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An environmentally compatible and less costly (greener) analytical method for the digestion of bone meal samples using microwave-assisted dilute nitric acid (HNO3) was developed and optimized. The method, employing a mixture of 1 mL concentrated HNO3 and 4 mL of deionized water, offered a comparable performance to the conventional method using 5 mL of concentrated HNO3. The accuracy of the method was validated by using certified reference material NIST 1486 (Bone Meal); percentage recoveries were within ±15% for all eight certified elements. Statistical analysis revealed no significant differences (p > 0.05) in percentage recoveries between the green and conventional methods for all elements except calcium. The greenness of the developed method was evaluated by using the analytical Eco-Scale, achieving a score of 87, categorizing it as an “excellent green analysis” method. This research highlights the potential for adopting greener practices in trace element analysis that reduce the environmental impact and safety risks associated with concentrated acids.

Changes in the macro and trace element composition of saliva might be indicative for pathological changes in periodontal tissues. However, there is a lack of evidence in the literature showing associations between mineral elements and periodontal status. The aim of this study was to determine whether such associations occur. Totally, 190 systemically healthy non-smoker participants (mean age 32.2 ± 6.02; 50 periodontally healthy, 50 gingivitis, 50 chronic periodontitis, and 40 aggressive periodontitis individuals) were included in this cross-sectional study. Salivary levels of some macro and trace elements were measured by using inductively coupled plasma mass spectrometry (ICP-MS). Kruskal-Wallis’s test was used for statistical analysis. Statistically significant differences were found in sodium (Na), magnesium (Mg), potassium (K), calcium (Ca), vanadium (V), chromium Cr), manganese (Mn), iron (Fe), rubidium (Rb), strontium (Sr), and selenium (Se) concentrations among the groups. Significant increases in the essential minerals Na, Mg, K, Ca, Fe, and Se occurred in both periodontitis groups when compared to the gingivitis and periodontally healthy groups. Lower Se, Sr, Fe, Mn, and V concentrations were found in the aggressive periodontitis group than in the chronic periodontitis group. The results of this study demonstrated that assessment of mineral element concentrations in saliva might be useful in assessing periodontal health and disease. However, further studies are required to determine whether the change in a specific mineral element is the result of periodontal disease or is involved in its pathogenesis.

Determination of whether magnesium (Mg) is a nutrient of public health concern has been hindered by questionable Dietary Recommended Intakes (DRIs) and problematic status indicators that make Mg deficiency assessment formidable. Balance data obtained since 1997 indicate that the EAR and RDA for 70-kg healthy individuals are about 175 and 250 mg/day, respectively, and these DRIs decrease or increase based on body weight. These DRIs are less than those established for the USA and Canada. Urinary excretion data from tightly controlled metabolic unit balance studies indicate that urinary Mg excretion is 40 to 80 mg (1.65 to 3.29 mmol)/day when Mg intakes are <250 mg (10.28 mmol)/day, and 80 to 160 mg (3.29 to 6.58 mmol)/day when intakes are >250 mg (10.28 mmol)/day. However, changing from low to high urinary excretion with an increase in dietary intake occurs within a few days and vice versa. Thus, urinary Mg as a stand-alone status indicator would be most useful for population studies and not useful for individual status assessment. Tightly controlled metabolic unit depletion/repletion experiments indicate that serum Mg concentrations decrease only after a prolonged depletion if an individual has good Mg reserves. These experiments also found that, although individuals had serum Mg concentrations approaching 0.85 mmol/L (2.06 mg/dL), they had physiological changes that respond to Mg supplementation. Thus, metabolic unit findings suggest that individuals with serum Mg concentrations >0.75 mmol/L (1.82 mg/L), or as high as 0.85 mmol/L (2.06 mg/dL), could have a deficit in Mg such that they respond to Mg supplementation, especially if they have a dietary intake history showing <250 mg (10.28 mmol)/day and a urinary excretion of <80 mg (3.29 mmol)/day.

Animal studies have shown that magnesium deficiency induces an inflammatory response that results in leukocyte and macrophage activation, release of inflammatory cytokines and acute-phase proteins, and excessive production of free radicals. Animal and in vitro studies indicate that the primary mechanism through which magnesium deficiency has this effect is through increasing cellular Ca , which is the signal that results in the priming of cells to give the inflammatory response. Primary pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin (IL)-1; the messenger cytokine IL-6; cytokine responders E-selectin, intracellular adhesion molecule-1 and vascular cell adhesion molecule-1; and acute-phase reactants C-reactive protein and fibrinogen have been determined to associate magnesium deficiency with chronic low-grade inflammation (inflammatory stress). When magnesium dietary intake, supplementation, and/or serum concentration suggest/s the presence of magnesium deficiency, it often is associated with low-grade inflammation and/or with pathological conditions for which inflammatory stress is considered a risk factor. When magnesium intake, supplementation, and/or serum concentration suggest/s an adequate status, magnesium generally has not been found to significantly affect markers of chronic low-grade inflammation or chronic disease. The consistency of these findings can be modified by other nutritional and metabolic factors that affect inflammatory and oxidative stress. In spite of this, findings to date provide convincing evidence that magnesium deficiency is a significant contributor to chronic low-grade inflammation that is a risk factor for a variety of pathological conditions such as cardiovascular disease, hypertension, and diabetes. Because magnesium deficiency commonly occurs in countries where foods rich in magnesium are not consumed in recommended amounts, magnesium should be considered an element of significant nutritional concern for health and well-being in these countries.

Increasing dietary intake of fish oil is frequently recommended for decreasing the risk for cardiovascular diseases and improving metabolic health. We hypothesised that dietary intake of chromista oil (a marine food product and a rich source of long-chain n-3 polyunsaturated fatty acids) ameliorates metabolic impairments in mice with established excess adiposity. Three-to 4-week-old mice (male) were fed a control (n = 12) or a high-fat diet (HFD, n = 24) for 12 weeks to establish body fat mass. Then, mice on the HFD were assigned to 2 groups (n = 12 each) with 1 continuing being fed the HFD and the other fed the HFD with chromista oil for an additional 12 weeks. Intake of chromista oil did not affect body weight and body adiposity of the mice fed the HFD; mice fed the HFD had significantly more body weight and fat mass than control mice. The flattened daily oscillations of respiratory exchange ratio induced by the HFD were not changed by chromista oil intake. Intake of chromista oil significantly increased plasma concentration of insulin, the calculated value of HOMA-IR, and plasma concentration of adiponectin in the mice fed the HFD. However, blood glucose was unaffected by chromista oil. Transcription of genes encoding circadian rhythm and fatty acid metabolism of the 2 HFD-fed groups were similar. Untargeted metabolomic analysis showed that intake of chromista oil altered the hepatic metabolomic profile with substantial alterations in amino acid metabolism. Findings from this study indicate that dietary intake of chromista oil does not improve glucose homeostasis or alter the diminished metabolic flexibility in mice with excess adiposity induced by the HFD. Targeted metabolomic analysis is warranted to investigate the effects of dietary chromista oil, as a source of n-3 poly unsaturated fatty acids, on metabolism in models of obesity.

In the past 20 years, a large number of epidemiological studies, randomized controlled trials, and meta-analyses have found an inverse relationship between magnesium intake or serum magnesium and cardiovascular disease, indicating that low magnesium status is associated with hypertension, coronary artery calcification, stroke, ischemic heart disease, atrial fibrillation, heart failure, and cardiac mortality. Controlled metabolic unit human depletion–repletion experiments found that a mild or moderate magnesium deficiency can cause physiological and metabolic changes that respond to magnesium supplementation, which indicates that these types of deficiencies or chronic latent magnesium deficiency are contributing factors to the occurrence and severity of cardiovascular disease. Mechanisms through which a mild or moderate magnesium deficiency can contribute to this risk include inflammatory stress, oxidative stress, dyslipidemia and deranged lipid metabolism, endothelial dysfunction, and dysregulation of cellular ion channels, transporters, and signaling. Based on USA official DRIs or on suggested modified DRIs based on body weight, a large number of individuals routinely consume less magnesium than the EAR. This especially occurs in populations that do not consume recommended amounts of whole grains, pulses, and green vegetables. Thus, inadequate magnesium status contributing to cardiovascular disease is widespread, making magnesium a nutrient of public health concern.

Monocyte chemotactic protein-1 (MCP-1), a small inducible cytokine, is involved in obesity-related chronic disorders. Adipocytes produce MCP-1 that is elevated in obese humans and in rodent models of obesity. This study examined the hepatic metabolomic alterations caused by adipose-specific MCP-1 deficiency in a rodent model of obesity. Wide-type (WT) and adipose-specific Mcp-1 knockdown mice (Mcp-1-/-) were each assigned randomly to 2 groups and fed the standard AIN93G diet or a high-fat diet (HFD) for 12 weeks. Compared to the AIN93G diet, the HFD increased body weight, body fat mass, and plasma concentrations of insulin and leptin, regardless of genotype. There were no differences in these variables between WT and Mcp-1-/- mice when they were fed the same diet. Eighty-seven of 172 identified metabolites met the criteria for metabolomic comparisons among the 4 groups. Thirty-nine metabolites differed significantly between the 2 dietary treatments and 15 differed when Mcp-1-/- mice were compared to WT mice. The metabolites that significantly differed in both comparisons included those involved in amino acid, energy, lipid, nucleotide, and vitamin metabolism. Network analysis found that both HFD and adipose Mcp-1 knockdown may considerably impact amino acid metabolism as evidenced by alteration in the aminoacyl-tRNA biosynthesis pathways, in addition to alteration in the phenylalanine, tyrosine, and tryptophan biosynthesis pathway in Mcp-1-/- mice. However, decreased signals of amino acid metabolites in mice fed the HFD and increased signals of amino acid metabolites in Mcp-1-/- mice indicate that HFD may have down-regulated and adipose Mcp-1 knockdown may have up-regulated amino acid metabolism.

Determination of the public health concern about magnesium (Mg) in health and disease has been confounded by the lack of a practical measure of status. This has resulted in a lack of consistency in associating Mg deficiency with specific pathological conditions. Some attempts at associating Mg with a chronic disease have used the Dietary Reference Intakes (DRIs) as a status assessment measure. Use of current DRIs for Mg is problematic because recent evidence suggests that they should be updated and based on body weight. An evidence-based suggested Estimated Average Requirement (EAR) and Recommended Dietary Allowance (RDA) for a 70-kg individual is 175 and 250 mg/day, respectively. However, numerous dietary and physiological factors can affect the need for Mg and thus affect the use of the current or suggested new DRIs to assess Mg status. Calcium intakes above normal requirements can decrease Mg balance and exacerbate signs of Mg deficiency. Mg deficiency apparently occurs often in obesity because of increased need to counteract the inflammatory stress induced by adipose tissue dysfunction. Deficiency in anti-oxidant nutrients such as vitamin E and selenium can exacerbate a response to low dietary Mg indicated by increased oxidative stress which can lead to chronic disease. Dietary modifiers of Mg absorption and excretion affect balance and thus the need for Mg. Factors decreasing Mg balance include low dietary protein and non-fermentable fiber, while factors that can increase balance include fructose and fermentable fiber and fructose-containing oligosaccharides. Use of the DRIs to assess the Mg status of a population or group needs to consider their physiological characteristics and dietary habits and be aware that the DRIs may need updating. The DRIs only can be considered a component of a toolbox that presently includes serum Mg concentration and the daily urinary Mg excretion to assess the Mg status of an individual.

Early studies on nickel essentiality with rats and goats indicated that nickel deprivation impaired reproductive performance. Nickel also has been found to influence cyclic nucleotide gated channels (CNG); these types of channels are important in sperm physiology. Thus, two experiments were conducted to test the hypothesis that nickel deficiency affects sperm physiology in a manner consistent with nickel having an essential function related to CNG channel functions. The experiments were factorially arranged with four treatment groups of eight weanling rats in each. In experiment 1, the treatments were supplemental dietary nickel of 0 and 1 mg/kg and N(ω)-nitro-l-arginine methyl ester (l-NAME, a nitric oxide synthase inhibitor) added to the drinking water (50 mg/100 mL) the last 3 wk of an 8-wk experiment. In experment 2, the treatments were supplemental dietary nickel at 0 and 1 mg/kg and supplemental dietary sodium chloride (NaCl) at 0 and 80 g/kg. The NaCl and l-NAME variables were included to act as stressors affecting CNG channel activity. The basal diet contained per kilogram about 27 µg of nickel and 1 g of sodium. After 8 wk in experiment 1 and 16 wk in experiment 2, urine while fasting and testes and epididymis in both experiments, and seminal vesicles and prostates in experiment 2 were harvested for analysis. Nickel deprivation significantly decreased spermatozoa motility and density in the epididymides, epididymal transit time of spermatozoa, and testes sperm production rate. Nickel deficiency also significantly decreased the weights of the seminal vesicles and prostate glands. Excessive NaCl had no effect on sperm physiology; however, it decreased prostate gland weights. The findings support the hypothesis that nickel has an essential function that possibly could affect reproductive performance in higher animals, perhaps through affecting a CNG channel function.

Nicotine, the major bioactive ingredient in tobacco, is a major risk factor for periodontal disease and destruction. Nicotine has been shown to stimulate the production of cytokines that are priming agents for inflammation that induces tissue destruction, such as IL-1β, IL-6, and IL-8, by gingival keratinocytes and human gingival fibroblasts (HGF). Boron as boric acid has been found to decrease pro-inflammatory cytokines and increase anti-inflammatory cytokines in cells with inflammatory stress. Thus, a study was performed to determine whether boric acid reverses negative effects of nicotine on human gingival fibroblasts (HGFs). The viability and cytokine expressions of HGFs cultured for 24 and 72 h in control medium with no nicotine or boric acid added and in media containing only nicotine, only boric acid, or a combination of BA and nicotine were determined. Nicotine in concentrations of 10 −1 , 10 −2 , 10 −3 ,10 −4 , 10 −5 , and 10 –6  mM significantly reduced cell viability compared to the control. Boric acid at 10 and 50 ng/mL in the media partially restored and 100 ng/mL in the media fully restored the nicotine-depressed HGF cell viability to the same level as the control group. Nicotine elevated the expression of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, IL-8, and IL-17 and decreased the anti-inflammatory IL-10 in HGFs at 24 and 72 h. Boric acid at 100 ng/mL in the medium prevented the changes induced by nicotine alone. The findings indicate that boric acid can inhibit or reverse nicotine-induced pathology in periodontal tissue and thus may help maintain oral and periodontal health in tobacco users.