scholarly journals 4- hydroxy-3,5-di-tret-butyl cinnamic acid restores the activity of the hippocampal mitochondria in rats under permanent focal cerebral ischemia

2021 ◽  
Author(s):  
Dmitry Pozdnyakov
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Respiratory Chain ◽  
Cinnamic Acid ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Mitochondrial Respiratory Chain ◽  
Respiratory Chain Complexes ◽  
Chain Complexes

Background and Purpose: Ischemic stroke remains one of the leading causes of death in the population. In addition, mitochondrial dysfunction is an essential part of the pathogenesis of cerebral ischemia and is a promising pharmacotherapeutic target. Experimental Approach: the work was performed on male Wistar rats, which were simulated cerebral ischemia by irreversible occlusion of the middle cerebral artery. 4-hydroxy-3,5-di-tret-butyl cinnamic acid (25 mg/kg, 50 mg/kg and 100 mg/kg) was injected intraperitoneally for 3 days after ischemia (daily). On the 4th day of the experiment, the changes of rat’s cognitive functions in the Morris water maze test, cellular respiration processes, the activity of the mitochondrial respiratory chain complexes and citrate synthase activity, the intensity of oxidative stress and apoptosis reactions were assessed. Key Results: it was found that the administration of 4-hydroxy-3,5-di-tret-butyl cinnamic acid at doses of 25 mg/kg and 50 mg/kg practically equivalently promotes the restoration of aerobic metabolism reactions and the activity of the mitochondrial respiratory chain complexes, decrease of the intensity of oxidative stress reactions and apoptosis, as well as an increase in the activity of citrate synthase. As a result, the restoration of mitochondrial function in the hippocampal cells contributed to the restoration of the animal’s spatial memory. Conclusion and Implications: a study showed that 4-hydroxy-3,5-di-tret-butyl cinnamic acid at doses of 25 mg/kg and 50 mg/kg has a neuroprotective effect on hippocampal neurons under conditions of permanent occlusion of the middle cerebral artery, realized by restoration of mitochondrial function.

Brain energy metabolism is increased by chronic administration of bupropion

2012 ◽  
Vol 24 (2) ◽  
pp. 115-121 ◽  
Author(s):  
Gabriela K. Ferreira ◽  
Gislaine T. Rezin ◽  
Mariane R. Cardoso ◽  
Cinara L. Gonçalves ◽  
Lislaine S. Borges ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Malate Dehydrogenase ◽  
Respiratory Chain ◽  
Citrate Synthase ◽  
Chronic Administration ◽  
Mitochondrial Respiratory Chain ◽  
Brain Energy Metabolism ◽  
Respiratory Chain Complexes ◽  
Chain Complexes ◽  
Brain Energy

Objectives: Based on the hypothesis that energy impairment may be involved in the pathophysiology of depression, we evaluated the activities of citrate synthase, malate dehydrogenase, succinate dehydrogenase (SDH), mitochondrial respiratory chain complexes I, II, II-III, IV and creatine kinase (CK) in the brain of rats submitted to chronic administration of bupropion.Methods: Animals received daily administration of bupropion dissolved in saline (10 mg/kg, intraperitoneal) at 1.0 ml/kg body weight. The rats received injections once a day for 14 days; control rats received an equivalent volume of saline. Twelve hours after the last administration, the rats were killed by decapitation and brain was rapidly removed and kept on an ice plate. The activities of the enzymes were measured in different brain areas.Results: We observed that the activities of citrate synthase and malate dehydrogenase, mithocondrial respiratory chain complexes I, II-III and IV and CK were not altered after chronic administration of bupropion. However, SDH activity was increased in the prefrontal cortex and cerebellum. In the hippocampus, cerebellum and striatum the activity of complex II was increased after chronic administration of bupropion.Conclusions: Our results demonstrated that bupropion increased some enzymes of brain energy metabolism. These findings are in accordance with other studies which showed that some antidepressants may improve energy metabolism. The present results reinforce the hypothesis that antidepressants modulate brain energy metabolism.

scholarly journals Activity of Mitochondrial Respiratory Chain Enzymes after Transient Focal Ischemia in the Rat

1997 ◽  
Vol 17 (11) ◽  
pp. 1166-1169 ◽  
Author(s):  
Laura Canevari ◽  
Satoshi Kuroda ◽  
Timothy E. Bates ◽  
John B. Clark ◽  
Bo K. Siesjö
Keyword(s):  
Respiratory Chain ◽  
Citrate Synthase ◽  
Mitochondrial Respiratory Chain ◽  
Artery Occlusion ◽  
Respiratory Chain Complexes ◽  
Secondary Damage ◽  
Chain Complexes ◽  
Postischemic Recirculation ◽  
Transient Focal Ischemia ◽  
Mitochondrial Respiratory

Previous results demonstrated that after 2-hour middle cerebral artery occlusion (MCAO) in the rat, 1- to 2-hour recirculation temporarily restored the bioenergetic state and mitochondrial function, but secondary deterioration took place after 4 hours. The authors measured the activity of mitochondrial respiratory chain complexes, citrate synthase, and glutamate dehydrogenase as possible targets of secondary damage. Focal and penumbral tissues were sampled in the control condition, after 2 hours of MCAO, and after 1, 2, or 4 hours of postischemic recirculation; two groups were treated with α-phenyl-N- tert-butyl-nitrone (PBN). Complex IV activity transiently decreased after MCAO, but after recirculation all measured activities returned to control values.

scholarly journals Age Modulates Fe3O4Nanoparticles Liver Toxicity: Dose-Dependent Decrease in Mitochondrial Respiratory Chain Complexes Activities and Coupling in Middle-Aged as Compared to Young Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Yosra Baratli ◽  
Anne-Laure Charles ◽  
Valérie Wolff ◽  
Lotfi Ben Tahar ◽  
Leila Smiri ◽  
...  
Keyword(s):  
Respiratory Chain ◽  
Rat Liver ◽  
Mitochondrial Function ◽  
Mitochondrial Respiratory Chain ◽  
Liver Mitochondria ◽  
Aged Rats ◽  
Middle Aged ◽  
Respiratory Chain Complexes ◽  
Chain Complexes ◽  
Mitochondrial Respiratory

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.

Physiological diversity of mitochondrial oxidative phosphorylation

2006 ◽  
Vol 291 (6) ◽  
pp. C1172-C1182 ◽  
Author(s):  
G. Benard ◽  
B. Faustin ◽  
E. Passerieux ◽  
A. Galinier ◽  
C. Rocher ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Respiratory Chain ◽  
Citrate Synthase ◽  
Intrinsic Activity ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Respiratory Chain Complexes ◽  
Mitochondrial Content ◽  
Physiological Diversity ◽  
Chain Complexes ◽  
Functional Features

To investigate the physiological diversity in the regulation and control of mitochondrial oxidative phosphorylation, we determined the composition and functional features of the respiratory chain in muscle, heart, liver, kidney, and brain. First, we observed important variations in mitochondrial content and infrastructure via electron micrographs of the different tissue sections. Analyses of respiratory chain enzyme content by Western blot also showed large differences between tissues, in good correlation with the expression level of mitochondrial transcription factor A and the activity of citrate synthase. On the isolated mitochondria, we observed a conserved molar ratio between the respiratory chain complexes and a variable stoichiometry for coenzyme Q and cytochrome c, with typical values of [1–1.5]:[30–135]:[3]:[9–35]:[6.5–7.5] for complex II:coenzyme Q:complex III:cytochrome c:complex IV in the different tissues. The functional analysis revealed important differences in maximal velocities of respiratory chain complexes, with higher values in heart. However, calculation of the catalytic constants showed that brain contained the more active enzyme complexes. Hence, our study demonstrates that, in tissues, oxidative phosphorylation capacity is highly variable and diverse, as determined by different combinations of 1) the mitochondrial content, 2) the amount of respiratory chain complexes, and 3) their intrinsic activity. In all tissues, there was a large excess of enzyme capacity and intermediate substrate concentration, compared with what is required for state 3 respiration. To conclude, we submitted our data to a principal component analysis that revealed three groups of tissues: muscle and heart, brain, and liver and kidney.

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