• 한국산림과학회지
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• 제80권1호
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• pp.97-102
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• 1991

포플러류의 식물체(植物體)와 그 식물체(植物體)에서 분리(分離)한 미토콘드라아를 동위효소(同位酵素) 분석(分析)하여, 각 동위효소(同位酵素)의 세포내(細胞內) 위치(位置)를 규명(糾明)하였다. 분석(分析)한 동위효소(同位酵素)는 ADH, 6-PGD, MDH, PGI와 Diaphorase였다. ADH는 세포질(細胞質)에 있으며, 핵내(核內)에 있는 한개의 유전자좌(遺傳子座)에 의(依)해 지배(支配)되는 것으로 나타났고, 6-PGD는 mitochondria에 있는 것으로 나타났다. MDH는 세포질(細胞質)에 3개의 band, mitochondria에 4개의 band가 있는 것으로 나타났다. PGI는 세포질(細胞質)에 3개의 band가 있는 듯하며, Diaphorase는 mitochondria에 1개의 band, 세포질(細胞質)에 2개의 band가 있는 것으로 나타났다. 세포질(細胞質)에 있는 두개의 band는 핵내(核內)에 있는 1개의 유전자좌(遺傳子座)에 있는 유전자(遺傳子)에 의(依)해 지배(支配)되는 것으로 판단되었다.

• BMB Reports
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• 제55권11호
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• pp.528-534
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• 2022

Mitochondria are cellular organelles that perform various functions within cells. They are responsible for ATP production, cell-signal regulation, autophagy, and cell apoptosis. Because the mitochondrial proteins that perform these functions need Ca²⁺ ions for their activity, mitochondria have ion channels to selectively uptake Ca²⁺ ions from the cytoplasm. The ion channel known to play the most important role in the Ca²⁺ uptake in mitochondria is the mitochondrial calcium uniporter (MCU) holo-complex located in the inner mitochondrial membrane (IMM). This ion channel complex exists in the form of a complex consisting of the pore-forming protein through which the Ca²⁺ ions are transported into the mitochondrial matrix, and the auxiliary protein involved in regulating the activity of the Ca²⁺ uptake by the MCU holo-complex. Studies of this MCU holo-complex have long been conducted, but we didn't know in detail how mitochondria uptake Ca²⁺ ions through this ion channel complex or how the activity of this ion channel complex is regulated. Recently, the protein structure of the MCU holo-complex was identified, enabling the mechanism of Ca²⁺ uptake and its regulation by the MCU holo-complex to be confirmed. In this review, I will introduce the mechanism of action of the MCU holo-complex at the molecular level based on the Cryo-EM structure of the MCU holo-complex to help understand how mitochondria uptake the necessary Ca²⁺ ions through the MCU holo-complex and how these Ca²⁺ uptake mechanisms are regulated.

• 한국영양학회:학술대회논문집
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• 한국영양학회 1992년도 춘계심포지움 및 발표논문 초록
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• pp.20-21
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• 1992

• 한국동물학회지
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• 제11권1호
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• pp.5-12
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• 1968

有尾兩棲類중 Triturus pyrrhogaster에서 人爲的으로 水晶體를 摘出하면, 虹彩의 瞳孔周緣上部中央의 色素上皮가 水晶體로 metaplasia 하는 것은 옛적부터 알려진 事實이다. 이 過程에는 色素上皮의 脫色增殖과 水晶體原基(水晶體胞)의 形成이 보이며 그 後의 水晶體形成은 正常發生의 그것과 全혀 같은 樣相으로 進行한다. 虹彩色素上皮의 細胞가 水晶體의 細胞로 變하는 過程에 대하여서는 벌써 Eguchi, Karasaki 等에 依하여 subcellular level의 解析 報告되었다. Eguchi(1964)의 報告에 依하면 細胞構成要素中 endoplasmic reticulum(ER) 및 mitochondria의 變化가 特히 興味를 끈다. ER 는 脫色이 完了된 細胞에서 核外膜의 泡狀變形에 依하여 形成된 事實로서 觀察되었으며, mitochondria 의 形態 크기 數의 變化도 顯著하였다. 本硏究는 ER 와 mitochondria를 問題의 焦點으로하여 活潑히 伸長되고있는 水晶體纖維細胞中 이 兩者의 細胞構造가 어떤 消長을 나타내는가를 電子顯微鏡으로서 調査한 것이다. 水晶體纖維는 立方狀의 水晶體上皮細胞가 水晶體의 後壁(網膜側)에서 伸長分化한 것인데 ER는 그의 基部 特히 核의 周邊에서만이 顯著한 發達을 나타내고 있었다. 또한 核外膜 은 顯著한 泡狀變化로서 近處의 ER에 連結되어 있었다. 核周邊의 ER는 一般的으로 reticular 構造를 나타내지 않고 큰 cisternae 空間을 가졌다. 그것은 外圍에 있는 粗面構成에 附着시키고 있었다. 一方 小型의 胞狀構造는 細胞質內에 散在 하고있었는데 여기에도 ribosome의 附着이 間或 觀察되는 까닭에 亦是 ER의 一斷面이라고 推定되었다. 纖維細胞의 核에서 먼 伸張端(apical portion)에 있는 ER의 構造는 漸次 沈滯하여 胞狀이 보였다. mitochondria에 對하여서도 ER와 같이 基部核周邊에 發達이 顯著하였다. ER의 周邊에도 密集하여 存在하며 間或 ER의 膜構造와 mitochondria의 外膜이 密接한 것도 觀察되었다. 이와같은 境遇의 ribosome은 polysome狀으로 되어서 緻密하게 散在하여 核의 周邊部에서 水晶體 protein의 合成이 旺盛하게 集行되고 있는 것이라고 推察될만한 微細構造上의 關係를 나타내고 있었다. 纖維의 伸張端近處의 mitochondria는 多少變形되어, 空胞化가 甚하며 때로는 mierin 狀重層膜構造를 連結시키며 大小多數의 胞狀構造와도 共存하고 있었다. 또 細胞間隔에도 이와같은 構造의 樣狀이 認定되는 것도 間或 있었다. 以上 水晶體纖維細胞의 核周邊部에 있어서 ER, mitochondria의 顯著한 發達像은, 核內 RNA 合成의 上昇에서 보이는 polysome의 增加에 뒷받침되는 硏究다. 卽 水晶體蛋白質의 合成에 큰 役割을 나타내는 것이라고 생각된다. 纖維가 伸張하는데 따라서 이들 膜構造는 漸次 細胞의 伸張端에서 退化를 始作하여 消失하는 像을 보이고 있으며 細胞의 退化消失에서도 確認되었다.

• The Korean Journal of Physiology and Pharmacology
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• 제16권3호
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• pp.181-186
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• 2012

Fenofibrate is a selective peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) activator and is prescribed to treat hyperlipidemia. The mechanism through which $PPAR{\alpha}$ agonists reduce food intake, body weight, and adiposity remains unclear. One explanation for the reduction of food intake is that fenofibrate promotes fatty acid oxidation and increases the production of ketone bodies upon a standard experimental dose of the drug (100~300 mg/kg/day). We observed that low-dose treatment of fenofibrate (30 mg/kg/day), which does not cause significant changes in ketone body synthesis, reduced food intake in Long-Evans Tokushima (LETO) rats. LETO rats are the physiologically normal controls for Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which are obese and cholecystokinin (CCK)-A receptor deficient. We hypothesized that the reduced food intake by fenofibrate-treated LETO rats may be associated with CCK production. To investigate the anorexic effects of fenofibrate in vivo and to determine whether CCK production may be involved, we examined the amount of food intake and CCK production. Fenofibrate-treated OLETF rats did not significantly change their food intake while LETO rats decreased their food intake. Treatment of fenofibrate increased CCK synthesis in the duodenal epithelial cells of both LETO and OLETF rats. The absence of a change in the food intake of OLETF rats, despite the increase in CCK production, may be explained by the absence of CCK-A receptors. Contrary to the OLETF rats, LETO rats, which have normal CCK receptors, presented a decrease in food intake and an increase in CCK production. These results suggest that reduced food intake by fenofibrate treatment may be associated with CCK production.

• Journal of Applied Biological Chemistry
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• 제57권3호
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• pp.259-265
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• 2014

Mitochondrial DNA (mtDNA)-depleted (${\rho}^0$) cells are often used as mtDNA recipients to study the interaction between the nucleus and mitochondria in mammalian cells. Therefore, it is crucial to obtain mtDNA-depleted cells with many different nuclear backgrounds for the study. Here, we demonstrate a rapid and reliable method to isolate mammalian mtDNA-depleted cells involving treatment with the antimitochondrial agents ethidium bromide (EtBr) and 2',3'-dideoxycytidine (ddC). After a short exposure to EtBr or ddC, followed by rapid clonal isolation, we were able to generate viable mtDNA-depleted cells from mouse and human cells and were able to successfully repopulate them with exogenous mitochondria from platelets isolated from mouse and human blood samples. These mtDNA-depleted cells can be used to characterize the nuclear mitochondrial interactions and to study mtDNA-associated defects in mammalian cells. Our method of isolating mtDNA-depleted cells is practical and applicable to a variety of cell types.

• 한국어류학회지
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• 제19권4호
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• pp.286-291
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• 2007

칼납자루 Acheilognathus koreensis 정자의 미세구조를 전자현미경으로 관찰하였다. 칼납자루 정자의 미세구조는 잉어과 어류정자의 일반적인 구조와 같이 둥근 두부, 얕은 핵와, 세포의 측면에 위치한 편모구조 그리고 비 대칭적인 편모구조의 특징을 취하고 있었다. 그러나 중편에 위치한 미토콘드리아는 대부분의 잉어류에서와는 달리 융합되어 하나를 형성하고 있으며 그 주위를 막성 구조물들이 둘러싸고 있었다. 하나로 융합된 미토콘드리아를 가지는 정자의 구조는 여러개로 나타나는 것에 비하여 경골어류에서는 파생형질로 알려져 있다. 잉어류 정자에서 미토콘드리아가 융합되어 하나로 나타나는 구조는 Rodeus와 Puntungia에서 보고되어 있으며 그 주위를 막성구조물이 둘러싸고 있는 것은 납자루류에서만 보고되고 있다.

• Journal of Chest Surgery
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• 제19권2호
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• pp.197-208
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• 1986

Propranolol is one of clinically useful antiarrhythmic agents and electrophysiologically classified as group II. And the negative inotropic effect which is not related to adrenolytic effect has been demonstrated with high concentration of propranolol. On the other hand, it has been well known that the calcium plays a central role in excitation-contraction coupling process of myocardium and also in electrophysiological changes of cell membrane. Author studies the effect of propranolol on calcium uptake and release in sarcoplasmic reticulum and mitochondria prepared from porcine myocardium to investigate the mechanism of action of propranolol on myocardium. The results are summarized as follow: 1] The maximum Ca++-uptake of sarcoplasmic reticulum is inhibited by propranolol in a dose dependent manner. 2] The release of calcium from sarcoplasmic reticulum is not affected by propranolol but with higher than 1x10-3 M of propranolol, rate of calcium release from sarcoplasmic reticulum is decreased. 3] Propranolol inhibits the maximum uptake and uptake rate of calcium in mitochondria non-competitively. [Ki = 6.21 x 10-4 M] 4] The rate of Na+ induced calcium release from mitochondrion shows a function of [Na+]2 and is inhibited by propranolol with the concentration significantly lower than that affect the calcium uptake in sarcoplasmic reticulum and in mitochondria [Ki = 2.91 x 10-5 M]. These results suggest that propranolol affects the intracellular calcium homeostasis which may considered to be one of the mechanism of action of propranolol on myocardium.

• Applied Microscopy
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• 제26권3호
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• pp.315-328
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• 1996

This study aims to demonstrate the effect of SOD (superoxide dismutase), one of the antioxidant enzymes, on the ultrastructural changes in the parietal cells caused by the administration of cisplatin in the rat. A total of 60 healthy Sprague-Dawley rats weighing about 200 gm were used as experimental animals. Cisplatin (6 mg/kg) was administered intraperitoneally to rats pretreated with 15,000 unit/kg of SOD or rats without the pretreatment. The experimental animals were sacrificed at 6 hours, 12 hours, 24 hours and 3 days after the administration of cisplatin. The results were as follows: 1. SOD alone did not affect the ultrastructural changes in the gastric parietal cells in the rat. 2. Irregular shaped mitochondria, mitochondria with dim cristae, dilated cristae, ruptured outer membrane, electron lucent matrix and degenerative mitochondria were seen in cisplatin treated rat. Whorled membranous body, many lysosomes and large vacuole were observed in the gastric parietal cells in cisplatin treated rat. 3. Mitochondria with dilated cristae and electron lucent matrix and irregular shaped mitochondria were observed in the gastric parietal cells of the cisplatin treated rat with pretreatment of SOD. These results suggest that SOD attenuates the toxic effect of the cisplatin in the gastric parietal cells of the rat.

• 한국동물번식학회:학술대회논문집
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• 한국동물번식학회 2001년도 춘계학술발표대회
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• pp.12-12
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• 2001

To get insight into the nature of foreign mitochondria and syngamy during mammalian fertilization we compared fertilization processes in porcine oocytes following microinjection of porcine or mouse spermatozoa. Pronuclear movement, sperm mitochondria, and DNA synthesis were imaged with propidium iodide, mitotracker, and BrdU under confocal laser scanning microscope. Intracytoplasmic injection of either porcine or mouse spermatzoon activated porcine oocytes without additional parthengenetic stimulation. Foreign mitochondria in either mouse or porcine sperm midpiece were introduced into porcine oocytes following sperm injection, but rapidly disappeared from the actively developing porcine oocytes. BrdU experiment showed new DNA synthesis in porcine oocytes following injection of mouse spermatozoon or sperm head. At 24 h after injection of mouse isolated sperm head or a spermatozoon, mitoic metaphase was seen in oocyte, but they did not go to normal cell division (Table). These results suggest that pronuclear formation, foreign mitochondria disruption, DNA synthesis and syngamy formation during fertilization are not species specific processes.(Table Omitted).