Antioxidant status in patients with osteoporosis: A controlled study

Şendur, Ömer Faruk; Turan, Yasemın; Tastaban, Engin; Serter, Mukadder

doi:10.1016/j.jbspin.2009.02.005

Cited by 174 publications

(120 citation statements)

References 36 publications

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“…Osteoporosis is a common skeletal disease in aged and is characterized by low bone mass and microstructure deterioration of bone tissue (Cummings & Melton, 2002; Ford, Bass, Zhao, Bai & Zhao, 2011; Reginster & Burlet, 2006). Numerous studies have proven that osteoporosis was associated with a higher oxidative stress index values and total plasma oxidant status (Almeida & O'Brien, 2013; Sendur, Turan, Tastaban & Serter, 2009; Zhang et al., 2011). Our previous study also demonstrated a positive relationship between AOPP accumulation and bone loss (Zeng et al., 2014).…”

Section: Discussionmentioning

confidence: 99%

Advanced oxidation protein products induce pre‐osteoblast apoptosis through a nicotinamide adenine dinucleotide phosphate oxidase‐dependent, mitogen‐activated protein kinases‐mediated intrinsic apoptosis pathway

et al. 2018

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SummaryOsteoblast apoptosis contributes to age‐related bone loss. Advanced oxidation protein products (AOPPs) are recognized as the markers of oxidative stress and potent inducers of apoptosis. We have demonstrated that AOPP accumulation was correlated with age‐related bone loss. However, the effect of AOPPs on the osteoblast apoptosis still remains unknown. Exposure of osteoblastic MC3T3‐E1 cells to AOPPs caused the excessive generation of reactive oxygen species (ROS) by activating nicotinamide adenine dinucleotide phosphate (NADPH) oxidases. Increased ROS induced phosphorylation of mitogen‐activated protein kinases (MAPKs), which subsequently triggered intrinsic apoptosis pathway by inducing mitochondrial dysfunction, endoplasmic reticulum stress, and Ca2+ overload and eventually leads to apoptosis. Chronic AOPP loading in aged Sprague‐Dawley rats induced osteoblast apoptosis and activated NADPH oxidase signaling cascade, in combination with accelerated bone loss and deteriorated bone microstructure. Our study suggests that AOPPs induce osteoblast apoptosis by the NADPH oxidase‐dependent, MAPK‐mediated intrinsic apoptosis pathway.

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Section: Discussionmentioning

confidence: 99%

Advanced oxidation protein products induce pre‐osteoblast apoptosis through a nicotinamide adenine dinucleotide phosphate oxidase‐dependent, mitogen‐activated protein kinases‐mediated intrinsic apoptosis pathway

et al. 2018

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“…Oxidative stress occurs as a result of an overproduction of ROS not balanced by adequate levels of antioxidants (1,2). This can be determined by both physiological events, such as aging and hormonal changes (decrease of estrogen) (16)(17)(18)(19) and pathological events related to the production of inflammatory cytokines involved in many pathological processes, exogenous and endogenous toxins, radiation exposure and drug therapies (2,6,20). Oxidative stress generates a cellular damage due to lipid oxidation, structural alteration of the membranes, oxidation of proteins and nucleic acids; the damage may extend to the organs and become systemic (21).…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress in bone remodeling: role of antioxidants

Domazetovic

Marcucci

Iantomasi

et al. 2017

ccmbm

544

524

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SummaryROS are highly reactive molecules which consist of a number of diverse chemical species, including radical and non-radical oxygen species. Oxidative stress occurs as a result of an overproduction of ROS not balanced by an adequate level of antioxidants. The natural antioxidants are: thiol compounds among which GSH is the most representative, and non-thiol compounds such as polyphenols, vitamins and also various enzymes. Many diseases have been linked to oxidative stress including bone diseases among which one of the most important is the osteoporosis. The redox state changes are also related to the bone remodeling process which allows the continuous bone regeneration through the coordinated action of bone cells: osteoclasts, osteoblasts and osteocytes. Changes in ROS and/or antioxidant systems seem to be involved in the pathogenesis of bone loss. ROS induce the apoptosis of osteoblasts and osteocytes, and this favours osteoclastogenesis and inhibits the mineralization and osteogenesis. Excessive osteocyte apoptosis correlates with oxidative stress causing an imbalance in favor of osteoclastogenesis which leads to increased turnover of bone remodeling and bone loss. Antioxidants either directly or by counteracting the action of oxidants contribute to activate the differentiation of osteoblasts, mineralization process and the reduction of osteoclast activity. In fact, a marked decrease in plasma antioxidants was found in aged or osteoporotic women. Some evidence shows a link among nutrients, antioxidant intake and bone health. Recent data demonstrate the antioxidant properties of various nutrients and their influence on bone metabolism. Polyphenols and anthocyanins are the most abundant antioxidants in the diet, and nutritional approaches to antioxidant strategies, in animals or selected groups of patients with osteoporosis or inflammatory bone diseases, suggest the antioxidant use in anti-resorptive therapies for the treatment and prevention of bone loss.

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“…(24)(25)(26)(27)(28)(29)(30) For example, glutathione peroxidase antioxidant activity was lower whereas the superoxide dismutase/glutathione peroxidase ratio was higher in older Mexicans with osteoporosis. (28) Similarly, among older men in the Framingham osteoporosis study, there appeared to be bone-protective effects of antioxidants such as vitamin C (29) and carotenoids.…”

Section: Introductionmentioning

confidence: 99%

Serum uric acid is associated with bone health in older men: A cross-sectional population-based study

Nabipour

Sambrook

Blyth

et al. 2010

Journal of Bone and Mineral Research

132

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Serum uric acid (UA) is a strong endogenous antioxidant. Since oxidative stress has been linked to osteoporosis, we examined the association between serum UA levels and bone mineral density (BMD), prevalent vertebral and nonvertebral fractures, and laboratory measures such as calcitropic hormones and bone turnover marker levels. This cross-sectional analysis consisted of 1705 communitydwelling men aged 70 years or over who participated in the baseline part of the Concord Health and Ageing in Men Project (CHAMP), a population-based study of older men in Sydney, Australia. BMD at all sites was significantly higher among men with serum UA levels above the group median than among men with UA levels below the median. In multiple regression analyses adjusted for potential confounders, serum UA remained associated with BMD at all sites (b ¼ 0.12 to 0.14, p < .

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Antioxidant status in patients with osteoporosis: A controlled study

Cited by 174 publications

References 36 publications

Advanced oxidation protein products induce pre‐osteoblast apoptosis through a nicotinamide adenine dinucleotide phosphate oxidase‐dependent, mitogen‐activated protein kinases‐mediated intrinsic apoptosis pathway

Advanced oxidation protein products induce pre‐osteoblast apoptosis through a nicotinamide adenine dinucleotide phosphate oxidase‐dependent, mitogen‐activated protein kinases‐mediated intrinsic apoptosis pathway

Oxidative stress in bone remodeling: role of antioxidants

Serum uric acid is associated with bone health in older men: A cross-sectional population-based study

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