Mitochondrial reactive oxygen species (ROS) have been demonstrated to play an important role as signaling and regulating molecules in human adipocytes. In order to evaluate the differential modulating roles of antioxidants, we treated human adipocytes differentiated from human bone marrow-derived mesenchymal stem cells with MitoQ, resveratrol and curcumin. The effects on ROS, viability, mitochondrial respiration and intracellular ATP levels were examined. MitoQ lowered both oxidizing and reducing ROS. Resveratrol decreased reducing and curcumin oxidizing radicals only. All three substances slightly decreased state III respiration immediately after addition. After 24 h of treatment, MitoQ inhibited both basal and uncoupled oxygen consumption, whereas curcumin and resveratrol had no effect. Intracellular ATP levels were not altered. This demonstrates that MitoQ, resveratrol and curcumin exert potent modulating effects on ROS signaling in human adipocyte with marginal effects on metabolic parameters.
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http://dx.doi.org/10.3109/10799893.2013.822887 | DOI Listing |
Mol Neurobiol
September 2024
GloNeuro, Sector 107, Vishwakarma Road, Noida, Uttar Pradesh, 201301, India.
Mitochondria are central to cellular energy production, and their dysfunction is a major contributor to oxidative stress and chronic inflammation, pivotal factors in aging, and related diseases. With aging, mitochondrial efficiency declines, leading to an increase in ROS and persistent inflammatory responses. Therapeutic interventions targeting mitochondrial health show promise in mitigating these detrimental effects.
View Article and Find Full Text PDFMol Nutr Food Res
May 2024
Department of Orthopedics, Haian Hospital of Traditional Chinese Medicine, Nantong, Jiangsu Province, 226600, P. R. China.
Pharmacol Res
May 2024
Department of Cardiology, Zhongshan Hospital of Traditional Chinese Medicine Affiliated to Guangzhou University of Traditional Chinese Medicine (Zhongshan Hospital of Traditional Chinese Medicine), Zhongshan, Guangdong, China; Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China. Electronic address:
The impact of mitochondrial dysfunction on the pathogenesis of cardiovascular disease is increasing. However, the precise underlying mechanism remains unclear. Mitochondria produce cellular energy through oxidative phosphorylation while regulating calcium homeostasis, cellular respiration, and the production of biosynthetic chemicals.
View Article and Find Full Text PDFNutrients
October 2023
CNC-UC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal.
Chronic diseases represent one of the major causes of death worldwide. It has been suggested that pregnancy-related conditions, such as gestational diabetes mellitus (GDM), maternal obesity (MO), and intra-uterine growth restriction (IUGR) induce an adverse intrauterine environment, increasing the offspring's predisposition to chronic diseases later in life. Research has suggested that mitochondrial function and oxidative stress may play a role in the developmental programming of chronic diseases.
View Article and Find Full Text PDFLife Sci
December 2022
Department of Nutrition and Integrative Physiology, College of Health and Human Sciences, Florida State University, Tallahassee, FL, United States. Electronic address:
Aims: Erectile dysfunction is a common complication within many pathological conditions associated with low testosterone. Testosterone deficiency increases oxidative stress in the penile tissue that contributes to endothelial dysfunction and subsequent erectile dysfunction. Current therapies do not ameliorate oxidative stress so targeting oxidative stress may improve erectile dysfunction.
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