• 대한방사선기술학회지:방사선기술과학
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• 제43권1호
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• pp.29-34
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• 2020

Mitochondria was observed much around the nuclear membrane of liver tissue where the energy metabolism process is active. Testis tissue had a large number of undifferentiated cells, and cristae in Inner membrane of Mitochondria was not observed clearly. Morphological damage occurred first in Inner membrane rather than the outer membrane. The kidney tissue was clearly observed in the form of cristae. Radiation-induced damage occurred at the edges of both ends, and the membrane was observed bursting with the thickness of the outer membrane. Small intestine cells were observed in many mitochondria in the tissues around the villus, where bowel movements were active. Morphological damage occurred with the outer and inner membranes getting tangled. Mitochondria sensitivity to radiation was sensitized in testis and small intestine tissues, and kidney, ovary and liver tissues were found to be resistant.

• Journal of Yeungnam Medical Science
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• 제41권2호
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• pp.61-73
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• 2024

Acute kidney ischemia-reperfusion (IR) injury is a life-threatening condition that predisposes individuals to chronic kidney disease. Since the kidney is one of the most energy-demanding organs in the human body and mitochondria are the powerhouse of cells, mitochondrial dysfunction plays a central role in the pathogenesis of IR-induced acute kidney injury. Mitochondrial dysfunction causes a reduction in adenosine triphosphate production, loss of mitochondrial dynamics (represented by persistent fragmentation), and impaired mitophagy. Furthermore, the pathological accumulation of succinate resulting from fumarate reduction under oxygen deprivation (ischemia) in the reverse flux of the Krebs cycle can eventually lead to a burst of reactive oxygen species driven by reverse electron transfer during the reperfusion phase. Accumulating evidence indicates that improving mitochondrial function, biogenesis, and dynamics, and normalizing metabolic reprogramming within the mitochondria have the potential to preserve kidney function during IR injury and prevent progression to chronic kidney disease. In this review, we summarize recent advances in understanding the detrimental role of metabolic reprogramming and mitochondrial dysfunction in IR injury and explore potential therapeutic strategies for treating kidney IR injury.

• Applied Microscopy
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• 제19권2호
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• pp.43-58
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• 1989

To investigate the effects of hexavalent chromium on mitochondrial respiration of rat kidney, various hexavalent chromium concentrations were treated, then respiration and electron transfer enzyme activities were measured. Ultrastructural changes at state IV respiration of mitochondria were also observed. Then, to investigate protective role against hexavalent chromium in the body, low-molecular-weight, chromium-binding substances (LMCr) were purified from livers of rabbits 2hr after intravenously administrated with sodium dichromate at a dose of 74mg per kg body weight. And then, respiration rates of mitochondria treated with LMCr, hexavalent chromium containing 0.7mM chromium were measured. Hexavalent chromium decreased state IV respiration rates and electron transfer enzyme activities of mitochondria, and increased labile membrane and swelling. And partial inhibitions of condensed to orthodox conformational change were observed. Respiration rates of mitochondria treated with LMCr containing 0.7mM chromium did not differ from that of the non-treated mitochondria. But respiration rates of 0.7mM hexavalent chromium-treated mitochondria decreased by 42%, compared to non-treated mitochondria. These results suggest that LMCr may play an important role in detoxification of toxic hexavalent chromium.

• Applied Microscopy
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• 제19권2호
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• pp.59-73
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• 1989

To investigate the effect of cadmium and cadmium binding protein on the electron transport system and conformational changes of rat kidney mitochondria, various cadmium concentration were treated in vitro and respiration rate, NADH-CoQ reductase activity were measured. Ultrastructural changes at state IV respiration were also observed. CdBP was isolated from the rat liver by Sephadex G-75 column fractionation and treated in vitro with cadmium. Also mitochondrial state IV respiration rate was measured. When cadmium was treated in vitro, state IV respiration and enzyme activity were decreased and ultrastructural transformation of mitochondria from a condensed to an orthodox conformation was inhibited under state IV respiration. In case cadmium and CdBP were treated together, oxygen consumption was more increased than cadmium only. Conformational changes of mitochondria from a condensed to orthodox conformation were also observed. This indicates that CdBP have a protective effect against cadmium toxicity.

• 한국동물학회지
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• 제21권3호
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• pp.87-102
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• 1978

수은이 붕어(Carassius carassius L.)의 간, 신장 아가미에 미치는 영향을 규명하기 위하여 붕어를 1 ppm, 2.5 ppm 농도의 $HgCl_2$에 노출시킨 후 전자현미경을 사용하여 그들의 미세구조 변화에 대한 연구를 수행한 바 다음과 같은 결과를 얻었다. 1. 수은에 처리된 간세포에서는 lysosome이 증가하였으며 결정상의 구조물들을 포함한 원형의 lysosome과 히ㅛ\ulcorner두과립이나 mitochondria를 탐식한 lysosome의 2가지 형태가 관찰되었고 mitochondria는 팽대되어 내부 기질의 전자밀도가 감소되었으며 핵에서는 인의 분리현상이 관찰되었다. 2. 신장의 변화로서는 신사구체 기저막의 비후와 기부선회소관에서는 공포들의 증가와 cytoplasmic body들이 출현하였으며 공포형성은 mitochondria와 연관되어 일어났다. 또한 2.5 ppm에서는 핵의 위축이 관찰되었다. 3. Gill lamella의 상피세포에서는 대, 소형의 lysosome이 증가했으며 lamella의 막에 fuzzy한 구조가 관찰되었다. 4. 본 실험에서 관찰된 결과로써 수은에 의해 초래된 세포의 미세구조의 변화는 세포의 해독과정을 활성화시키며 energy대사과정을 손상시키는 것으로 생각된다.

• The Korean Journal of Physiology and Pharmacology
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• 제3권6호
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• pp.631-640
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• 1999

The present study investigated the stimulatory effects of iron (or ascorbate) on cyclosporine-induced kidney mitochondrial damage. Damaging effect of $50\;{\mu}M$ cyclosporine plus $20\;{\mu}M\;Fe^{2+}$ on mitochondrial lipids and proteins of rat kidney and hyaluronic acid was greater than the summation of oxidizing action of each compound alone, except sulfhydryl oxidation. Cyclosporine and $100\;{\mu}M$ ascorbate showed an enhanced damaging effect on lipids but not on proteins. The peroxidative action of cyclosporine on lipids was enhanced with increasing concentrations of $Fe^{2+}.$ Ferric ion $(20\;{\mu}M)$ also interacted with cyclosporine to stimulate lipid peroxidation. Damaging action of cyclosporine on mitochondrial lipids was enhanced by ascorbate $(100\;{\mu}M\;and\;1\;mM)$. Iron chelators, DTPA and EDTA, attenuated carbonyl formation induced by cyclosporine plus ascorbate. Cyclosporine $(100\;{\mu}M)$ and $50\;{\mu}M\;Fe^{2+}$ $(or\;100\;{\mu}M\;ascorbate)$ synergistically stimulated degradation of $2-{\alpha}$ deoxyribose. Cyclosporine $(1\;to\;100\;{\mu}M)$ reduced ferric ion in a dose dependent manner, which is much less than ascorbate action. Addition of $Fe^{2+}$ caused a change in absorbance spectrum of cyclosporine in $230{\sim}350$ nm of wavelengths. The results show that cyclosporine plus iron (or ascorbate) exerts an enhanced damaging effect on kidney mitochondria. Iron and ascorbate appear to promote the nephrotoxicity induced by cyclosporine.

• 한국동물학회지
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• 제30권3호
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• pp.239-247
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• 1987

생쥐 신장의 근위세뇨관과 원위세뇨관 세포의 미세구조에 미치는 염화 메틸수은의 독성에 대한 홍삼유출물의 첨독성적 영향을 전자현징경적으로 연구하였다. 염화 메틸수은 처리군의 근위세뇨관 세포에서는 대조군에서 보다 철세 융모가 다소 축소되고 불규칙한 배열을 하였다. Brush border의 인접 부위에서는 작은 경계들이 나타나고 세포질 중앙 부위에서는 치밀체를 함유한 큰 육포들이 관색되었다. Mitochondria는 상당히 팽대되고 기양막은 부분적으로 비후되었으며 다수의 ITsosome이 나타났다. 염화 메틸수은 처리군의 원위세뇨관 세롱에서는 불규칙한 세포 표면, 양사된 세포, 그리고 다수의 ribosome과 소수의 지방사이 나타났으며 mitochondria 는 팽대되고 기고막은 부분적으로 비후되었다. 염화 메틸수은-홍삼추출물 병행 처리군의 근위세뇨관 세포에서는 염화 메틸수은 처리군에서 보다 mitochondria의 팽대 정도가 감소되었으며 육포의 크기와 수도 상당히 감소되었다. 염화 메틸수은-홍모적출물 병행 처리군의 원위세뇨관 세롱에서는 세포 표면이 어느정도 규칙적이고 mitochondria의 정해와 기저막의 비후 정도가 감소되어 정상 세포와 거의 유사하였다.

• 대한약리학회지
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• 제14권1_2호
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• pp.1-11
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• 1978

가토 심실근에서 추출한 mitochondria에서 $Na^+$ 및 $K^+$이온에 의한 $Ca^{++}$ 유리작용을 관찰하였다. 반응액에 첨가한 1-3mM의 소량 $Na^+$은 mitochondria막에 미리 결합되어있던 $Ca^{++}$을 현저히 유리시켰으며, $K^+$은 단독으로는 $Ca^{++}$ 유리를 유도하지 않았으나 $Na^+$에 의한 $Ca^{++}$ 유리에 대하여는 $Na^+/K^+$비에 따라 그것이 클수록 $Ca^{++}$ 유리를 증가시켰다. 간 및 신장 mitochondria에서도 $Na^+$에 의하 $Ca^{++}$ 유리현상을 보였으나 심근mitochondria에 비하여 $Na^+$에 대한 감수성이 훨씬 미약하여 약 $1/10{\sim}1/5$에 지나지 않았다. 이와같은 mitochondria의 $Ca^{++}$ 유리현상은 비교적 $Na^+$에 특이한 작용이었으며 다른 일가양이온중에서는 $Li^+$에 의해서만 어느 정도 보였다. 부전심근 mitochondria에서의 $Na^+$에 의한 $Ca^{++}$유리는 정상심근 mitochondria에서와 같았으며 이때 digitalis 강심배당체가 직접적으로는 별 영향을 미치지 않았다. 이상에서 심근의 경우 mitochondria는 세포내 $Ca^{++}$을 조절할 수 있는 기구로서 심근수축의 E-C coupling과정에서 세포막의 전기적 흥분현상과 결부하여 $Ca^{++}$을 유리할 수 있을 것으로 추정하였으며, 한편 digitalis배당체의 강심작용기전에 있어서는 digitalis 배당체에 의한 세포막의 $Na^+$, $K^+$-ATPase 억제결과 초래될 수 있는 세포내의 $Na^+$ 증가 및(또는) $K^+$감소가 간접적으로 mitochondria에서부터 $Ca^{++}$ 유리를 증가하여 E-C coupling 과정을 촉진할 수 있을 것을 사료하였다.

• Applied Microscopy
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• 제17권1호
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• pp.115-130
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• 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.

• Journal of Medicine and Life Science
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• 제15권2호
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• pp.37-41
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• 2018

Mitochondrial injury in renal tubule has been recognized as a major contributor in acute kidney injury (AKI) pathogenesis. Ischemic insult, nephrotoxin, endotoxin and contrast medium destroy mitochondrial structure and function as well as their biogenesis and dynamics, especially in renal proximal tubule, to elicit ATP depletion. Mitochondrial fatty acid ${\beta}$-oxidation (FAO) is the preferred source of ATP in the kidney, and its impairment is a critical factor in AKI pathogenesis. This review explores current knowledge of mitochondrial dysfunction and energy depletion in AKI and prospective views on developing therapeutic strategies targeting mitochondrial dysfunction in AKI.