, apoptosis inducing factor (AIF), endonuclease G and Smac. The cellular events activated by $A{\beta}$ to induce death of non-neuronal cells are complex. Understanding these apoptosis signalling processes will aid in the development of more effective strategies to slow down age-dependent cerebrovascular degeneration caused by progressive cerebrovascular $A{\beta}$ deposition.

• BMB Reports
• /
• v.52 no.1
• /
• pp.13-23
• /
• 2019

Aging is accompanied by a time-dependent progressive deterioration of multiple factors of the cellular system. The past several decades have witnessed major leaps in our understanding of the biological mechanisms of aging using dietary, genetic, pharmacological, and physical interventions. Metabolic processes, including nutrient sensing pathways and mitochondrial function, have emerged as prominent regulators of aging. Mitochondria have been considered to play a key role largely due to their production of reactive oxygen species (ROS), resulting in DNA damage that accumulates over time and ultimately causes cellular failure. This theory, known as the mitochondrial free radical theory of aging (MFRTA), was favored by the aging field, but increasing inconsistent evidence has led to criticism and rejection of this idea. However, MFRTA should not be hastily rejected in its entirety because we now understand that ROS is not simply an undesired toxic metabolic byproduct, but also an important signaling molecule that is vital to cellular fitness. Notably, mitochondrial function, a term traditionally referred to bioenergetics and apoptosis, has since expanded considerably. It encompasses numerous other key biological processes, including the following: (i) complex metabolic processes, (ii) intracellular and endocrine signaling/communication, and (iii) immunity/inflammation. Here, we will discuss shortcomings of previous concepts regarding mitochondria in aging and their emerging roles based on recent advances. We will also discuss how the mitochondrial genome integrates with major theories on the evolution of aging.

• BMB Reports
• /
• v.56 no.9
• /
• pp.488-495
• /
• 2023

Mitochondrial transplantation is a promising therapeutic approach for the treatment of mitochondrial diseases caused by mutations in mitochondrial DNA, as well as several metabolic and neurological disorders. Animal studies have shown that mitochondrial transplantation can improve cellular energy metabolism, restore mitochondrial function, and prevent cell death. However, challenges need to be addressed, such as the delivery of functional mitochondria to the correct cells in the body, and the long-term stability and function of the transplanted mitochondria. Researchers are exploring new methods for mitochondrial transplantation, including the use of nanoparticles or CRISPR gene editing. Mechanisms underlying the integration and function of transplanted mitochondria are complex and not fully understood, but research has revealed some key factors that play a role. While the safety and efficacy of mitochondrial transplantation have been investigated in animal models and human trials, more research is needed to optimize delivery methods and evaluate long-term safety and efficacy. Clinical trials using mitochondrial transplantation have shown mixed results, highlighting the need for further research in this area. In conclusion, although mitochondrial transplantation holds significant potential for the treatment of various diseases, more work is needed to overcome challenges and evaluate its safety and efficacy in human trials.

• Applied Microscopy
• /
• v.24 no.3
• /
• pp.55-66
• /
• 1994

This study was carried out to investigate the histological changes of sperm cells in testis, obtained from 100 of 3-year-old male rainbow trout (Oncorhynchus mykiss) collected and analysed from March in 1992 to February in 1993. Especially, the ultrastructural changes of spermatogonia, primary and secondary spermatocytes, spermatids, and spermatozoa were examined to describe the reproductive cycles of this species. The results obtained in this study were as follows: The ultrastructures of the gonadotrophs largely parallel the cyclical changes in the testes. Each nest of cells belongs to one spermatogenetic stage, although nests at different stages can be found within the one lobule. At first keterochromatin is dispersed and then is condensed. In mature gamete, the nucleus is dense and homogeneous. The nuclear membrane appeared at the beginning of differentiation. In spermatogonia, Sertoli cells are located at the periphery of their cytoplasm. In the primary spermatocytes, the small mitochondria are abundant over the outer cytoplasm. During cell differentiation, the cytoplasm decreases and the nucleus increases. In spermatids, the protein masses moved towards the posterior part of the nucleus. In late spermatids, the two large mitochondria are located over the cytoplasm. In spermatozoa, two spheroidal mitochondria (about 145nm long) are situated in parallel between the nucleus and the axoneme. Spermatozoa mitochondria are assembled into an organized sheath surrounding the outer dense fibres and axoneme of the flagellar midpiece. The two centrioles are quite separate and the central pair and sheath complex of the flagellum is inserted into the base of the distal centriole.

• Development and Reproduction
• /
• v.2 no.2
• /
• pp.141-148
• /
• 1998

The fine structure of spermatozoa of Pungtungia herzi was examined with scanning and transmission electron microscopies. The spermatozoa of p. herzi are approximately 37.4 ${\mu}{\textrm}{m}$ in length and a relatively simple cell with a spherical nucleus, a short midpiece and a tail. The acrosome is not present as in most teleost fishes. The ultrastructure of spermatozoa represents typical characteristics of cyprinid spermatozoa including the lateral insertion of flagellum, the organization of centriolar complex in shallow nuclear fossa, and the occurrence and asymmetrical arrangement of mitochondria. In the nuclear envelope and mitochondrion, however there were some morphological differences for their ultrastructure. The nuclear envelope is severely undulated and the shallow nuclear fossa contains two centrioles which are at the angle of some 130$^{\circ}$ each other. The most significant feature can be observed with the mitochondrion; five or more mitochondria, which are shown in primary spermatocyte, fuse to form a single one in the mature spermatozoon. The mitochondrial aspect is different from that of other cyprinid spermatozoa, where their mitochondria have a conventional aspect and never fuse to form a mitochondrial derivative. In terms of sperm evolution the fused mitochondria are regarded as the apomorphic character in comparison with the separate mitochondria. The single mitochondrion is not reported in cyprinid spermatozoon except the case of Rhodeus.

• Journal of Korean Neurosurgical Society
• /
• v.29 no.10
• /
• pp.1283-1288
• /
• 2000

Objectives : The subcellular locations of Bad, Bid, Bax and Bcl-XL change during apoptosis and this change is important for the regulation of cell death. The purpose this study was to elucidate binding of Bad with Bcl-XL in vivo Methods : We mads Bad with Green Fluorescent Protein(GFP) using PCR method. We transfected and overexpressed GFP-Bad with or without Bcl-XL cotransfection in living COS-7 cell. Results : Bad and Bcl- XL bind one another in healthy living cells and this association controled mitochondrial docking. In the absence of Bad-XL, Bad was mainly cytosolic and partially bound to mitochondria. Upon coexpression of Bad and Bcl-XL, most of Bad translocated to mitochondria. These should suggest that Bad binds to the mitochondrial and cytoplasmic forms of Bcl-XL and Bad bound to cytoplasmic Bcl-XL translocates to mitochondria. These in vivo findings confirm that Bad make a complexes with Bcl- XL and cause mitochondrial translocation of Bad-Bcl-XL complex.

• The Korean Journal of Zoology
• /
• v.16 no.1
• /
• pp.43-53
• /
• 1973

The flight muscles in Pieris rapae have been examined to study ultrastructural changes in mitochondria with aging. All the mitochondira of flight muscle from the butterfly are recognized as type A which has the simple folded cristae and light matrix, and type B which possesses the complex multicristae and dense matrix. In just newly emerged butterflies both A and B type mitochondria are almost equally present. About ten days after emergence the type A mitochondria rapidly decrease, compared with the type B. In ten-day-old butterflies the type B mitochondria vary in ultrastructure with age. Ultrastructural changes of these aged mitochondria are supposed to occur, in part, by reorganization of inner membranes into myelin-like structures which represent the phase of degeneration of the B type with age. Age-dependent increase in size and number of concentric rings in myelin-like whorl are also found. Glycogen particles penetrated from the cytoplasmic matrix of the muscle cell into the mitochondrial matrix to be in the center of their concentric rings.

• Korean Journal of Veterinary Research
• /
• v.37 no.1
• /
• pp.87-101
• /
• 1997

The development of trachea in fetuses on 60, 90 and 120 days of gestation and neonates of Korean native goats was investigated by microscopy and scanning and transmission electron microscopy. The results were summarized as follows; Light microscopic studies: 1. In the 60-day-old fetuses, the tracheal walls were differentiated and divided into four layers of the mucosa, submucosa, muscle and cartilage, and adventitia. The tracheal epithelium is composed of stratified ciliated columnar epithelium at 60- and 90-day-old fetuses while the epithelium observed at 120-day-old fetuses was pseudostraified ciliated colummar epithelium. 2. In the 90-day-old fetuses, tracheal glands extended into the submucosa and peripheral area of the tracheal cartilage. The blood vessels were observed in the submucosa and adventitia. The elastic and collagenous fibers were observed in the tracheal walls. 3. In the neonates, the tracheal walls consisted of mucosa with well-developed folds, submucosa, tracheal glands, muscle and cartilage, collagenous and elastic fibers, and adventitia, which were more developed than those of 120-day-old fetuses. The tracheal epithelium was developed as that in adults. Scanning electron microscopic studies: 4. In the 60-day-old fetuses, most of tracheal epithelial cells were nonciliated but short microvilli were sporadically observed on the luminal surface. On rare occasions, a few cells have solitary cilium. 5. In the 90-day-old fetuses, the ciliated cells appeared increasingly and cilia elongated longer than those of 60-day-old fetuses. 6. In the 120-day-old fetuses, the nonciliated cells covered with microvilli in dome-shape were barriered by thick carpet of cilia. The nonciliated cells also have many papillary projectons on the apical surface. 7. In the neonates, the nonciliated cells in tracheal epithelium were covered compactly with numerous cilia, and many secretory droplets were found on the cilia. Transmission electron microscopic studies: 8. In the 60-day-old fetuses, nonciliated cells of the tracheal epithelium contain large amounts of glycogen granules in the supernuclear and subnuclear areas meanwhile a few cell organelles were formed. Cilia were well formed along the apical cell membranes of the ciliated cells. Also found in the ciliated cells were basal corpuscles, mitochondria and short chains in granular endoplasmic reticulum(GER). Between the epithelial cells presented were well-defined junctional complex with zonula occludens and desmosomes. The nuclei were variable in size and shape. The more developed nucleoli were observed conspicuosly. 9. In the 90-day-old fetuses, nonciliated cells contained large glycogen granules. Accumulated glycogen granules were observed in the subnuclear and supranuclear portion of the cytoplasm. A few short microvilli were covered with glycocalyx. Ciliated cells contained numerous mitochondria and short chains of GER. 10. In the 120-day-old fetuses, the ciliated cells contained numerous mitochondria, abundant short chains of GER and nucleoli. Nonciliated cells contained some Golgi complex and mitochondria. The cell borders were well-defined and distinct junctional complex with zonula occludens, desmosomes, and interdigitorum. 11. In the neonates, well-developed goblet cells were observed in the tracheal epithelium. Ultrastructures of ciliated and nonciliated cells on the tracheal epithelia were similar in pattern as those in adults.