Estimation of the hydrogen peroxide producing capacities of liver and cardiac mitochondria isolated from C57BL/6N and C57BL/6J mice

Oldford, Catherine; Kuksal, Nidhi; Gill, Robert M.; Young, Adrian; Mailloux, Ryan J.

doi:10.1016/j.freeradbiomed.2019.02.012

Cited by 41 publications

(52 citation statements)

References 36 publications

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“…Our group recently profiled the native rates of ROS production by several 'unconventional' generators using mitochondria collected from 6N and 6J mice. This included measuring the rates of production by KGDH, PDH, BCKDH, complex II, PRODH, and G3PDH in liver mitochondria and KGDH, PDH, PRODH, and G3PDH in heart mitochondria, respectively [12]. Mitochondria were permeabilized with Triton-X and treated with complex I and III inhibitors to curtail ROS production by the electron transport chain.…”

Section: Ros Sources In Liver Tissue Vary According To Mouse Strainmentioning

confidence: 99%

“…Our group also recently demonstrated that other key physiological and phenotypic factors must be considered when studying how mitochondria maintain cellular ROS balance. This includes factors such as mouse strain and sex and tissue type, which can have a strong impact on the native rate of H 2 O 2 production by several "unconventional" ROS generators such as α-keto acid dehydrogenases [12]. Additionally, important advances have been made in identifying other ROS sources such as long-chain fatty acid dehydrogenase (LCAD) and very long-chain fatty acid dehydrogenase (VLCAD), two integral components of the fatty acid oxidation (FAO) pathway [13,14].…”

Section: Introductionmentioning

confidence: 99%

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An Update on Mitochondrial Reactive Oxygen Species Production

Mailloux

2020

Antioxidants

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183

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Mitochondria are quantifiably the most important sources of superoxide (O2●−) and hydrogen peroxide (H2O2) in mammalian cells. The overproduction of these molecules has been studied mostly in the contexts of the pathogenesis of human diseases and aging. However, controlled bursts in mitochondrial ROS production, most notably H2O2, also plays a vital role in the transmission of cellular information. Striking a balance between utilizing H2O2 in second messaging whilst avoiding its deleterious effects requires the use of sophisticated feedback control and H2O2 degrading mechanisms. Mitochondria are enriched with H2O2 degrading enzymes to desensitize redox signals. These organelles also use a series of negative feedback loops, such as proton leaks or protein S-glutathionylation, to inhibit H2O2 production. Understanding how mitochondria produce ROS is also important for comprehending how these organelles use H2O2 in eustress signaling. Indeed, twelve different enzymes associated with nutrient metabolism and oxidative phosphorylation (OXPHOS) can serve as important ROS sources. This includes several flavoproteins and respiratory complexes I-III. Progress in understanding how mitochondria generate H2O2 for signaling must also account for critical physiological factors that strongly influence ROS production, such as sex differences and genetic variances in genes encoding antioxidants and proteins involved in mitochondrial bioenergetics. In the present review, I provide an updated view on how mitochondria budget cellular H2O2 production. These discussions will focus on the potential addition of two acyl-CoA dehydrogenases to the list of ROS generators and the impact of important phenotypic and physiological factors such as tissue type, mouse strain, and sex on production by these individual sites.

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Section: Ros Sources In Liver Tissue Vary According To Mouse Strainmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

An Update on Mitochondrial Reactive Oxygen Species Production

Mailloux

2020

Antioxidants

Self Cite

183

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“…A cocktail of ROS generation inhibitors was utilized to ensure the fluorescent signal corresponded to production. Inhibitors were selected based on recent findings that have demonstrated the site for ROS production by mitochondria can vary significantly depending on which fuel is being combusted [ 5 , 16 ]. Mitochondria were pre-treated with the various inhibitors for 10 min at 25°C prior to starting assays.…”

Section: Methodsmentioning

confidence: 99%

An investigation into the impact of deleting one copy of the glutaredoxin-2 gene on diet-induced weight gain and the bioenergetics of muscle mitochondria in female mice fed a high fat diet

et al. 2020

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Our group recently documented that male mice containing a deletion for one copy of the glutaredoxin-2 (Grx2) gene were completely protected from developing diet-induced obesity (DIO). Objectives: Here, we conducted a similar investigation but with female littermates. Results: In comparison to our recent publication using male mice, exposure of WT and GRX2+/- female mice to a HFD from 3-to-10 weeks of age did not induce any changes in body mass, circulating blood glucose, food intake, hepatic glycogen levels, or abdominal fat pad mass. Examination of the bioenergetics of muscle mitochondria revealed no changes in the rate of superoxide ( )/hydrogen peroxide (H 2 O 2 ) or O 2 consumption under different states of respiration or alterations in lipid peroxidation adduct levels regardless of mouse strain or diet. Additionally, we measured the bioenergetics of mitochondria isolated from liver tissue and found that partial loss of GRX2 augmented respiration but did not alter ROS production. Discussion: Overall, our findings demonstrate there are sex differences in the protection of female GRX2+/- mice from DIO, fat accretion, intrahepatic lipid accumulation, and the bioenergetics of mitochondria from muscle and liver tissue.

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“…In the reaction catalyzed by GPx, glutathione is oxidized to glutathione disulfate, which can be converted to glutathione by glutathione reductase in an "NADPH-consuming" process [106]. Catalase (CAT) is a high molecular weight tetrameric enzyme containing porphyrin in the active site.…”

Section: Exercise and Ros Production: How To Prevent Oxidative Damagementioning

confidence: 99%

“…It is one of the fundamental antioxidant enzymes that mitigates oxidative stress to a significant extent by destroying cellular hydrogen peroxide to produce water and oxygen [107] (Figure 3). In the reaction catalyzed by GPx, glutathione is oxidized to glutathione disulfate, which can be converted to glutathione by glutathione reductase in an "NADPH-consuming" process [106]. Catalase (CAT) is a high molecular weight tetrameric enzyme containing porphyrin in the active site.…”

Section: Exercise and Ros Production: How To Prevent Oxidative Damagementioning

confidence: 99%

Antioxidants in Sport Sarcopenia

et al. 2020

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The decline of skeletal muscle mass and strength that leads to sarcopenia is a pathology that might represent an emergency healthcare issue in future years. Decreased muscle mass is also a condition that mainly affects master athletes involved in endurance physical activities. Skeletal muscles respond to exercise by reshaping the biochemical, morphological, and physiological state of myofibrils. Adaptive responses involve the activation of intracellular signaling pathways and genetic reprogramming, causing alterations in contractile properties, metabolic status, and muscle mass. One of the mechanisms leading to sarcopenia is an increase in reactive oxygen and nitrogen species levels and a reduction in enzymatic antioxidant protection. The present review shows the recent experimental models of sarcopenia that explore molecular mechanisms. Furthermore, the clinical aspect of sport sarcopenia will be highlighted, and new strategies based on nutritional supplements, which may contribute to reducing indices of oxidative stress by reinforcing natural endogenous protection, will be suggested.

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Estimation of the hydrogen peroxide producing capacities of liver and cardiac mitochondria isolated from C57BL/6N and C57BL/6J mice

Cited by 41 publications

References 36 publications

An Update on Mitochondrial Reactive Oxygen Species Production

An Update on Mitochondrial Reactive Oxygen Species Production

An investigation into the impact of deleting one copy of the glutaredoxin-2 gene on diet-induced weight gain and the bioenergetics of muscle mitochondria in female mice fed a high fat diet

Antioxidants in Sport Sarcopenia

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