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4. Guidelines for measuring reactive oxygen species and oxidative damage in cells and in vivo

Author

Murphy, Michael P, Bayir, Hülya, Belousov, Vsevolod, Chang, Christopher J, Davies, Kelvin JA, Davies, Michael J, Dick, Tobias P, Finkel, Toren, Forman, Henry J, Janssen-Heininger, Yvonne, Gems, David, Kagan, Valerian E, Kalyanaraman, Balaraman, Larsson, Nils-Göran, Milne, Ginger L, Nyström, Thomas, Poulsen, Henrik E, Radi, Rafael, Van Remmen, Holly, Schumacker, Paul T, Thornalley, Paul J, Toyokuni, Shinya, Winterbourn, Christine C, Yin, Huiyong, and Halliwell, Barry

Subjects
Generic health relevance, Antioxidants, Oxidation-Reduction, Oxidative Stress, Reactive Oxygen Species, Signal Transduction
Abstract

Multiple roles of reactive oxygen species (ROS) and their consequences for health and disease are emerging throughout biological sciences. This development has led researchers unfamiliar with the complexities of ROS and their reactions to employ commercial kits and probes to measure ROS and oxidative damage inappropriately, treating ROS (a generic abbreviation) as if it were a discrete molecular entity. Unfortunately, the application and interpretation of these measurements are fraught with challenges and limitations. This can lead to misleading claims entering the literature and impeding progress, despite a well-established body of knowledge on how best to assess individual ROS, their reactions, role as signalling molecules and the oxidative damage that they can cause. In this consensus statement we illuminate problems that can arise with many commonly used approaches for measurement of ROS and oxidative damage, and propose guidelines for best practice. We hope that these strategies will be useful to those who find their research requiring assessment of ROS, oxidative damage and redox signalling in cells and in vivo.

Published
2022

14. Molecular changes associated with spinal cord aging

Author

Piekarz, Katarzyna M., Bhaskaran, Shylesh, Sataranatarajan, Kavithalakshmi, Street, Kaitlyn, Premkumar, Pavithra, Saunders, Debra, Zalles, Michelle, Gulej, Rafal, Khademi, Shadi, Laurin, Jaime, Peelor, Rick, Miller, Benjamin F., Towner, Rheal, and Van Remmen, Holly

Published
2020
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16. Time-restricted feeding improves aortic endothelial relaxation by enhancing mitochondrial function and attenuating oxidative stress in aged mice

Author

Milan, Madison, Brown, Jacob, O'Reilly, Colleen L., Bubak, Matthew P., Negri, Sharon, Balasubramanian, Priya, Dhanekula, Arjune S., Pharaoh, Gavin, Reyff, Zeke, Ballard, Cade, Shi, Helen, Yabluchanskiy, Andriy, Rudolph, Michael C., Ungvari, Zoltan, Marcinek, David J., Miller, Benjamin F., Van Remmen, Holly, and Tarantini, Stefano

Published
2024
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19. Insulin-like growth factor receptor signaling regulates working memory, mitochondrial metabolism, and amyloid-β uptake in astrocytes

Author

Logan, Sreemathi, Pharaoh, Gavin A., Marlin, M. Caleb, Masser, Dustin R., Matsuzaki, Satoshi, Wronowski, Benjamin, Yeganeh, Alexander, Parks, Eileen E., Premkumar, Pavithra, Farley, Julie A., Owen, Daniel B., Humphries, Kenneth M., Kinter, Michael, Freeman, Willard M., Szweda, Luke I., Van Remmen, Holly, and Sonntag, William E.

Published
2018
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23. Modulation of sarcopenia phenotypes by glutathione peroxidase 4 overexpression in mice.

Author

Xu, Hongyang, Czyżowska, Agnieszka, Van Remmen, Holly, and Brown, Jacob L.

Abstract

Our laboratory previously showed lipid hydroperoxides and oxylipin levels are elevated in response to loss of skeletal muscle innervation and are associated with muscle pathologies. To elucidate the pathological impact of lipid hydroperoxides, we overexpressed glutathione peroxidase 4 (GPx4), an enzyme that targets reduction of lipid hydroperoxides in membranes, in adult CuZn superoxide dismutase knockout (Sod1KO) mice that show accelerated muscle atrophy associated with loss of innervation. The gastrocnemius muscle from Sod1KO mice shows reduced mitochondrial respiration and elevated oxidative stress (F2‐isoprostanes and hydroperoxides) compared to wild‐type (WT) mice. Overexpression of GPx4 improved mitochondrial respiration and reduced hydroperoxide generation in Sod1KO mice, but did not attenuate the muscle loss that occurs in Sod1KO mice. In contrast, contractile force generation is reduced in EDL muscle in Sod1KO mice relative to WT mice, and overexpression of GPx4 restored force generation to WT levels in Sod1KO mice. GPx4 overexpression also prevented loss of muscle contractility at the single fibre level in fast‐twitch fibres from Sod1KO mice. Muscle fibres from Sod1KO mice were less sensitive to both depolarization and calcium at the single fibre level and exhibited a reduced activation by S‐glutathionylation. GPx4 overexpression in Sod1KO mice rescued the deficits in both membrane excitability and calcium sensitivity of fast‐twitch muscle fibres. Overexpression of GPx4 also restored the sarco/endoplasmic reticulum Ca2+‐ATPase activity in Sod1KO gastrocnemius muscles. These data suggest that GPx4 plays an important role in preserving excitation–contraction coupling function and Ca2+ homeostasis, and in maintaining muscle and mitochondrial function in oxidative stress‐induced sarcopenia. Key points: Knockout of CuZn superoxide dismutase (Sod1KO) induces elevated oxidative stress with accelerated muscle atrophy and weakness.Glutathione peroxidase 4 (GPx4) plays a fundamental role in the reduction of lipid hydroperoxides in membranes, and overexpression of GPx4 improves mitochondrial respiration and reduces hydroperoxide generation in Sod1KO mice.Muscle contractile function deficits in Sod1KO mice are alleviated by the overexpression of GPx4.GPx4 overexpression in Sod1KO mice rescues the impaired muscle membrane excitability of fast‐twitch muscle fibres and improves their calcium sensitivity.Sarco/endoplasmic reticulum Ca2+‐ATPase activity in Sod1KO muscles is decreased, and it is restored by the overexpression of GPx4.Our results confirm that GPx4 plays an important role in preserving excitation–contraction coupling function and Ca2+ homeostasis, and maintaining muscle and mitochondrial function in oxidative stress‐induced sarcopenia. [ABSTRACT FROM AUTHOR]

Published
2023
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24. Modulation of Lon protease activity and aconitase turnover during aging and oxidative stress

Author

Bota, Daniela A, Van Remmen, Holly, and Davies, Kelvin JA

Subjects
Aging, ATP-Dependent Proteases, Aconitate Hydratase, Aldehydes, Animals, Down-Regulation, Heat-Shock Proteins, Mice, Mice, Knockout, Mitochondria, Muscle, Skeletal, Oxidative Stress, Serine Endopeptidases, Superoxide Dismutase, Lon protease, aconitase, protein oxidation, mitochondria, aging, Sod2, Medicinal and Biomolecular Chemistry, Biochemistry and Cell Biology, Evolutionary Biology, Biochemistry & Molecular Biology
Abstract

We compared Lon protease expression in murine skeletal muscle of young and old, wild-type and Sod2(-/+) heterozygous mice, and studied Lon involvement in the accumulation of damaged (oxidized) proteins. Lon protease protein levels were lower in old and oxidatively challenged animals, and this Lon deficiency was associated with increased levels of carbonylated proteins. We identified one of these proteins as aconitase, and another as an aconitase fragmentation product, which we can also generate in vitro by treating purified aconitase with H(2)O(2). These results imply that aging and oxidative stress down-regulate Lon protease expression which, in turn, may be responsible for the accumulation of damaged proteins, such as aconitase, within mitochondria.

Published
2002

25. Neuronal deletion of MnSOD in mice leads to demyelination, inflammation and progressive paralysis that mimics phenotypes associated with progressive multiple sclerosis

Author

Bhaskaran, Shylesh, primary, Kumar, Gaurav, additional, Thadathil, Nidheesh, additional, Piekarz, Katarzyna M., additional, Mohammed, Sabira, additional, Lopez, Sergio Dominguez, additional, Qaisar, Rizwan, additional, Walton, Dorothy, additional, Brown, Jacob L., additional, Murphy, Ashley, additional, Smith, Nataliya, additional, Saunders, Debra, additional, Beckstead, Michael J., additional, Plafker, Scott, additional, Lewis, Tommy L., additional, Towner, Rheal, additional, Deepa, Sathyaseelan S., additional, Richardson, Arlan, additional, Axtell, Robert C., additional, and Van Remmen, Holly, additional

Published
2023
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26. Molecular changes associated with spinal cord aging

Author

Piekarz, Katarzyna M., Bhaskaran, Shylesh, Sataranatarajan, Kavithalakshmi, Street, Kaitlyn, Premkumar, Pavithra, Saunders, Debra, Zalles, Michelle, Gulej, Rafal, Khademi, Shadi, Laurin, Jaime, Peelor, Rick, Miller, Benjamin F., Towner, Rheal, and Van Remmen, Holly

Abstract

Age-related muscle weakness and loss of muscle mass (sarcopenia) is a universal problem in the elderly. Our previous studies indicate that alpha motor neurons (α-MNs) play a critical role in this process. The goal of the current study is to uncover changes in the aging spinal cord that contribute to loss of innervation and the downstream degenerative processes that occur in skeletal muscle. The number of α-MNs is decreased in the spinal cord of wildtype mice during aging, beginning in middle age and reaching a 41% loss by 27 months of age. There is evidence for age-related loss of myelin and mild inflammation, including astrocyte and microglia activation and an increase in levels of sICAM-1. We identified changes in metabolites consistent with compromised neuronal viability, such as reduced levels of N-acetyl-aspartate. Cleaved caspase-3 is more abundant in spinal cord from old mice, suggesting that apoptosis contributes to neuronal loss. RNA-seq analysis revealed changes in the expression of a number of genes in spinal cord from old mice, in particular genes encoding extracellular matrix components (ECM) and a 172-fold increase in MMP-12 expression. Furthermore, blood-spinal cord barrier (BSCB) permeability is increased in old mice, which may contribute to alterations in spinal cord homeostasis and exacerbate neuronal distress. Together, these data show for the first time that the spinal cord undergoes significant changes during aging, including progressive α-MNs loss that is associated with low-grade inflammation, apoptosis, changes in ECM, myelination, and vascular permeability.

Published
2024
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38. Senolytic treatment reduces cell senescence and necroptosis in Sod1 knockout mice that is associated with reduced inflammation and hepatocellular carcinoma

Author

Thadathil, Nidheesh, primary, Selvarani, Ramasamy, additional, Mohammed, Sabira, additional, Nicklas, Evan H., additional, Tran, Albert L., additional, Kamal, Maria, additional, Luo, Wenyi, additional, Brown, Jacob L., additional, Lawrence, Marcus M., additional, Borowik, Agnieszka K., additional, Miller, Benjamin F., additional, Van Remmen, Holly, additional, Richardson, Arlan, additional, and Deepa, Sathyaseelan S., additional

Published
2022
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39. Selective Ablation of Sod2 in Astrocytes Induces Sex-Specific Effects on Cognitive Function, d-Serine Availability, and Astrogliosis

Author

Baier, Matthew P., primary, Nagaraja, Raghavendra Y., additional, Yarbrough, Hannah P., additional, Owen, Daniel B., additional, Masingale, Anthony M., additional, Ranjit, Rojina, additional, Stiles, Megan A., additional, Murphy, Ashley, additional, Agbaga, Martin-Paul, additional, Ahmad, Mohiuddin, additional, Sherry, David M., additional, Kinter, Michael T., additional, Van Remmen, Holly, additional, and Logan, Sreemathi, additional

Published
2022
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42. Guidelines for measuring reactive oxygen species and oxidative damage in cells and in vivo

Author

Murphy, Michael P., Bayir, Hülya, Belousov, Vsevolod, Chang, Christopher J., Davies, Kelvin J.A., Davies, Michael J., Dick, Tobias P., Finkel, Toren, Forman, Henry J., Janssen-Heininger, Yvonne, Gems, David, Kagan, Valerian E., Kalyanaraman, Balaraman, Larsson, Nils Göran, Milne, Ginger L., Nyström, Thomas, Poulsen, Henrik E., Radi, Rafael, Van Remmen, Holly, Schumacker, Paul T., Thornalley, Paul J., Toyokuni, Shinya, Winterbourn, Christine C., Yin, Huiyong, Halliwell, Barry, Murphy, Michael P., Bayir, Hülya, Belousov, Vsevolod, Chang, Christopher J., Davies, Kelvin J.A., Davies, Michael J., Dick, Tobias P., Finkel, Toren, Forman, Henry J., Janssen-Heininger, Yvonne, Gems, David, Kagan, Valerian E., Kalyanaraman, Balaraman, Larsson, Nils Göran, Milne, Ginger L., Nyström, Thomas, Poulsen, Henrik E., Radi, Rafael, Van Remmen, Holly, Schumacker, Paul T., Thornalley, Paul J., Toyokuni, Shinya, Winterbourn, Christine C., Yin, Huiyong, and Halliwell, Barry

Abstract

Multiple roles of reactive oxygen species (ROS) and their consequences for health and disease are emerging throughout biological sciences. This development has led researchers unfamiliar with the complexities of ROS and their reactions to employ commercial kits and probes to measure ROS and oxidative damage inappropriately, treating ROS (a generic abbreviation) as if it were a discrete molecular entity. Unfortunately, the application and interpretation of these measurements are fraught with challenges and limitations. This can lead to misleading claims entering the literature and impeding progress, despite a well-established body of knowledge on how best to assess individual ROS, their reactions, role as signalling molecules and the oxidative damage that they can cause. In this consensus statement we illuminate problems that can arise with many commonly used approaches for measurement of ROS and oxidative damage, and propose guidelines for best practice. We hope that these strategies will be useful to those who find their research requiring assessment of ROS, oxidative damage and redox signalling in cells and in vivo.

Published
2022

45. Scavenging mitochondrial hydrogen peroxide by peroxiredoxin 3 overexpression attenuates contractile dysfunction and muscle atrophy in a murine model of accelerated sarcopenia

Author

Ahn, Bumsoo, primary, Ranjit, Rojina, additional, Kneis, Parker, additional, Xu, Hongyang, additional, Piekarz, Katarzyna M., additional, Freeman, Willard M., additional, Kinter, Michael, additional, Richardson, Arlan, additional, Ran, Qitao, additional, Brooks, Susan V., additional, and Van Remmen, Holly, additional

Published
2022
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