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Cannabis Flavonoids—Antioxidant & Anti-Inflammatory Benefits
Published in Betty Wedman-St Louis, Cannabis as Medicine, 2019
Mitochondria are the center of cellular energy production in the body and the major source of ROS [51]. Mitochondria produce superoxide anions as byproducts of electron leakage [52]. Under normal physiological conditions, mitochondrial ROS is removed by the cellular antioxidant defense system—superoxide dismutases (SOD), catalase, and glutathione peroxidase. However, under pathological conditions, the mitochondrial ROS is over produced leading to excess radicals that damage the mitochondria and cells [53]. The uncontrolled overproduction of ROS overwhelms the cellular antioxidant capacity and impairs the mitochondria.
Mitochondrial Dysfunction in Multiple Sclerosis
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Angela Dziedzic, Elzbieta Miller, Joanna Saluk-Bijak, Michał Bijak
Numerous studies demonstrate that over-production of nitric oxide (NO) plays a significant role in damage of oligodendrocytes in MS. Increased expression of inducible nitric oxide synthase (iNOS) has been detected in MS lesions (Liu et al. 2001; Boullerne and Benjamins 2006; Witherick et al. 2011). What more, both endogenous NO, released by glial cells and NO generated from exogenous NO-donors, are known to induce death of oligodendrocytes (Jana and Pahan 2013). Generation of mitochondrial ROS mainly takes place at the respiratory chain located on the inner mitochondrial membrane during the process of oxidative phosphorylation. ROS production by mitochondria can lead to oxidative damage to mitochondrial proteins, membranes and DNA, impairing the ability of mitochondria to synthesized ATP (Murphy 2009).
Exercise Training, Mitochondrial Adaptations, and Aging
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Nashwa Cheema, Matthew Triolo, David A. Hood
One of the most popular theories of ageing is the mitochondrial free radical theory. The theory postulates that ageing results from a gradual accumulation of mitochondrial damage from ROS. The free radical theory became known as the mitochondrial theory following the discovery that the majority of the ROS were produced in the mitochondria at complex I and complex III (112). Mitochondrial ROS production is most critical to longevity and health span. Supporting this theory, research on transgenic mice overexpressing catalase targeted to the mitochondria had an extension in median and maximal life span (151). The mitochondrial theory of ageing states that there is an age-dependent increase in mitochondrial dysfunction, which results in a decline in energy levels and an increase in cell death. Mitochondria are susceptible to damage, as mtDNA lacks histones, has an inefficient DNA repair system, and is in proximity to ROS production by the electron transport chain. A vicious cycle of events occurs, where ROS-induced damage to DNA and proteins results in further enhanced ROS production from faulty complexes in the ETC. With normal ageing, muscles that exhibit mitochondrial dysfunction have the greatest muscle atrophy and fibre loss (24), suggesting that the organelle can contribute to the age-related decline in muscle function. Mitochondria's direct role on sarcopenia was tested in transgenic mice expressing a proofreading-deficient mtDNA polymerase. The mice had high levels of mtDNA mutations and exhibited premature ageing phenotypes such as shortened life span, accelerated osteoporosis, weight loss, sarcopenia, and increased apoptosis (93).
HYAL1 deficiency attenuates lipopolysaccharide-triggered renal injury and endothelial glycocalyx breakdown in septic AKI in mice
Published in Renal Failure, 2023
Hongxia Xing, Shensen Li, Yongchao Fu, Xin Wan, Annan Zhou, Feifei Cao, Qing Sun, Nana Hu, Mengqing Ma, Wenwen Li, Changchun Cao
Oxidative stress is a key factor in regulation of programmed cell death [52,53]. Intracellular antioxidant enzymes (e.g., SOD) play key roles in inhibiting excessive free radical production [54]. During AKI progression, SOD activity is restrained and superoxide generation is accelerated [55]. As the end product of lipid peroxidation, MDA has been reported to be elevated in renal tissues after ischemia/reperfusion (I/R) injury [56] and contribute to increased apoptotic renal cells in AKI [57]. iNOS is an isoform of nitric oxide synthase and iNOS is usually activated in renal tissues under pathological conditions [58]. Suppression of iNOS production has been demonstrated to mitigate oxidative stress and subsequently alleviate I/R induced renal injury [59] and LPS-induced AKI [60]. Mitochondrial ROS induces electron transport chain dysfunction and disturbs the balance of energy production [61]. Here, we reported that HYAL1 knockdown attenuated LPS-induced oxidative stress by in septic AKI in vivo. Endogenous apoptosis of mitochondrial pathways is activated by various stimuli, including oxidative stress [62]. Here, we confirmed that HYAL1 depletion reversed the promotive impact of LPS stimulation on cell apoptosis of kidneys of mice. Cell survival in response to increased oxidative stress depends on many factors, one of which is nuclear factor erythroid 2-related factor 2 (Nrf2) [63]. Therefore, work in the future should be focused on whether HYAL1 is related to Nrf2/HO-1 signaling pathway-related oxidative stress.
3-Bromopyruvate elevates ROS and induces hormesis to exert a caloric restriction mimetic effect in young and old rats
Published in Archives of Physiology and Biochemistry, 2023
Jitendra Kumar Arya, Raushan Kumar, Shambhoo Sharan Tripathi, Syed Ibrahim Rizvi
There are a plethora of reports to document an increase in oxidative stress during aging, which has been linked to a higher production of mitochondrial ROS (Sena and Chandel 2012). However, it is evident that ROS does not necessarily lead to increased oxidative stress, but instead may act as a signalling molecule that improves health by reducing or delaying a variety of chronic diseases and eventually extending their life span (Schieber and Chandel 2014). ROS can activate enzymes capable of detoxifying oxygen radicals, effectively contributing to improved ROS defense capability (Schulz et al.2007). It is believed that if biological systems are intentionally exposed to moderate stress in order to challenge and activate their hemodynamic maintenance and repair mechanisms, this will lead to desirable hormetic effects, especially health and longevity-promoting effects (Rattan 2008). Significantly it has been reported that in states of elevated mitochondrial activity, increased ROS levels can trigger a series of events that induce stress resistance resulting in improved defense mechanisms against oxidative stress (Ristow and Schmeisser 2011). Some studies show that elevated ROS levels, due to regular exercise and intermittent fasting, induces a hormetic effect and promote antioxidant levels (Ristow et al.2009, Wegman et al.2015).
Dexamethasone as an anti-cancer or hepatotoxic
Published in Toxicology Mechanisms and Methods, 2023
Farzaneh Motafeghi, Parham Mortazavi, Nasrin Ghassemi-Barghi, Mohammad Zahedi, Mohammad Shokrzadeh
Currently, many pathological changes are associated with mitochondrial dysfunction, such as decreased OXPHOS and ATP production and increased ROS accumulation. Although intracellular ROS production itself is an inevitable process, cells have an adaptive defense system to clear ROS. However, the endogenous antioxidant system is not sufficient to eliminate excess ROS when oxidative stress occurs. As a result, ROS accumulation causes oxidative damage to lipids, DNA, and proteins and causes various diseases. Research has focused on maintaining redox homeostasis and normal mitochondrial function through antioxidants for the past decade. Current research focuses on drugs that restore mitochondrial function and regulate mitochondrial ROS production. The drug must selectively accumulate in the mitochondria, interact with mitochondrial targets, and ultimately maintain normal cellular function (Jiang et al. 2020).