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C60 INTERESTING ANTIOXIDANT for BONES, HEALTH, \u0026 CELL SUPPORT? w/ Ken Swartz + BoneCoach™Antioxidant and bone health -
A previous study indicated that the total SOD level decreased in menopausal mice, as measured by ELISA Cao et al. Hidetoshi Nojiri found that bone mass decreased significantly in SOD-deficient mice Nojiri et al.
Increasing mitochondrial SOD activity prevented osteoblast apoptosis induced by ROS Yang et al. Moreover, SOD has a significant regulatory effect on the differentiation trend of bone marrow mesenchymal stem cells BM-MSCs. Catalase CAT is the marker enzyme of peroxisomes and is widely present in various tissues of the body Shin et al.
As the second defense system of antioxidant enzymes, the antioxidant mechanism of CAT mainly acts on the dismutation reaction on H 2 O 2 produced in SOD-mediated processes Ray and Husain, A large number of studies have reported that H 2 O 2 increased lipid peroxidation following the decrease of CAT in a postmenopausal osteoporosis model Ozgocmen et al.
In addition, CAT can have a positive effect on bone mass by inhibiting H 2 O 2 -induced osteoclastic resorption Fraser et al. However, the physiological role of CAT is mainly dependent on the regulation of forkhead box O1 FOXO1 Venkatesan et al.
FOXO1 increased the expression of SIRT1 participating in the mitochondrial biosynthesis to maintain the level of CAT Alcendor et al. Estrogen deficiency decreases the expression of FOXO1 protein, leading to the inhibition of BM-MSCs into osteoblasts Liao et al.
Glutathione peroxidase GSH-Px is an important peroxidase enzyme characterized by each subunit containing a selenium Se atom in the form of selenocysteine Liu et al. The antioxidant effect of GSH-Px is determined by the Se cysteine in its active center Zachara, The Se of the GSH-Px enzyme system catalyzes GSH to GSSG and reduces toxic peroxides to non-toxic hydroxyl compounds.
GSH-Px can intervene in the development of osteoporosis through the abovementioned GSH-dependent pathways and endoplasmic reticulum-mediated osteogenic differentiation of BM-MSCs via the mTOR pathway Wiswedel et al.
Additionally, GSH-Px can relieve inflammation-induced osteolytic bone destruction by breaking down LPS Islam et al. Upregulating GSH-PX activity can inhibit pro-inflammatory factors associated with osteoclast maturation genes, such as iNOS, IL-1β, and tumor necrosis factor-alpha TNF-α Kruger et al.
GSH-Px may be the key link in the oxidative stress-inflammation reaction in postmenopausal osteoporosis with great potential research value. However, the content of peroxidase in the fracture site was increased to compensate for fracture-induced stress damage when fractures occurred in patients with osteoporosis Föger-Samwald et al.
The metabolism of free purine bases after DNA damage aggravates oxidative stress damage. In contrast, a growing number of studies have shown that high uric acid levels can lead to decreased bone density and osteoporosis Sharaf El Din et al.
The ROS produced by the oxidation of purine inhibits osteoblast differentiation from BM-MSCs and bone mineralization through the ERK and NF-KB pathways Chang et al.
ROS can stimulate the proliferation and differentiation of osteoclast progenitor cells through the RANKL pathway Garrett et al. In addition to direct effects, purine metabolism also regulates bone homeostasis through the indirect activation of inflammatory cytokines Martinon, At high uric acid levels, mononuclear cell-derived inflammasomes phagocytose monosodium urate MSU and release IL-1, TNF-α, IL-6, and IL-8 Chhana et al.
They further activate RANK and macrophage colony-stimulating factor M-CSF , resulting in a large number of osteoclasts Ritchlin et al. Therefore, the damaged DNA must be repaired to ensure genomic integrity Radak and Boldogh, DNA repair enzymes reduce the production of purine bases to prevent further damage to the skeletal system, as well as the occurrence of osteoporosis Yao et al.
Lipid peroxide, a peroxidation product of unsaturated fatty acids with ROS, is the core of lipofuscin Adibhatla and Hatcher, ; Zadlo et al. Previous studies indicated that a large amount of lipid peroxide is deposited in the bone tissue of ovariectomized mice Al et al.
It triggers oxidative damage and inflammation in the bone microenvironment, destroying bone homeostasis Wu et al.
Oxidized lipids cannot be repaired and need to be broken down into non-toxic products by specific enzymes. Phospholipase A2 PLA2 and acyltransferase AT are the important metabolic enzymes of lipid peroxide. AT directly participates in lipid mobilization and β-oxidation Wang et al.
PLA2 catalyzes the hydrolysis of the ester bond formed by the C2 hydroxyl group on the glycerol backbone in the phospholipid Prunonosa Cervera et al. Compared with AT, the effect of PLA2 on the skeletal system is not limited to accelerate the metabolism of lipid peroxide.
PLA2 can increase the expression of PGE2 to promote osteogenesis through the cyclooxygenase 2 COX2 pathway Yoshida et al. At present, osteoporosis affects approximately one-third of postmenopausal women worldwide Gosset et al.
In the past, scientific researchers and clinicians focused on the skeletal system, especially the inhibition of osteoclasts, to treat postmenopausal osteoporosis Ukon et al. Although the deterioration has been improved to a certain extent, the pathogenesis of the disease has not been clarified, and effective control has not been achieved.
Oxidative stress damage, as a mediator linking estrogen, aging, and bone, is regarded as a breakthrough in exploring the development of postmenopausal osteoporosis.
Overloaded ROS break the balance between osteogenesis and osteoclastogenesis, leading to bone mass loss and bone quality decline Lee et al.
The ROS accumulation is due to excessive production and inefficient removal. The DNA damage caused by ROS and the metabolism of DNA purine bases form a closed loop, which continuously increases the production of free radicals Calkins et al.
DNA repair enzymes are essential to break this vicious cycle Figure 4. The endogenous hormone melatonin maintains these antioxidant processes by protecting mitochondrial function Yang et al. The ROS activation of the NF-κB pathway involved in osteoclast maturation is also inhibited by antioxidant systems.
Inflammation is also an important connection between oxidative stress and postmenopausal osteoporosis. Oxidative stress causes biomolecular damage and releases cytokines and chemokines to recruit and activate inflammatory cells, resulting in chronic inflammation in the body Sindhu et al.
ROS can induce the hyperactivation of NF-κB by modulating the activity of AP-1 Arcambal et al. Activated NF-κB also induces the expression of inflammatory factors, such as IL-1β, IL-6, and TNF-α to exacerbate inflammation Ma et al.
These inflammatory factors also stimulate ROS production to exacerbate oxidative damage Zhu et al. A vicious cycle exists between oxidative stress and inflammation. Osteoporosis is also regarded as a chronic inflammatory disease Montalcini et al. Estrogen deficiency could induce an inflammatory storm and decrease antioxidant capacity Mohamad et al.
The secretion of inflammatory factors activates osteoclasts to worsen osteoporosis Wu et al. Therefore, anti-inflammatory drugs have been applied to treat osteoporosis and have the ability to improve bone mass Tao et al.
Due to the unclear pathogenesis of postmenopausal osteoporosis, past studies have obvious limitations. Our review clarified the nature of postmenopausal osteoporosis from the perspective of oxidative stress damage induced by aging and described the potential ability of antioxidants to treat it in detail.
Antioxidants not only systematically improve the oxidation state of the body, but also locally regulate the imbalance of the skeletal system.
At present, antioxidant substances have been verified to improve bone mass in animal models, such as vitamin C, vitamin E, and GSH Deng et al. However, there is no special drug designed based on the antioxidant ability that is being applied for osteoporosis treatment.
Three classes of antioxidant systems are very important for the prevention and treatment of postmenopausal osteoporosis. Our review contributes to antioxidant drug designs for postmenopausal osteoporosis.
KY contributed to data curation, formal analysis, data curation, methodology, and writing — original draft. FC contributed to investigation, methodology, software, and writing — original draft. YX contributed to software and validation. LT contributed to conceptualization, software, validation, writing, review, and editing.
YZ contributed to funding acquisition, project administration, resources, writing, reviewing, and editing. All authors read and approved the manuscript.
This study was supported by the Shenyang Young and Middle-aged Innovative Talent Project RC The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.
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Ahmad Hamouda on his efforts and critical revision of this chapter. Department of Orthopedics, College of Medicine, Taibah University, AlMadinah Almmunawarah, Kingdom of Saudi Arabia. Department of Clinical Biochemistry, College of Medicine, Taibah University, AlMadinah Almmunawarah, Kingdom of Saudi Arabia.
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Osteoporosis and Oxidative Stress — Role of Antioxidants. In: Laher, I. eds Systems Biology of Free Radicals and Antioxidants. Springer, Berlin, Heidelberg.
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Abstract Osteoporosis is a systemic metabolic bone disorder characterized by a decrease of bone strength with fragility fracture. Keywords Antioxidants Free radicals Osteoporosis Oxidative stress Vitamins.
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Hfalth Maggio, Mauro Barabani, Marco Immune-boosting supplements, M. Although recent epidemiological studies found a positive correlation between Antioxidant and bone health vitamin C intake and bone mineral density, hralth on plasma levels Antioidant vitamin C or other antioxidants in osteoporotic subjects are bon. The aim of hfalth study was to evaluate whether Hydration and sports performance defenses are Antioxidant and bone health in elderly osteoporotic women and, if this is the case, to understand whether osteoporosis is a condition characterized by increased oxidative stress. To answer these questions, plasma vitamins C, E, and A; uric acid; and the enzymatic activities of superoxide dismutase in plasma and erythrocytes and of glutathione peroxidase in plasma were measured in 75 subjects with osteoporosis and 75 controls. Dietary and endogenous antioxidants were consistently lower in osteoporotic than in control subjects. On the other hand, plasma levels of malondialdehyde, a byproduct of lipid peroxidation, did not differ between groups. Our results reveal that antioxidant defenses are markedly decreased in osteoporotic women. Osteoporosis is nealth systemic metabolic bone disorder characterized by a decrease hralth bone strength with Minerals for cardiovascular health fracture. There Antioxidant and bone health only heapth few studies hsalth Antioxidant and bone health ahd stress bnoe a risk factor linked to osteoporosis OP. This Good gut bacteria discusses the Antioxidant and bone health of Antioxidantt factors involved in OP and in particular the role of oxidative stress OS in this disease. Moreover, our aim is extended to show the role of antioxidants in the prevention of OP. Mutations or polymorphism of nitric oxide NO synthase genes increase susceptibility of many subjects to OP through changes in both bone mass gain and regulation of signal factors involved in bone turnover. Moreover, NO itself changes bone remodeling signals and bone loss since administration of nitroglycerin and nitrates NO donors decreases bone resorption and increases both bone mineral density and bone formation through inhibition of the osteoclastic cells activities.
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