ArticleThe Journal of pharmacology and experimental therapeutics2011
Inhibition of NADPH oxidases prevents chronic ethanol-induced bone loss in female rats.
Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
- Dexamethasone Induced Osteocyte Apoptosis in Steroid-Induced Femoral Head Osteonecrosis through ROS-Mediated Oxidative Stress.Orthopaedic surgery · 2024Article
- The role of N-acetylcysteine in osteogenic microenvironment for bone tissue engineering.Frontiers in cell and developmental biology · 2024Review
- Nox4 expression in osteo-progenitors controls bone development in mice during early life.Communications biology · 2022Article
- Binge Ethanol Exposure in Mice Represses Expression of Genes Involved in Osteoblast Function and Induces Expression of Genes Involved in Osteoclast Differentiation Independently of Endogenous Catalase.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Natural Recovery by the Liver and Other Organs after Chronic Alcohol Use.Alcohol research : current reviews · 2021Review
- Antagonistic Impact of Acrylamide and Ethanol on Biochemical and Morphological Parameters Consistent with Bone Health in Mice.Animals : an open access journal from MDPI · 2020Article
- Impact of Alcohol on Bone Health, Homeostasis and Fracture repair.Current pathobiology reports · 2020Article
- Nox4 Expression Is Not Required for OVX-Induced Osteoblast Senescence and Bone Loss in Mice.JBMR plus · 2020Article
- Chronic Ethanol Feeding in Mice Decreases Expression of Genes for Major Structural Bone Proteins in a Nox4-Independent Manner.The Journal of pharmacology and experimental therapeutics · 2020Article
- Dehydrocostus lactone inhibits NFATc1 via regulation of IKK, JNK, and Nrf2, thereby attenuating osteoclastogenesis.BMB reports · 2020Article
- Reduced Serum Osteocalcin in High-Risk Alcohol Using People Living With HIV Does Not Correlate With Systemic Oxidative Stress or Inflammation: Data From the New Orleans Alcohol Use in HIV Study.Alcoholism, clinical and experimental research · 2019Article
- 3-(3-Hydroxyphenyl)-Propionic Acid (PPA) Suppresses Osteoblastic Cell Senescence to Promote Bone Accretion in Mice.JBMR plus · 2019Article
- NADPH Oxidase Isoforms Are Involved in Glucocorticoid-Induced Preosteoblast Apoptosis.Oxidative medicine and cellular longevity · 2019Article
- Changes in the microstructure of compact and trabecular bone tissues of mice subchronically exposed to alcohol.Journal of biological research (Thessalonike, Greece) · 2018Article
- NOX4 Deletion in Male Mice Exacerbates the Effect of Ethanol on Trabecular Bone and Osteoblastogenesis.The Journal of pharmacology and experimental therapeutics · 2018Article
- N-Acetyl Cysteine Treatment Restores Early Phase Fracture Healing in Ethanol-Fed Rats.Alcoholism, clinical and experimental research · 2018Article
- Effects of Episodic Alcohol Exposure on BMP2 Signaling During Tibia Fracture Healing.Journal of orthopaedic trauma · 2018Article
- Cellular and molecular mechanisms of alcohol-induced osteopenia.Cellular and molecular life sciences : CMLS · 2017Review
- Partial Protection by Dietary Antioxidants Against Ethanol-Induced Osteopenia and Changes in Bone Morphology in Female Mice.Alcoholism, clinical and experimental research · 2017Article
- Reactive Oxygen Species Differentially Regulate Bone Turnover in an Age-Specific Manner in Catalase Transgenic Female Mice.The Journal of pharmacology and experimental therapeutics · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Previous in vitro data suggest that ethanol (EtOH) activates NADPH oxidase (Nox) in osteoblasts leading to accumulation of reactive oxygen species (ROS). This might be a mechanism underlying inhibition of bone formation and increased bone resorption observed in vivo after EtOH exposure. In a rat model in which cycling females were infused intragastrically with EtOH-containing liquid diets, EtOH significantly decreased bone formation and stimulated osteoblast-dependent osteoclast differentiation. These effects were reversed by exogenous 17-β-estradiol coadministration. Moreover, coadministration of N-acetyl cysteine (NAC), an antioxidant, or diphenylene iodonium (DPI), a specific Nox inhibitor, also abolished chronic EtOH-associated bone loss. EtOH treatment up-regulated mRNA levels of Nox1, 2, 4, and the receptor activator of nuclear factor-κB ligand (RANKL), an essential factor for differentiation of osteoclasts in bone. Protein levels of Nox4, a major Nox isoform expressed in nonphagocytic cells, was also up-regulated by EtOH in bone. 17-β-Estradiol, NAC, and DPI were able to normalize EtOH-induced up-regulation of Nox and RANKL. In vitro experiments demonstrated that EtOH directly up-regulated Nox expression in osteoblasts. Pretreatment of osteoblasts with DPI eliminated EtOH-induced RANKL promoter activity. Furthermore, EtOH induced RANKL gene expression, and RANKL promoter activation in osteoblasts was ROS-dependent. These data suggest that inhibition of Nox expression and activity may be critical for prevention of chronic EtOH-induced osteoblast-dependent bone loss.
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