Pharmacological significance of MitoQ in ameliorating mitochondria-related diseases

Sulaimon, Lateef Adegboyega; Afolabi, Lukman O.; Adisa, Rahmat Adetutu; Ayankojo, Akinrinade George; Afolabi, Mariam Olanrewaju; Adewolu, Abiodun Mohammed; Wan, Xiaochun

doi:10.1016/j.arres.2022.100037

Cited by 18 publications

(13 citation statements)

References 164 publications

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“…The relationship between MitoBENs structure and their toxicity on NHDF cells was subsequently studied and compared with their respective parental antioxidants and MitoQ and SkQ1, two mitochondria-targeted antioxidants with current cosmetic applications [ 37 , 38 ]. Cytotoxicity of MitoBENs (1–100 μM) on NHDF cells was determined by measuring cell mass, metabolic activity, and intracellular ATP levels after a 48 h incubation.…”

Section: Discussionmentioning

confidence: 99%

“…Firstly, we evaluated the chemical stability of the four MitoBENs tested here (MB1, MB2, MB3, and MB4, Figure 1 A), followed by investigating their toxicity on normal human dermal fibroblasts (NHDF) cells (cell viability, ATP content, mitochondrial toxicity and genotoxicity). A comparison was made with parental compounds, and with MitoQ and SkQ1, which are well-characterized mitochondria-targeted antioxidants, now having commercial applications in cosmetic products [ 37 , 38 ]. After this preliminary screening, MitoBENs that showed low cytotoxicity were investigated for their protective effects against H 2 O 2 cytotoxicity on 2D cell cultures.…”

Section: Introductionmentioning

confidence: 99%

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Targeting Hydroxybenzoic Acids to Mitochondria as a Strategy to Delay Skin Ageing: An In Vitro Approach

et al. 2022

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Targeting antioxidants to mitochondria is considered a promising strategy to prevent cellular senescence and skin ageing. In this study, we investigate whether four hydroxybenzoic acid-based mitochondria-targeted antioxidants (MitoBENs, MB1-4) could be used as potential active ingredients to prevent senescence in skin cells. Firstly, we evaluated the chemical stability, cytotoxicity, genotoxicity and mitochondrial toxicity of all compounds. We followed this by testing the antioxidant protective capacity of the two less toxic compounds on human skin fibroblasts. We then assessed the effects of the best hit on senescence, inflammation and mitochondrial remodeling on a 3D skin cell model, while also testing its mutagenic potential. Cytotoxicity and mitochondrial toxicity rankings were produced: MB3 < MB4 ≃ MB1 < MB2 and MB3 < MB1 < MB4 < MB2, respectively. These results suggest that pyrogallol-based compounds (MB2 and MB4) have lower cytotoxicity. The pyrogallol derivative, MB2, containing a 6-carbon spacer, showed a more potent antioxidant protective activity against hydrogen peroxide cytotoxicity. In a 3D skin cell model, MB2 also decreased transcripts related to senescence. In sum, MB2’s biological safety profile, good chemical stability and lack of mutagenicity, combined with its anti-senescence effect, converts MB2 into a good candidate for further development as an active ingredient for skin anti-ageing products.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Targeting Hydroxybenzoic Acids to Mitochondria as a Strategy to Delay Skin Ageing: An In Vitro Approach

et al. 2022

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“…Consequently, concentrations of MTAs in the lung of COPD patients may be inadequate, and optimal dosing may be difficult to achieve. Again, nanocarriers may present a promising way to combat these limitations, as MTAs can be loaded into nanosized drug carriers that can be engineered to selectively accumulate in specific disease sites/tissues [ 156 ].…”

Section: Limitations and Future Perspectives For Mtas In Copdmentioning

confidence: 99%

Mitochondria-Targeted Antioxidants as a Therapeutic Strategy for Chronic Obstructive Pulmonary Disease

et al. 2023

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Oxidative stress is a major hallmark of COPD, contributing to inflammatory signaling, corticosteroid resistance, DNA damage, and accelerated lung aging and cellular senescence. Evidence suggests that oxidative damage is not solely due to exogenous exposure to inhaled irritants, but also endogenous sources of oxidants in the form of reactive oxygen species (ROS). Mitochondria, the major producers of ROS, exhibit impaired structure and function in COPD, resulting in reduced oxidative capacity and excessive ROS production. Antioxidants have been shown to protect against ROS-induced oxidative damage in COPD, by reducing ROS levels, reducing inflammation, and protecting against the development of emphysema. However, currently available antioxidants are not routinely used in the management of COPD, suggesting the need for more effective antioxidant agents. In recent years, a number of mitochondria-targeted antioxidant (MTA) compounds have been developed that are capable of crossing the mitochondria lipid bilayer, offering a more targeted approach to reducing ROS at its source. In particular, MTAs have been shown to illicit greater protective effects compared to non-targeted, cellular antioxidants by further reducing apoptosis and offering greater protection against mtDNA damage, suggesting they are promising therapeutic agents for the treatment of COPD. Here, we review evidence for the therapeutic potential of MTAs as a treatment for chronic lung disease and discuss current challenges and future directions.

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“…Mitochondria are the primary source of reactive oxygen species, and their malfunction can be a major contributor to oxidative stress and apoptosis during ischemic reperfusion injury in various tissues (9,10). Mito Q is a potent endogenous antioxidant produced from the combination of coenzyme Q10 and triphenylphosphine in mitochondria, which can prevent the production of ROS and mitochondrial oxidative damage (11,12). A wealth of preclinical research has demonstrated that Mito Q can protect the liver, kidney, brain, and heart from oxidative injury caused by ischemia/reperfusion (12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

“…Mito Q is a potent endogenous antioxidant produced from the combination of coenzyme Q10 and triphenylphosphine in mitochondria, which can prevent the production of ROS and mitochondrial oxidative damage (11,12). A wealth of preclinical research has demonstrated that Mito Q can protect the liver, kidney, brain, and heart from oxidative injury caused by ischemia/reperfusion (12)(13)(14). Moreover, a clinical trial study revealed that administering Mito Q for a period of one year in patients with chronic hepatitis C resulted in a signi cant reduction of liver damage (15).…”

Section: Introductionmentioning

confidence: 99%

Combination of alpha-lipoic acid and mitoquinone improves myocardial function in an experimental model of myocardial infarction in aged rats

Nemati,

Badalzadeh,

Zavvari-Oskuye

et al. 2023

Preprint

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This study aimed to investigate whether a combination of two potent antioxidants, alpha-lipoic acid (ALA) and mitoquinone (Mito Q), could improve myocardial function and the underlying mechanisms in an experimental model of myocardial infarction in aged rats. To develop a myocardial infarction model in aged rats the left anterior descending artery (LADA) was transiently occluded for 30 minutes and then re-perfused for 24 hours. Mito Q (10 mg/kg, IP) and ALA (100 mg/kg, gavage) was given daily for 2 weeks before occlusion of LADA. Subsequently, 24 hours after ischemia, left ventricular function was measured, and inflammatory factors (IL-6, IL-1β, TNF-α), tissue apoptosis, expression of Bax, Bcl-2, cytochrome C (Cyt-c), and caspase-3 were evaluated using ELISA, TUNEL, real-time PCR methods, respectively. The findings of this study indicated that the administration of the combination of ALA and Mito Q significantly improved cardiac function. This improvement was linked to a reduction in the expression of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β (P < 0.001) and apoptotic markers (Bax, caspase-3, and Cyt-c), as well as a decrease in the percentage of TUNEL-positive cells (P < 0.001). The combined administration of ALA and Mito Q was found to synergistically reduce cardiac dysfunction in aged rats with myocardial infarction by inhibiting both the inflammatory and apoptotic pathways. This compound may offer a promising solution for elderly individuals who are at risk of heart attack, however, further research is needed to validate its potential

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Pharmacological significance of MitoQ in ameliorating mitochondria-related diseases

Cited by 18 publications

References 164 publications

Targeting Hydroxybenzoic Acids to Mitochondria as a Strategy to Delay Skin Ageing: An In Vitro Approach

Targeting Hydroxybenzoic Acids to Mitochondria as a Strategy to Delay Skin Ageing: An In Vitro Approach

Mitochondria-Targeted Antioxidants as a Therapeutic Strategy for Chronic Obstructive Pulmonary Disease

Combination of alpha-lipoic acid and mitoquinone improves myocardial function in an experimental model of myocardial infarction in aged rats

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