An association between polymorphism of the NADH/NADPH oxidase p22phox (phagocyte oxidase) subunit and aging in Turkish population

Kayaaltı, Zeliha; Kaya, Dilek; Bacaksız, Ayşegül; Söylemezoğlu, Tülın

doi:10.1007/s40520-013-0129-3

Cited by 5 publications

(2 citation statements)

References 30 publications

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“…By contrast, there is an association between single nucleotide polymorphism (SNP) CC for C242T in NADPH oxidase subunit (p22phox) and longevity (people >85 years) in the Turkish population [ 96 ]. In the Korean centenarian cohort, no significant difference between C242T genotype frequency was found between centenarian vs non-centenarians [ 97 ].…”

Section: Implication Of Nadph Oxidases In Human Agingmentioning

confidence: 99%

Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging

Ewald

2018

Antioxidants

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An accumulating body of evidence suggests that transient or physiological reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases act as a redox signal to re-establish homeostasis. The capacity to re-establish homeostasis progressively declines during aging but is maintained in long-lived animals to promote healthy aging. In the model organism Caenorhabditis elegans, ROS generated by dual oxidases (Duox) are important for extracellular matrix integrity, pathogen defense, oxidative stress resistance, and longevity. The Duox enzymatic activity is tightly regulated and under cellular control. Developmental molting cycles, pathogen infections, toxins, mitochondrial-derived ROS, drugs, and small GTPases (e.g., RHO-1) can activate Duox (BLI-3) to generate ROS, whereas NADPH oxidase inhibitors and negative regulators, such as MEMO-1, can inhibit Duox from generating ROS. Three mechanisms-of-action have been discovered for the Duox/BLI-3-generated ROS: (1) enzymatic activity to catalyze crosslinking of free tyrosine ethyl ester in collagen bundles to stabilize extracellular matrices, (2) high ROS bursts/levels to kill pathogens, and (3) redox signaling activating downstream kinase cascades to transcription factors orchestrating oxidative stress and immunity responses to re-establish homeostasis. Although Duox function at the cell surface is well established, recent genetic and biochemical data also suggests a novel role for Duoxs at the endoplasmic reticulum membrane to control redox signaling. Evidence underlying these mechanisms initiated by ROS from NADPH oxidases, and their relevance for human aging, are discussed in this review. Appropriately controlling NADPH oxidase activity for local and physiological redox signaling to maintain cellular homeostasis might be a therapeutic strategy to promote healthy aging.

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Section: Implication Of Nadph Oxidases In Human Agingmentioning

confidence: 99%

Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging

Ewald

2018

Antioxidants

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show abstract

“…In humans, there is an association between single nucleotide polymorphism (SNP) CC for C242T in NADPH oxidase subunit (p22phox) and longevity (people >85 years) in the Turkish population [95]. In the Korean centenarian cohort, no significant difference between C242T genotype frequency was found between centenarian vs non-centenarians [96].…”

Section: Conclusive Remarks and Relevance To Human Agingmentioning

confidence: 99%

Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity, and Aging

Ewald¹

2018

Preprint

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An accumulating body of evidence suggests that physiological reactive oxygen species (ROS) generated by NADPH oxidases act as a redox signal to re-establish homeostasis, a capacity that progressively declines during aging, but is maintained in long-lived animals to promote healthy aging. In the model organism Caenorhabditis elegans, ROS generated by dual oxidases (Duox) are important for extracellular matrix integrity, pathogen defense, oxidative stress resistance, and longevity. The Duox enzymatic activity is tightly regulated and under cellular control. Developmental molting cycles, pathogen infections, toxins, mitochondrial-derived ROS, drugs, and small GTPases (RHO-1) can activate Duox (BLI-3) to generate ROS, whereas NADPH oxidase inhibitors and negative regulators, such as MEMO-1, can inhibit Duox to generate ROS. Three mechanisms-of-action have been discovered for the Duox/BLI-3-generated ROS: 1) enzymatic activity to catalyze cross-linking of free tyrosine ethyl ester in collagen bundles to stabilize extracellular matrices, 2) high ROS bursts/levels to kill pathogens, and 3) Redox signaling activating downstream kinase cascades to transcription factors orchestrating oxidative stress- and immunity responses to re-establish homeostasis. Although Duox function at the cell surface is well established, recent genetic and biochemical data also suggests a novel role for Duoxs at the endoplasmic reticulum membrane to control redox signaling. Evidence underlying these mechanisms initiated by ROS from NADPH oxidases and their relevance for human aging are discussed in this review. Appropriately controlling NADPH oxidase activity for local and physiological redox signaling to maintain cellular homeostasis might be a therapeutic strategy to promote healthy aging.

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Doxorubicin–transferrin conjugate alters mitochondrial homeostasis and energy metabolism in human breast cancer cells

Wigner

Zieliński

Łabieniec-Watała

et al. 2021

Sci Rep

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Doxorubicin (DOX) is considered one of the most powerful chemotherapeutic agents but its clinical use has several limitations, including cardiomyopathy and cellular resistance to the drug. By using transferrin (Tf) as a drug carrier, however, the adverse effects of doxorubicin as well as drug resistance can be reduced. The main objective of this study was to determine the exact nature and extent to which mitochondrial function is influenced by DOX–Tf conjugate treatment, specifically in human breast adenocarcinoma cells. We assessed the potential of DOX–Tf conjugate as a drug delivery system, monitoring its cytotoxicity using the MTT assay and ATP measurements. Moreover, we measured the alterations of mitochondrial function and oxidative stress markers. The effect of DOX–Tf was the most pronounced in MDA-MB-231, triple-negative breast cancer cells, whereas non-cancer endothelial HUVEC-ST cells were more resistant to DOX–Tf conjugate than to free DOX treatment. A different sensitivity of two investigate breast cancer cell lines corresponded to the functionality of their cellular antioxidant systems and expression of estrogen receptors. Our data also revealed that conjugate treatment mediated free radical generation and altered the mitochondrial bioenergetics in breast cancer cells.

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An association between polymorphism of the NADH/NADPH oxidase p22phox (phagocyte oxidase) subunit and aging in Turkish population

Cited by 5 publications

References 30 publications

Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging

Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging

Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity, and Aging

Doxorubicin–transferrin conjugate alters mitochondrial homeostasis and energy metabolism in human breast cancer cells

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