scholarly journals The Influence Of Central Asian Cobra Poison On The Activity Of Rothenon Sensitive And Insensitive Over.H-Oxidase Of Rat Liver Mitochondria And Their Correction With Flavosan (Flateron)

2020 ◽  
Vol 02 (11) ◽  
pp. 96-103
Author(s):  
M. M. Mamajanov ◽  

In the presence of cobra venom, the rate of NAD.H oxidation along the internal pathway of the mitochondrial respiratory chain is suppressed, and the rate of NAD.H oxidation along the external pathway increases. These changes occur against the background of cytochrome c deserption from the inner mitochondrial membrane and a significant increase in the process of mitochondrial lipid peroxidation. These facts indicate that when animals are poisoned with cobra venom, profound disturbances are observed in the system of oxidative phosphorylation and the electron transport chain. The introduction of flavosan into the body of animals poisoned with cobra venom leads to an increase in the rate of NAD.H oxidation along the internal pathway of the mitochondrial respiratory chain and suppression of the rate of NAD.H oxidation through the external pathway.

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Yosra Baratli ◽  
Anne-Laure Charles ◽  
Valérie Wolff ◽  
Lotfi Ben Tahar ◽  
Leila Smiri ◽  
...  

We examined the effects of iron oxide nanoparticles (IONPs) on mitochondrial respiratory chain complexes activities and mitochondrial coupling in young (3 months) and middle-aged (18 months) rat liver, organ largely involved in body iron detoxification. Isolated liver mitochondria were extracted using differential centrifugations. Maximal oxidative capacities (Vmax, complexes I, III, and IV activities),Vsucc(complexes II, III, and IV activities), andVtmpd, (complex IV activity), together with mitochondrial coupling (Vmax/V0) were determined in controls conditions and after exposure to 250, 300, and 350 μg/ml Fe3O4in young and middle-aged rats. In young liver mitochondria, exposure to IONPs did not alter mitochondrial function. In contrast, IONPs dose-dependently impaired all complexes of the mitochondrial respiratory chain in middle-aged rat liver:Vmax(from 30 ± 1.6 to 17.9 ± 1.5;P<0.001),Vsucc(from 33.9 ± 1.7 to 24.3 ± 1.0;P<0.01),Vtmpd(from 43.0 ± 1.6 to 26.3 ± 2.2 µmol O2/min/g protein;P<0.001) using Fe3O4350µg/ml. Mitochondrial coupling also decreased. Interestingly, 350 μg/ml Fe3O4in the form of Fe3+solution did not impair liver mitochondrial function in middle-aged rats. Thus, IONPs showed a specific toxicity in middle-aged rats suggesting caution when using it in old age.


2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Mårten Wikström ◽  
Roger Springett

AbstractThe protonmotive mitochondrial respiratory chain, comprising complexes I, III and IV, transduces free energy of the electron transfer reactions to an electrochemical proton gradient across the inner mitochondrial membrane. This gradient is used to drive synthesis of ATP and ion and metabolite transport. The efficiency of energy conversion is of interest from a physiological point of view, since the energy transduction mechanisms differ fundamentally between the three complexes. Here, we have chosen actively phosphorylating mitochondria as the focus of analysis. For all three complexes we find that the thermodynamic efficiency is about 80–90% and that the degree of coupling between the redox and proton translocation reactions is very high during active ATP synthesis. However, when net ATP synthesis stops at a high ATP/ADP.Pi ratio, and mitochondria reach “State 4” with an elevated proton gradient, the degree of coupling drops substantially. The mechanistic cause and the physiological implications of this effect are discussed.


2021 ◽  
Vol 10 (22) ◽  
pp. 5235
Author(s):  
Daniele Orsucci

Mitochondrial disorders are a remarkably complex group of diseases caused by impairment of the mitochondrial respiratory chain (or electron transport chain) [...]


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