Dietary zinc deficiency induces oxidative stress and promotes tumor necrosis factor-α- and interleukin-1β-induced RANKL expression in rat bone
Autor: | Hiroshi Matsuzaki, Shin-ichi Katsumata, Takako Suzuki, Kazuharu Suzuki |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
medicine.medical_specialty medicine.medical_treatment Clinical Biochemistry Medicine (miscellaneous) medicine.disease_cause Bone morphogenetic protein 2 Bone remodeling 03 medical and health sciences iron Internal medicine zinc deficiency cytokine medicine oxidative stress Nutrition and Dietetics biology Activator (genetics) RANKL medicine.disease 030104 developmental biology Cytokine Endocrinology Immunology biology.protein Zinc deficiency Original Article Tumor necrosis factor alpha Oxidative stress |
Zdroj: | Journal of Clinical Biochemistry and Nutrition |
ISSN: | 1880-5086 0912-0009 |
DOI: | 10.3164/jcbn.15-87 |
Popis: | We investigated the effects of dietary zinc deficiency on oxidative stress and bone metabolism. Four-week-old male Wistar rats were randomly assigned to one of three groups for 4 weeks: a zinc-adequate group (30 ppm); a zinc-deficient group (1 ppm); and a pair-fed group (30 ppm) that was pair-fed to the zinc-deficient group. The iron content and the thiobarbituric acid reactive substance level in bone were higher in the zinc-deficient group than in the zinc-adequate and pair-fed groups. The mRNA expression level of osteoblastogenesis-related genes such as bone morphogenetic protein 2 and runt-related transcription factor 2 was lower in the zinc-deficient group than in the zinc-adequate and pair-fed groups. In contrast, the mRNA expression levels of tumor necrosis factor-α, interleukin-1β and osteoclastogenesis-related genes such as receptor activator of nuclear factor-κB ligand and nuclear factor of activated T cells cytoplasmic 1 were higher in the zinc-deficient group than in the zinc-adequate and pair-fed groups. These findings suggested that dietary zinc deficiency reduced osteoblastogenesis via a decrease in the expression of bone morphogenetic protein 2 and increased osteoclastogenesis via enhancement of the expression of receptor for activator of nuclear factor-κB ligand induced by oxidative stress-stimulated tumor necrosis factor-α and interleukin-1β. |
Databáze: | OpenAIRE |
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