Effects of α-tocopherol on bone marrow mesenchymal cells derived from type II diabetes mellitus rats

Noguchi, Masahiro; Yamawaki, Isao; Takahashi, Saitatsu; Taguchi, Yoichiro; Umeda, Makoto

doi:10.2334/josnusd.17-0422

Cited by 3 publications

(2 citation statements)

References 55 publications

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“…To do so, they not only form complexes with lipid-destabilizing molecules but like vitamin C and D also act as a potent chain-breaking antioxidant which inhibits lipid peroxidation (Mehta & Gowder, 2015;Niki & Abe, 2019). The antioxidant properties of vitamin E are very important in cell therapy; hence, the antagonizing effectiveness of vitamin E variants with ROS in MSC has been well fully investigated in some recent studies (Bhatti et al, 2017;Bhatti, Kim, Yi, Hasty & Cho, 2018;Godoy-Parejo, Deng, Zhang, Liu, & Chen, 2019;Noguchi, Yamawaki, Takahashi, Taguchi, & Umeda, 2018). They are also the well-known regulators of many enzymes and signaling pathways which can influence the viable properties of stem cells (Niki & Abe, 2019).…”

Section: Vitamin Ementioning

confidence: 99%

Cytoprotective effects of antioxidant supplementation on mesenchymal stem cell therapy

Panahi

Rahimi

et al. 2020

Journal Cellular Physiology

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Mesenchymal stem cells (MSCs) are earmarked as perfect candidates for cell therapy and tissue engineering due to their capacity to differentiate into different cell types. However, their potential for application in regenerative medicine declines when the levels of the reactive oxygen and nitrogen species (RONS) increase from the physiological levels, a phenomenon which is at least inevitable in ex vivo cultures and air-exposed damaged tissues. Increased levels of RONS can alter the

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Section: Vitamin Ementioning

confidence: 99%

Cytoprotective effects of antioxidant supplementation on mesenchymal stem cell therapy

Panahi

Rahimi

et al. 2020

Journal Cellular Physiology

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“…Considering that pro-oxidant conditions were found to increase the cytotoxicity of EE [31], a plausible explanation for these results might be that AT exerts its antioxidant effect at low concentrations, while at high concentrations, it increases oxidative stress. In a study by Noguchi et al, it has been shown that AT 100 µM did not affect the proliferation of bone marrow mesenchymal cells but increased the activity of H2O2 while reducing catalase expression [21].…”

Section: Resultsmentioning

confidence: 94%

In Vitro Evaluation of Alpha-Tocopherol as Potential Agent in Combating the Hepatotoxicity Induced by Ethinylestradiol

ILIESCU

2023

FARMACIA

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Drug-induced hepatotoxicity (DIH) represents the main cause of drug withdrawal from therapy. Despite their numerous benefits, oral contraceptives (OCs) present several adverse effects, including a high risk of liver complications. Thus, the main objective of this in vitro study was to assess the potential of alpha-tocopherol (AT) in reducing the cytotoxicity of ethinylestradiol (EE), the primary ingredient of modern OCs, against the HepaRG cell line. The results showed that AT exerted no cytotoxicity in HepaRG cells at the tested concentrations, while EE reduced cell viability and confluence, altered cellular morphology, and induced apoptotic-like nuclear features at 100 µM. These cytotoxic effects were reversed by the co-treatment of EE 100 µM with AT 1 µM -the viability, morphology, and nuclear parameters of the treated cells were similar to those of control cells. However, at 100 µM, AT significantly augmented the hepatotoxicity of EE 100 µM, leading to the highest reduction in cell viability, loss of confluence, fragmentation of cell nuclei, increase of the apoptotic index, and reduction of nuclear area and circumference. Further studies should investigate the hepatoprotective effect of AT at low concentrations against EE-induced liver damage, also considering the potential toxicity resulting from their co-administration in high doses. RezumatHepatotoxicitatea reprezintă principala cauză a retragerii medicamentelor din terapie. Deși au numeroase beneficii, contraceptivele orale (CO) prezintă o serie de reacții adverse, printre care se numără și riscul crescut de apariție a complicațiilor la nivel hepatic. Obiectivul principal al acestui studiu in vitro a fost evaluarea eficienței alfa-tocoferolului (AT) în combaterea citotoxicității indusă de etinilestradiol (EE), componenta majoră a CO moderne, asupra liniei celulare HepaRG. Rezultatele au arătat că AT nu a prezentat citotoxicitate asupra celulelor HepaRG la concentrațiile testate, însă EE la concentrația de 100 µM a redus viabilitatea celulară și confluența, a afectat morfologia celulară și a determinat alterări la nivel nuclear similare procesului de apoptoză. Aceste efecte citotoxice au fost reduse prin asocierea EE 100 µM cu AT 1 µMvaloarea viabilității, morfologia celulară și aspectul nuclear al celulelor tratate au fost similare cu cele ale celulelor Control. Cu toate acestea, la concentrația de 100 µM, AT a crescut hepatotoxicitatea indusă de EE 100 µM, ducând la cea mai mare scădere a viabilității celulare, reducere a confluenței și fragmentare a nucleilor celulari. Efectul hepatoprotector al AT la concentrații mici împotriva hepatotoxicității indusă de EE necesită studii suplimentare, considerând potențialul toxic al co-administrării acestor compuși la doze mari.

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Role of oxidative stress in impaired type II diabetic bone repair: scope for antioxidant therapy intervention?

Li,

Alenazi,

Dally

et al. 2024

Front. Dent. Med

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Impaired bone healing is a significant complication observed in individuals with type 2 diabetes mellitus (T2DM), leading to prolonged recovery, increased risk of complications, impaired quality of life, and increased risk of patient morbidity. Oxidative stress, resulting from an imbalance between the generation of reactive oxygen species (ROS) and cellular/tissue antioxidant defence mechanisms, has been identified as a critical contributor to the pathogenesis of impaired bone healing in T2DM. Antioxidants have shown promise in mitigating oxidative stress and promoting bone repair, particularly non-enzymic antioxidant entities. This comprehensive narrative review aims to explore the underlying mechanisms and intricate relationship between oxidative stress, impaired bone healing and T2DM, with a specific focus on the current preclinical and clinical evidence advocating the potential of antioxidant therapeutic interventions in improving bone healing outcomes in individuals with T2DM. From the ever-emerging evidence available, it is apparent that exogenously supplemented antioxidants, especially non-enzymic antioxidants, can ameliorate the detrimental effects of oxidative stress, inflammation, and impaired cellular function on bone healing processes during uncontrolled hyperglycaemia; and therefore, hold considerable promise as novel efficacious therapeutic entities. However, despite such conclusions, several important gaps in our knowledge remain to be addressed, including studies involving more sophisticated enzymic antioxidant-based delivery systems, further mechanistic studies into how these antioxidants exert their desirable reparative effects; and more extensive clinical trial studies into the optimisation of antioxidant therapy dosing, frequency, duration and their subsequent biodistribution and bioavailability. By enhancing our understanding of such crucial issues, we can fully exploit the oxidative stress-neutralising properties of these antioxidants to develop effective antioxidant interventions to mitigate impaired bone healing and reduce the associated complications in such T2DM patient populations.

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Effects of α-tocopherol on bone marrow mesenchymal cells derived from type II diabetes mellitus rats

Cited by 3 publications

References 55 publications

Cytoprotective effects of antioxidant supplementation on mesenchymal stem cell therapy

Cytoprotective effects of antioxidant supplementation on mesenchymal stem cell therapy

In Vitro Evaluation of Alpha-Tocopherol as Potential Agent in Combating the Hepatotoxicity Induced by Ethinylestradiol

Role of oxidative stress in impaired type II diabetic bone repair: scope for antioxidant therapy intervention?

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