scholarly journals EFFECT OF GAMMA IRRADIATION ON THE DESOXYRIBONUCLEASE II ACTIVITY OF ISOLATED MITOCHONDRIA

1957 ◽  
Vol 3 (2) ◽  
pp. 239-248 ◽  
Author(s):  
Shigefumi Okada ◽  
Lee D. Peachey
Keyword(s):  
Structural Damage ◽  
Liver Homogenate ◽  
Liver Mitochondria ◽  
Structural Elements ◽  
Dnase Ii ◽  
Mitochondrial Structure ◽  
Co60 Source ◽  
Mitochondrial Suspension ◽  
High Doses ◽  
Isolated Liver

1. Exposure of isolated liver mitochondria to high doses of gamma rays from a Co60 source causes the level of DNase II activity to increase. Treatment of the mitochondria with sonic vibration causes a further elevation of the activity to a level which is independent of the prior radiation dose. 2. Such increased mitochondrial DNase II activity appears to be due to the "structural damage" of the subcellular particulates caused by the ionizing radiation. Other methods of disrupting the mitochondrial structure also cause increased DNase II activity. A causal relationship between the structural alteration and the increased enzymatic activity is postulated. 3. The DNase II activity appears to be closely associated with the structural elements of the mitochondria and remains associated with the fragments after irradiation. 4. Upon irradiation, the mitochondrial suspension releases ultraviolet-absorbing materials which are probably nucleotide in nature. 5. The possibility of localization of DNase activity in the lysosome fraction of de Duve (15) is discussed. It is felt that DNase II is at least in part a mitochondrial enzyme and that probably the conclusions drawn here would be applicable to any DNase II present in the lysosomes as well. 6. Irradiation of whole liver homogenate causes no increased DNase II activity. The experiments do not provide any information on the presence or action of protective substances in the homogenate.

scholarly journals Studies on the Mechanism of Ascorbate-induced Swelling and Lysis of Isolated Liver Mitochondria

1964 ◽  
Vol 239 (2) ◽  
pp. 604-613 ◽  
Author(s):  
F. Edmund Hunter ◽  
A. Scott ◽  
P.E. Hoffsten ◽  
Francisco Guerra ◽  
J. Weinstein ◽  
...  
Keyword(s):  
Liver Mitochondria ◽  
Isolated Liver

scholarly journals Stability of Oxidative Phosphorylation and Related Reactions in Isolated Liver Mitochondria

1959 ◽  
Vol 234 (6) ◽  
pp. 1580-1586 ◽  
Author(s):  
Eugene C. Weinbach ◽  
With the technical assistance of C. Elwood Claggett
Keyword(s):  
Oxidative Phosphorylation ◽  
Liver Mitochondria ◽  
Isolated Liver

Oxidation and Phosphorylation Reactions in Isolated Liver Mitochondria in Normal and Icteric Conditions

1966 ◽  
Vol 1 (4) ◽  
pp. 284-291 ◽  
Author(s):  
T. Scherstén ◽  
S. Björkerud ◽  
L. Jakoi ◽  
P. Björntorp
Keyword(s):  
Liver Mitochondria ◽  
Isolated Liver

scholarly journals Cyclosporine in the treatment of idiopathic nephrosis.

1994 ◽  
Vol 5 (4) ◽  
pp. 1049-1056
Author(s):  
P Niaudet ◽  
R Habib
Keyword(s):  
Structural Damage ◽  
Therapeutic Effects ◽  
Steroid Resistant ◽  
The Past ◽  
Cyclosporine Nephrotoxicity ◽  
Steroid Sensitive ◽  
Idiopathic Nephrosis ◽  
High Doses ◽  
Functional Toxicity

Within the past decade, there have been numerous reports on the use of cyclosporine in idiopathic nephrosis. In this review, the results of both uncontrolled and controlled studies of the therapeutic effects of cyclosporine in steroid-sensitive/dependent idiopathic nephrosis and in steroid-resistant idiopathic nephrosis are analyzed. Cyclosporine is efficient in up to 80% of patients with steroid-sensitive/dependent idiopathic nephrosis. Most patients, however, relapse when the drug is withdrawn, thus necessitating prolonged treatments. Although cyclosporine is less efficient in patients with steroid-resistant idiopathic nephrosis, a few studies seem to indicate that this drug may be successful in some patients, especially if combined with corticosteroids. There is no evidence that cyclosporine can prevent the recurrence of nephrotic syndrome on the graft after renal transplantation. However, in patients in whom disease has recurred, high doses of cyclosporine may be effective alone or in combination with plasma exchanges. The main worrisome side effect of cyclosporine is chronic nephrotoxicity, which should be differentiated from acute or "functional" toxicity. Follow-up studies including pretreatment and posttreatment renal biopsies show a lack of correlation between structural damage and renal function, suggesting that a histologic examination of the renal parenchyma is the only reliable way of evaluating chronic cyclosporine nephrotoxicity.

Rosuvastatin: Morphological and Respiratory Effects of High Doses on Liver Mitochondria from Hypercholesterolemic Mice

2020 ◽  
Author(s):  
Juan C Diaz Zagoya ◽  
Alejandro Marín-Medina ◽  
Alma M. Zetina-Esqu ◽  
Jorge L. Blé-Castillo ◽  
Andrés E. Castell-Rodríguez ◽  
...  
Keyword(s):  
Respiratory Function ◽  
Respiratory Control ◽  
Premature Death ◽  
Liver Mitochondria ◽  
Hepatic Tissue ◽  
High Dose ◽  
Main Site ◽  
Functional Changes ◽  
Microscopic Studies ◽  
High Doses

Abstract Background: Statins are the cornerstone of therapy in patients with hyperlipidemia. In high risk patients statins are employed for aggressive therapy, however part of the users are intolerant to these drugs. The aim of this study was to analyze the undesirable effects of moderate, median and high doses of rosuvastatin in CD-1 male mice that received a cholesterol-rich diet, focusing in the morphological and functional changes on hepatocyte mitochondria. Methods: We studied in a mouse model the combined administration of a cholesterol-rich diet (HD) along with a moderate high dose of rosuvastatin (Ro): 1, 2.5 or 5 mg/Kg/day during several days. Animals (n=6) were sacrificed, the liver mitochondria were isolated for analysis of respiratory function and microscopic studies. The respiratory control (state 3/state 4) and the O2 expenditure (nanoatoms/min/mg proteins) were evaluated. Results: Rosuvastatin doses higher than 20 mg/Kg/day induced premature death in hypercholesterolemic mice but not in mice with a cholesterol-free diet. Doses from 2.5 to 5 mg/Kg/day also induced morphological and functional alterations in mitochondria but the hypercholesterolemic animals survived longer. A dose of 1 mg/Kg/day, which is close to the maximal therapeutic dose employed in humans, did not affect mitochondrial architecture or respiratory function after two months of treatment. We analyzed the effect of rosuvastatin on the hepatic tissue where statins are most retained after their administration, and the main site of endogenous cholesterol synthesis. Conclusions: Our results contribute to understand the undesirable side effects of rosuvastatin in hypercholesterolemic mice, effects that can also be present in human being intolerant to statins.

A Rational Definition of Yield Strength

1940 ◽  
Vol 44 (356) ◽  
pp. 653-656
Author(s):  
W. R. Osgood
Keyword(s):  
Yield Strength ◽  
Structural Damage ◽  
Structural Elements ◽  
Conventional Methods ◽  
Definition Of ◽  
Maximum Stresses

Explicitly or implicitly the yield strength of a material is often used as a measure of incipient structural damage. With the yield strength determined by conventional methods, however, it cannot be said in general for two structural elements geometrically alike but of different materials that similar loads, producing maximum stresses equal to the yield strengths in the two cases, are simply related to the yield strengths. A definition of yield strength is proposed in this paper which often has the advantage that, for geometrically similar structures of different materials, loads producing maximum stresses equal to the yield strength are proportional to the yield strength.

scholarly journals Renal ischemia alters expression of mitochondria-related genes and impairs mitochondrial structure and function in swine scattered tubular-like cells

2020 ◽  
Vol 319 (1) ◽  
pp. F19-F28 ◽  
Author(s):  
Rahele A. Farahani ◽  
Xiang-Yang Zhu ◽  
Hui Tang ◽  
Kyra L. Jordan ◽  
Lilach O. Lerman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Structural Damage ◽  
Nuclear Dna ◽  
Mitochondrial Genes ◽  
Structure And Function ◽  
Mitochondrial Damage ◽  
Renal Ischemia ◽  
Gene Gain ◽  
Mitochondrial Structure ◽  
And Function

Scattered tubular-like cells (STCs) are dedifferentiated surviving tubular epithelial cells that repair neighboring injured cells. Experimental renal artery stenosis (RAS) impairs STC reparative potency by inducing mitochondrial injury, but the exact mechanisms of mitochondrial damage remain unknown. We hypothesized that RAS alters expression of mitochondria-related genes, contributing to mitochondrial structural damage and dysfunction in swine STCs. CD24+/CD133+ STCs were isolated from pig kidneys after 10 wk of RAS or sham ( n = 3 each). mRNA sequencing was performed, and nuclear DNA (nDNA)-encoded mitochondrial genes and mitochondrial DNA (mtDNA)-encoded genes were identified. Mitochondrial structure, ATP generation, biogenesis, and expression of mitochondria-associated microRNAs were also assessed. There were 96 nDNA-encoded mitochondrial genes upregulated and 12 mtDNA-encoded genes downregulated in RAS-STCs versus normal STCs. Functional analysis revealed that nDNA-encoded and mtDNA-encoded differentially expressed genes were primarily implicated in mitochondrial respiration and ATP synthesis. Mitochondria from RAS STCs were swollen and showed cristae remodeling and loss and decreased ATP production. Immunoreactivity of the mitochondrial biogenesis marker peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and expression of the mitochondria-associated microRNAs miR-15a, miR-181a, miR-196a, and miR-296-3p, which target several mtDNA genes, were higher in RAS-STCs compared with normal STCs, suggesting a potential modulation of mitochondria-related gene expression. These results demonstrate that RAS induces an imbalance in mtDNA- and nDNA-mitochondrial gene expression, impairing mitochondrial structure and function in swine STCs. These observations support development of gene gain- and loss-of-function strategies to ameliorate mitochondrial damage and preserve the reparative potency of STCs in patients with renal ischemia.

scholarly journals Effects of 2-mercaptoacetate in isolated liver mitochondria in vitro. Competitive inhibition of 3-hydroxybutyrate dehydrogenase and depression of the β-oxidation pathway

1982 ◽  
Vol 206 (1) ◽  
pp. 53-59 ◽  
Author(s):  
F Bauché ◽  
D Sabourault ◽  
Y Giudicelli ◽  
J Nordmann ◽  
R Nordmann
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Competitive Inhibition ◽  
Liver Mitochondria ◽  
Inhibitory Effect ◽  
Acid Oxidation ◽  
Membrane Bound ◽  
Energy Dependent ◽  
Isolated Liver

The effects of 2-mercaptoacetate on the respiration rates induced by different substrates were studied in vitro in isolated liver mitochondria. With palmitoyl-L-carnitine or 2-oxoglutarate as the substrate, the ADP-stimulated respiration (State 3) was dose-dependently inhibited by 2-mercaptoacetate. with glutamate or succinate as the substrate. State-3 respiration was only slightly inhibited by 2-mercaptoacetate. In contrast, the oxidation rate of 3-hydroxybutyrate was competitively inhibited by 2-mercaptoacetate in both isolated mitochondria and submitochondrial particles. In uncoupled mitochondria and in mitochondria in which ATP- and GTP-dependent acyl-CoA biosynthesis was inhibited, the inhibitory effect of 2-mercaptoacetate on palmitoyl-L-carnitine oxidation was abolished; under the same conditions, however, inhibition of 3-hydroxybutyrate oxidation by 2-mercaptoacetate still persisted. These results led to the following conclusions: 2-mercaptoacetate itself enters the mitochondrial matrix, inhibits fatty acid oxidation through a mechanism requiring an energy-dependent activation of 2-mercaptoacetate and itself inhibits 3-hydroxybutyrate oxidation through a competitive inhibition of the membrane-bound 3-hydroxybutyrate dehydrogenase. This study also strongly suggests that the compound responsible for the inhibition of fatty acid oxidation is 2-mercaptoacetyl-CoA.

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