Low Calcium Diet Increases Radical Production of Polymorphonuclear Leukocytes from Mice

2009 ◽  
Vol 79 (56) ◽  
pp. 375-380 ◽  
Author(s):  
Junji Takaya ◽  
Fumiko Yamato ◽  
Shoji Tsuji ◽  
Kazunari Kaneko

Although calcium is an essential mineral for bones, little is known about its effect on inflammatory or oxidative regulation. We hypothesize that calcium plays the role in the production of reactive oxygen species (ROS) and nitric oxide (NO) from polymorphonuclear leukocytes (PMNs). Our purpose was to determine the relationship of NO and ROS produced from PMNs, taking into account the role of calcium and magnesium in diet. Using flow cytometry, we compared ROS and NO production from PMNs after the stimulation by S. aureus or phorbol myristate acetate (PMA). PMNs taken from three murine groups were analyzed: C57BL/6 wild-type mice, low-calcium diet (Low Ca Group), or low-magnesium diet fed for 2 weeks. ROS production at baseline in the Low Ca Group was highest among the groups. PMA- and S. aureus-stimulated ROS production was also highest in the Low Ca Group. On the contrary, NO production at baseline in the Low Ca Group was lowest among the groups, while there was no significant difference among the groups in S. aureus-stimulated PMNs. A low-calcium diet increases ROS production from stimulated PMNs and decreases NO production at baseline. This finding suggests that calcium regulates ROS production from PMNs.

Author(s):  
SANDEEP DAS ◽  
DIPAYAN CHOUDHURI

Objective: Emerging evidence established the role of dietary calcium in the modulation of obesity. Obesity is known to induce inflammatory and oxidative stress in adipocytes resulting in several metabolic complications. In the present study, we evaluated the role of low and high calcium diet on systemic inflammatory response and oxidative stress markers in both plasma and hepatic tissues in male rats. Methods: A total of 30 male rats were divided into three groups and fed with control, low calcium (0.25%), and high calcium (1.0%) diet for 3 months. All the diets were isocaloric in nature. At the end of the treatment, all rats were sacrificed, followed by collection of blood and hepatic tissue for inflammatory, oxidative, antioxidant, and histological study. Results: Rats fed with a low calcium diet showed a significant increase in the body weight gain, liver mass, plasma inflammatory markers C-reactive protein, interleukin-6, and tumor necrosis factor-alpha. Low calcium diet significantly increased the lipid peroxidation and protein carbonylation and decreased the superoxide dismutase and glutathione peroxidase activities in both plasma and liver. High calcium diet, on the other hand, showed the reversed effect. Conclusion: Low calcium in the diet, along with obesity, increases the systemic inflammatory response, which in turn increases oxidative stress both in blood and hepatic tissues. This might be associated with obesity-induced hepatic disorder. High calcium in diet attenuates this effect.


Blood ◽  
1964 ◽  
Vol 23 (6) ◽  
pp. 786-794 ◽  
Author(s):  
KARL GUGGENHEIM

Abstract The suggestion that the "meat anemia" of mice is due to a dietary lack of copper accompanied by an excess of zinc in meat was investigated. Muscle meat contains small amounts of copper and much more zinc whereas liver which protects against "meat anemia" contains more copper and less zinc than muscle. Supplementation of meat with copper or liver, which reduce the zinc-copper ratio of the diet, prevents anemia. Addition of zinc, which increases the zinc-copper ratio, leads to anemia. Calcium prevents anemia even when the zinc-copper ratio is high. Treatment with vitamin D does not protect against anemia. It is concluded that calcium acts before its absorption in the intestinal tract, probably by interfering with the absorption of zinc. Anemia also develops in mice which are maintained on a semisynthetic low-calcium diet with a higher content of zinc than of copper. Supplementation of this diet with calcium likewise alleviates the anemia. Rats, which are resistant to "meat anemia," are less susceptible to the toxic effects of zinc than mice. "Meat anemia" of mice seems, therefore, to result mainly from the presence in meat of insufficient amounts of copper accompanied by an excess of zinc, the effects of which are accentuated by a concomitant lack of calcium. Genetic factors determining the particular sensitivity to zinc seem to play an important role as well.


2021 ◽  
Vol 1 (1) ◽  
Author(s):  
Zhengwang Yu ◽  
Jie Huang ◽  
Zhongxin Zhou

AbstractCage layer osteoporosis (CLO) is a common bone metabolism disease in the breeding industry of China. However, effective prevention for CLO has not been developed. Icariin (ICA), the main bioactive component of the Chinese herb Epimedium, has been shown to have good therapeutic effects on bone-related diseases. In this study, the effects of ICA were further evaluated in a low-calcium diet-induced CLO, and a serum metabolomics assay was performed to understand the underlying mechanisms. A total of 144 31-wk-old Lohmann pink-shell laying hens were randomly allocated to 4 groups with 6 replicates of 6 hens per replicate. The 4 dietary treatment groups consisted of a basal diet (3.5% calcium), a low-calcium diet (2.0% calcium), and a low-calcium diet supplemented with 0.5 or 2.0 g/kg ICA. The results showed that ICA exerted good osteoprotective effects on low-calcium diet-induced CLO. ICA significantly increased femur bone mineral density, improved bone microstructure, decreased bone metabolic level, and upregulated mRNA expression of bone formation genes in femoral bone tissue. Serum untargeted metabolomics analysis showed that 8 metabolite levels were significantly changed after ICA treatment, including increased contents of 7-dehydrocholesterol, 7-oxocholesterol, desmosterol, PC (18:1(9Z)/18:1(9Z)), PS (18:0/18:1(9Z)), N,N-dimethylaniline and 2-hydroxy-butanoic acid and decreased N2,N2-dimethylguanosine. Metabolic pathway analysis based on the above 8 metabolites indicated that ICA mainly perturbed steroid biosynthesis and glycerophospholipid metabolism. These findings suggest that ICA can effectively prevent bone loss in low-calcium diet-induced CLO by mediating steroid biosynthesis and glycerophospholipid metabolism and provide new information for the regulation of bone metabolic diseases.


Endocrinology ◽  
2007 ◽  
Vol 148 (3) ◽  
pp. 1396-1402 ◽  
Author(s):  
Yurong Song ◽  
James C. Fleet

We tested the hypothesis that low vitamin D receptor (VDR) level causes intestinal vitamin D resistance and intestinal calcium (Ca) malabsorption. To do so, we examined vitamin D regulated duodenal Ca absorption and gene expression [transient receptor potential channel, vallinoid subfamily member 6 (TRPV6), 24-hydroxylase, calbindin D9k (CaBP) mRNA, and CaBP protein] in wild-type mice and mice with reduced tissue VDR levels [i.e. heterozygotes for the VDR gene knockout (HT)]. Induction of 24-hydroxylase mRNA levels by 1,25 dihydroxyvitamin D3 [1,25(OH)2 D3] injection was significantly reduced in the duodenum and kidney of HT mice in both time-course and dose-response experiments. TRPV6 and CaBP mRNA levels in duodenum were significantly induced after 1,25(OH)2 D3 injection, but there was no difference in response between wild-type and HT mice. Feeding a low-calcium diet for 1 wk increased plasma PTH, renal 1α-hydroxylase (CYP27B1) mRNA level, and plasma 1,25(OH)2 D3, and this response was greater in HT mice (by 88, 55, and 37% higher, respectively). In contrast, duodenal TRPV6 and CaBP mRNA were not higher in HT mice fed the low-calcium diet. However, the response of duodenal Ca absorption and CaBP protein to increasing 1,25(OH)2 D3 levels was blunted by 40% in HT mice. Our data show that low VDR levels lead to resistance of intestinal Ca absorption to 1,25(OH)2 D3, and this resistance may be due to a role for the VDR (and VDR level) in the translation of CaBP.


2020 ◽  
Vol 514 ◽  
pp. 110891
Author(s):  
Rougin Khalil ◽  
Ioannis Simitsidellis ◽  
Na Ri Kim ◽  
Ferran Jardi ◽  
Dieter Schollaert ◽  
...  

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