scholarly journals Administration of 4-Hydroxy-3,5-Di-Tertbutyl Cinnamic Acid Restores Mitochondrial Function in Rabbits with Cerebral Ischemia

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Dmitriy I. Pozdnyakov ◽  
Zara J. Hadzhieva ◽  
Anastasiya E. Pozdnyakova
Keyword(s):  
Membrane Potential ◽  
Cerebral Ischemia ◽  
Mitochondrial Membrane Potential ◽  
Cinnamic Acid ◽  
Mitochondrial Function ◽  
Neurological Deficit ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Mitochondrial Permeability Transition ◽  
Time Interval

Abstract The aim of the study is to evaluate the effect of 4-hydroxy-3,5- di-tertbutyl cinnamic acid on the change in mitochondrial function under conditions of experimental cerebral ischemia in rabbits. The study was performed on 48 male rabbits, which were used for modeling permanent cerebral ischemia by occlusion of the common carotid arteries. The test compound was administered before modeling ischemia for 14 days and after the occurrence of reproducing ischemia, in a similar time interval. After that, neurological deficit and the parameters of mitochondrial respiration, the intensity of anaerobic processes, the latent opening time of the mitochondrial permeability transition pore, the value of the mitochondrial membrane potential and the concentration of caspase – 3 were determined. The administration of 100 mg/kg of 4-hydroxy-3,5-di-tertbutyl cinnamic acid into the animals reduced neurological deficit and restored the mitochondrial membrane potential. Prophylactic administration of 4-hydroxy- 3,5-di-tertbutyl cinnamic acid, contributed to an increase in ATPgenerating ability, the maximum level of respiration and respiratory capacity by 4.1 times (p<0.01), 4.8 times (p<0.01) and 4.3 times (p<0.01), respectively. With therapeutic administration, these indicators increased by 11 times (p<0.01), 12.2 times (p<0.01) and 8.6 times (p<0.01), respectively. Also, both the prophylactic and therapeutic use of 4-hydroxy-3,5-di-tret-butyl cinnamic acid normalized aerobic/anaerobic metabolism, as well as reduced the concentration of caspase-3. Based on the obtained data, significant cerebroprotective properties of 4-hydroxy-3,5- di-tertbutyl cinnamic acid can be assumed. Moreover, the potential mechanism of action of this compound may be mediated by the normalization of mitochondrial function.

Δ9-Tetrahydrocannabinol disrupts mitochondrial function and cell energetics

2003 ◽  
Vol 284 (2) ◽  
pp. L298-L306 ◽  
Author(s):  
Theodore A. Sarafian ◽  
Shaghig Kouyoumjian ◽  
Farnaz Khoshaghideh ◽  
Donald P. Tashkin ◽  
Michael D. Roth
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Mitochondrial Inhibitors ◽  
Transformed Cell Line ◽  
Important Health

We have observed rapid and extensive depletion of cellular energy stores by Δ9-tetrahydrocannabinol (THC) in the pulmonary transformed cell line A549. ATP levels declined dose dependently with an IC50 of 7.5 μg/ml of THC after 24-h exposure. Cell death was observed only at concentrations >10 μg/ml. Studies using JC-1, a fluorescent probe for mitochondrial membrane potential, revealed diminished mitochondrial function at THC concentrations as low as 0.5 μg/ml. At concentrations of 2.5 or 10 μg/ml of THC, a decrease in mitochondrial membrane potential was observed as early as 1 h after THC exposure. Mitochondrial function remained diminished for at least 30 h after THC exposure. Flow cytometry studies on cells exposed to particulate smoke extracts indicate that JC-1 red fluorescence was fivefold lower in cells exposed to marijuana smoke extract relative to cells exposed to tobacco smoke extract. Comparison with a variety of mitochondrial inhibitors demonstrates that THC produced effects similar to that of carbonyl cyanide p-trifluoromethoxyphenylhydrazone, suggesting uncoupling of electron transport. Loss of red JC-1 fluorescence by THC was suppressed by cyclosporin A, suggesting mediation by the mitochondrial permeability transition pore. This disruption of mitochondrial function was sustained for at least 24 h after removal of THC by extensive washing. These results suggest that exposure of the bronchopulmonary epithelium to THC may have important health and physiological consequences.

scholarly journals Correction of mitochondrial dysfunction by succinic acid derivatives under experimental cerebral ischemia conditions

2021 ◽  
Vol 34 (1) ◽  
pp. 42-48
Author(s):  
Dmitry I. Pozdnyakov ◽  
Denis S. Zolotych ◽  
Michael V. Larsky
Keyword(s):  
Membrane Potential ◽  
Cerebral Ischemia ◽  
Succinic Acid ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Anaerobic Metabolism ◽  
Mitochondrial Pore ◽  
Apoptosis Inducing Factor ◽  
Test Objects

Abstract The aim of the study. To evaluate the effect of succinic acid derivatives on changes of mitochondrial function in rats under cerebral ischemia conditions. Materials and methods. In this work, the effect of succinic acid, ethylmethylhydroxypyridine succinate, and acetylaminosuccinic acid at doses of 50 mg/kg, 100 mg/kg, and 200 mg/kg (per os) on the change of the neuronal mitochondria function was studied. Cerebral ischemia was reproduced by the Tamura method. The following parameters were evaluated: changes in aerobic/anaerobic metabolism, mitochondrial membrane potential, the opening rate of the mitochondrial pore of transitional permeability and the activity of apoptotic systems. Results. During the study, it was found that the use of the test-compounds at doses of 100 mg/kg and 200 mg/kg contributed to an increase in ATP-generating activity, as well as the maximum respiration level and respiratory capacity, while accompanied by a decrease in the intensity of anaerobic metabolism reactions. Also, upon administration of the test succinic acid derivatives, an increase in the mitochondrial membrane potential and latent opening time of the mitochondrial pore transitional permeability were observed. Moreover, the activity of caspase-3 and apoptosis-inducing factor on groups treated by test objects at doses of 100 mg/kg and 200 mg/kg was significantly lower than that in untreated animals. Conclusion. The studied succinic acid derivatives contribute to the restoration of mitochondrial function in cerebral ischemia conditions, while the most effective dose can be considered to be 100 mg/kg.

scholarly journals Two Subpopulations of Human Monocytes That Differ by Mitochondrial Membrane Potential

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 153
Author(s):  
Nikita G. Nikiforov ◽  
Anastasia Ryabova ◽  
Marina V. Kubekina ◽  
Igor D. Romanishkin ◽  
Kirill A. Trofimov ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Primary Culture ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Aminolevulinic Acid ◽  
Protoporphyrin Ix ◽  
Intima Media Thickness ◽  
Mtdna Mutations ◽  
Proinflammatory Activity

Atherosclerosis is associated with a chronic local inflammatory process in the arterial wall. Our previous studies have demonstrated the altered proinflammatory activity of circulating monocytes in patients with atherosclerosis. Moreover, atherosclerosis progression and monocyte proinflammatory activity were associated with mitochondrial DNA (mtDNA) mutations in circulating monocytes. The role of mitochondria in the immune system cells is currently well recognized. They can act as immunomodulators by releasing molecules associated with bacterial infection. We hypothesized that atherosclerosis can be associated with changes in the mitochondrial function of circulating monocytes. To test this hypothesis, we performed live staining of the mitochondria of CD14+ monocytes from healthy donors and atherosclerosis patients with MitoTracker Orange CMTMRos dye, which is sensitive to mitochondrial membrane potential. The intensity of such staining reflects mitochondrial functional activity. We found that parts of monocytes in the primary culture were characterized by low MitoTracker staining (MitoTracker-low monocytes). Such cells were morphologically similar to cells with normal staining and able to metabolize 5-aminolevulinic acid and accumulate the heme precursor protoporphyrin IX (PplX), indicative of partially preserved mitochondrial function. We assessed the proportion of MitoTracker-low monocytes in the primary culture for each study subject and compared the results with other parameters, such as monocyte ability to lipopolysaccharide (LPS)-induced proinflammatory activation and the intima-media thickness of carotid arteries. We found that the proportion of MitoTracker-low monocytes was associated with the presence of atherosclerotic plaques. An increased number of such monocytes in the primary culture was associated with a reduced proinflammatory activation ability of cells. The obtained results indicate the presence of circulating monocytes with mitochondrial dysfunction and the association of such cells with chronic inflammation and atherosclerosis development.

scholarly journals Genomic instability induced by radiation-mimicking chemicals is not associated with persistent mitochondrial degeneration

2021 ◽  
Author(s):  
Luukkonen Jukka ◽  
Höytö Anne ◽  
Sokka Miiko ◽  
Syväoja Juhani ◽  
Juutilainen Jukka ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Ionizing Radiation ◽  
Genomic Instability ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Neuroblastoma Cells ◽  
Superoxide Production ◽  
Mitochondrial Activity ◽  
Mitochondrial Superoxide

AbstractIonizing radiation has been shown to cause induced genomic instability (IGI), which is defined as a persistently increased rate of genomic damage in the progeny of the exposed cells. In this study, IGI was investigated by exposing human SH-SY5Y neuroblastoma cells to hydroxyurea and zeocin, two chemicals mimicking different DNA-damaging effects of ionizing radiation. The aim was to explore whether IGI was associated with persistent mitochondrial dysfunction. Changes to mitochondrial function were assessed by analyzing mitochondrial superoxide production, mitochondrial membrane potential, and mitochondrial activity. The formation of micronuclei was used to determine immediate genetic damage and IGI. Measurements were performed either immediately, 8 days, or 15 days following exposure. Both hydroxyurea and zeocin increased mitochondrial superoxide production and affected mitochondrial activity immediately after exposure, and mitochondrial membrane potential was affected by zeocin, but no persistent changes in mitochondrial function were observed. IGI became manifested 15 days after exposure in hydroxyurea-exposed cells. In conclusion, immediate responses in mitochondrial function did not cause persistent dysfunction of mitochondria, and this dysfunction was not required for IGI in human neuroblastoma cells.

scholarly journals Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cells

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Junqiang Yan ◽  
Hongxia Ma ◽  
Xiaoyi Lai ◽  
Jiannan Wu ◽  
Anran Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Protein Expression ◽  
Mitochondrial Membrane Potential ◽  
Western Blotting ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects

Abstract Background Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. The oxidative stress is an important component of the pathogenesis of PD. Artemisinin (ART) has antioxidant and neuroprotective effects. The purpose of this study is to explore the neuroprotective effect of ART on 1-methyl-4-phenyliodine iodide (MPP +)-treated SH-SY5Y cells and underlying mechanism. Methods We used MPP+-treated SH-SY5Y cells to study the neuroprotective effect of ART. Cell viability was measured by MTT assay after incubating the cells with MPP+ and/or ART for 24 h. DCFH-DA was used to detect the level of intracellular reactive oxygen species (ROS), and WST-8 was used to detect the level of superoxide dismutase (SOD). The level of intracellular reduced glutathione (GSH) was detected with 5,5΄-dithiobis-(2-nitrobenzoic acid), and the level of malondialdehyde (MDA) was assessed based on the reaction of MDA and thiobarbituric acid. A mitochondrial membrane potential detection kit (JC-1) was used to detect changes in the mitochondrial membrane potential (MMP), and an Annexin V-FITC cell apoptosis kit was used to detect cell apoptosis. The expression levels of caspase-3, cleaved caspase-3 and the autophagy-related proteins LC3, beclin-1, and p62 were detected by Western blotting. In addition, to verify the change in autophagy, we used immunofluorescence to detect the expression of LC3 and p62. Results No significant cytotoxicity was observed at ART concentrations up to 40 μM. ART could significantly increase the viability of SH-SY5Y cells treated with MPP+ and reduce oxidative stress damage and apoptosis. In addition, the Western blotting and immunofluorescence results showed that MPP+ treatment could increase the protein expression of beclin1 and LC3II/LC3I and decrease the protein expression of p62, indicating that MPP+ treatment could induce autophagy. Simultaneous treatment with ART and MPP+ could decrease the protein expression of beclin1 and LC3II/LC3I and increase the protein expression of p62, indicating that ART could decrease the level of autophagy induced by MPP+. Conclusion Our results indicate that ART has a protective effect on MPP+-treated SH-SY5Y cells by the antioxidant, antiapoptotic activities and inhibition of autophagy. Our findings may provide new hope for the prevention and treatment of PD.

Abstract P352: Prostaglandin E2 Reduces Mitochondrial Function in Adult Mouse Cardiomyocytes

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Pamela Harding ◽  
Timothy D Bryson ◽  
Indrani Datta ◽  
Yun Wang ◽  
Albert Levin
Keyword(s):  
Membrane Potential ◽  
Ejection Fraction ◽  
Prostaglandin E2 ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Complex I ◽  
Mitochondrial Membrane ◽  
Receptor Subtypes ◽  
Atp Levels ◽  
Complex I Activity

Hypertension is a leading cause of heart failure and both conditions are characterized by increased prostaglandin E2 (PGE2) which signals through 4 receptor subtypes (EP1-EP4) to elicit diverse physiologic effects. We previously reported that cardiomyocyte-specific deletion of the EP4 receptor results in a phenotype of dilated cardiomyopathy in male mice that is characterized by reduced ejection fraction. Subsequent gene array on left ventricles from these mice, coupled with Ingenuity Pathway Analysis (IPA) demonstrated that genes differentiating WT mice and EP4 KO mice with low ejection fraction were significantly overrepresented in mitochondrial (p=2.51x10 -28 ) and oxidative phosphorylation (p=3.16 x10 -30 ) pathways. We therefore hypothesized that PGE2 could reduce mitochondrial function. To test this hypothesis, we used isolated mouse cardiomyocytes (AVM) from 16-18 week old male C57Bl/6 mice and treated them with 1 μM PGE2 for various times. Mitochondrial gene expression was examined using a RT-profiler kit for mitochondrial energy metabolism, complex I activity with a spectrophotometric assay, ATP levels with a bioluminescence assay and mitochondrial membrane potential using JC-1 staining. Treatment of AVM with PGE2 for 4 hrs reduced expression of multiple genes from mitochondrial pathways including sub units of mitochondrial NADH dehydrogenase ubiquinone flavoprotein (Nduf), a component of complex I. In accord with the mRNA data, Complex I activity was reduced by 50% (p < 0.05) by 4 hr treatment with PGE2, from 1.32 ± 0.36 to 0.66 ± 0.08 mOD/min. Cytochrome c oxidase subunit 8 (Cox8c) mRNA was also reduced from a control value of 1.00 to -1.75 ± 0.20 (p < 0.005) after PGE2 treatment. Immuno-fluorescence showed that JC-1 aggregates were reduced after 1 or 3 hr treatment with either 1 μM PGE2 or the EP3 agonist, sulprostone, suggesting reduced mitochondrial membrane potential. Subsequent experiments also showed that ATP levels were reduced 16% from 11.18 ± 0.71 nmol to 9.39 ± 0.83 nmol after treatment with sulprostone for only 1 hr. Taken together, these results suggest that increased PGE2 in hypertension may contribute to impaired mitochondrial function and provide yet another link between inflammation and cardiac dysfunction.

scholarly journals Alpha-Tocotrienol Prevents Oxidative Stress-Mediated Post-Translational Cleavage of Bcl-xL in Primary Hippocampal Neurons

2019 ◽  
Vol 21 (1) ◽  
pp. 220 ◽  
Author(s):  
Han-A Park ◽  
Nelli Mnatsakanyan ◽  
Katheryn Broman ◽  
Abigail U. Davis ◽  
Jordan May ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Mitochondrial Membrane ◽  
Antioxidant Properties ◽  
B Cell Lymphoma ◽  
Atp Depletion ◽  
Primary Hippocampal Neurons

B-cell lymphoma-extra large (Bcl-xL) is an anti-apoptotic member of the Bcl2 family of proteins, which supports neurite outgrowth and neurotransmission by improving mitochondrial function. During excitotoxic stimulation, however, Bcl-xL undergoes post-translational cleavage to ∆N-Bcl-xL, and accumulation of ∆N-Bcl-xL causes mitochondrial dysfunction and neuronal death. In this study, we hypothesized that the generation of reactive oxygen species (ROS) during excitotoxicity leads to formation of ∆N-Bcl-xL. We further proposed that the application of an antioxidant with neuroprotective properties such as α-tocotrienol (TCT) will prevent ∆N-Bcl-xL-induced mitochondrial dysfunction via its antioxidant properties. Primary hippocampal neurons were treated with α-TCT, glutamate, or a combination of both. Glutamate challenge significantly increased cytosolic and mitochondrial ROS and ∆N-Bcl-xL levels. ∆N-Bcl-xL accumulation was accompanied by intracellular ATP depletion, loss of mitochondrial membrane potential, and cell death. α-TCT prevented loss of mitochondrial membrane potential in hippocampal neurons overexpressing ∆N-Bcl-xL, suggesting that ∆N-Bcl-xL caused the loss of mitochondrial function under excitotoxic conditions. Our data suggest that production of ROS is an important cause of ∆N-Bcl-xL formation and that preventing ROS production may be an effective strategy to prevent ∆N-Bcl-xL-mediated mitochondrial dysfunction and thus promote neuronal survival.

Melatonin and Nicotinamide Mononucleotide Attenuate Myocardial Ischemia/Reperfusion Injury via Modulation of Mitochondrial Function and Hemodynamic Parameters in Aged Rats

2019 ◽  
Vol 25 (3) ◽  
pp. 240-250 ◽  
Author(s):  
Leila Hosseini ◽  
Manouchehr S. Vafaee ◽  
Reza Badalzadeh
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Ischemia Reperfusion ◽  
Combined Therapy ◽  
Aged Rats ◽  
Hemodynamic Parameters ◽  
Nicotinamide Mononucleotide

Ischemic heart diseases are the major reasons for disability and mortality in elderly individuals. In this study, we tried to examine the combined effects of nicotinamide mononucleotide (NMN) preconditioning and melatonin postconditioning on cardioprotection and mitochondrial function in ischemia/reperfusion (I/R) injury of aged male rats. Sixty aged Wistar rats were randomly allocated to 5 groups, including sham, control, NMN-receiving, melatonin-receiving, and combined therapy (NMN+melatonin). Isolated hearts were mounted on Langendorff apparatus and then underwent 30-minue ligation of left anterior descending coronary artery to induce regional ischemic insult, followed by 60 minutes of reperfusion. Nicotinamide mononucleotide (100 mg/kg/d intraperitoneally) was administered for every other day for 28 days before I/R. Melatonin added to perfusion solution, 5 minutes prior to the reperfusion up to 15 minutes early reperfusion. Myocardial hemodynamic and infarct size (IS) were measured, and the left ventricles samples were obtained to evaluate cardiac mitochondrial function and oxidative stress markers. Melatonin postconditioning and NMN had significant cardioprotective effects in aged rats; they could improve hemodynamic parameters and reduce IS and lactate dehydrogenase release compared to those of control group. Moreover, pretreatment with NMN increased the cardioprotection by melatonin. All treatments reduced oxidative stress and mitochondrial reactive oxygen species (ROS) levels and improved mitochondrial membrane potential and restored NAD+/NADH ratio. The effects of combined therapy on reduction of mitochondrial ROS and oxidative status and improvement of mitochondrial membrane potential were greater than those of alone treatments. Combination of melatonin and NMN can be a promising strategy to attenuate myocardial I/R damages in aged hearts. Restoration of mitochondrial function may substantially contribute to this cardioprotection.

scholarly journals The spatio-temporal dynamics of mitochondrial membrane potential during oocyte maturation

2019 ◽  
Vol 25 (11) ◽  
pp. 695-705 ◽  
Author(s):  
Usama AL-Zubaidi ◽  
Jun Liu ◽  
Ozgur Cinar ◽  
Rebecca L Robker ◽  
Deepak Adhikari ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Oocyte Maturation ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Local Level ◽  
Meiotic Spindle ◽  
Mitochondrial Activity ◽  
Wide Range ◽  
Spatio Temporal

Abstract Mitochondria are highly dynamic organelles and their distribution, structure and activity affect a wide range of cellular functions. Mitochondrial membrane potential (∆Ψm) is an indicator of mitochondrial activity and plays a major role in ATP production, redox balance, signaling and metabolism. Despite the absolute reliance of oocyte and early embryo development on mitochondrial function, there is little known about the spatial and temporal aspects of ΔΨm during oocyte maturation. The one exception is that previous findings using a ΔΨm indicator, JC-1, report that mitochondria in the cortex show a preferentially increased ΔΨm, relative to the rest of the cytoplasm. Using live-cell imaging and a new ratiometric approach for measuring ΔΨm in mouse oocytes, we find that ΔΨm increases through the time course of oocyte maturation and that mitochondria in the vicinity of the first meiotic spindle show an increase in ΔΨm, compared to other regions of the cytoplasm. We find no evidence for an elevated ΔΨm in the oocyte cortex. These findings suggest that mitochondrial activity is adaptive and responsive to the events of oocyte maturation at both a global and local level. In conclusion, we have provided a new approach to reliably measure ΔΨm that has shed new light onto the spatio-temporal regulation of mitochondrial function in oocytes and early embryos.

scholarly journals Differential Effects of Silibinin A on Mitochondrial Function in Neuronal PC12 and HepG2 Liver Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Carsten Esselun ◽  
Bastian Bruns ◽  
Stephanie Hagl ◽  
Rekha Grewal ◽  
Gunter P. Eckert
Keyword(s):  
Membrane Potential ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Membrane Potential ◽  
Cell Lines ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Nitrosative Stress ◽  
Citrate Synthase ◽  
Atp Levels ◽  
Age Related

The Mediterranean plant Silybum marianum L., commonly known as milk thistle, has been used for centuries to treat liver disorders. The flavonolignan silibinin represents a natural antioxidant and the main bioactive ingredient of silymarin (silybin), a standard extract of its seeds. Mitochondrial dysfunction and the associated generation of reactive oxygen/nitrogen species (ROS/RNS) are involved in the development of chronic liver and age-related neurodegenerative diseases. Silibinin A (SIL A) is one of two diastereomers found in silymarin and was used to evaluate the effects of silymarin on mitochondrial parameters including mitochondrial membrane potential and ATP production with and without sodium nitroprusside- (SNP-) induced nitrosative stress, oxidative phosphorylation, and citrate synthase activity in HepG2 and PC12 cells. Both cell lines were influenced by SIL A, but at different concentrations. SIL A significantly weakened nitrosative stress in both cell lines. Low concentrations not only maintained protective properties but also increased basal mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) levels. However, these effects could not be associated with oxidative phosphorylation. On the other side, high concentrations of SIL A significantly decreased MMP and ATP levels. Although SIL A did not provide a general improvement of the mitochondrial function, our findings show that SIL A protects against SNP-induced nitrosative stress at the level of mitochondria making it potentially beneficial against neurological disorders.

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