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Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Phosphorus makes up about 0.65–1.1% of the adult body (~600 g). In the adult body 85% of phosphorus is in bone and the remaining 15% is distributed in soft tissues (3). Total phosphorus concentration in whole blood is 13 mmol/l, most of which is in the phospholipids of erythrocytes and plasma lipoproteins, with approximately 1 mmol/l present as inorganic phosphate (3). P deficiency is unusual, but symptoms of hypophosphatemia are described as bone pain, irregular breathing, fatigue, anxiety, numbness, changes in body weight and skin sensitivity (7). If Ca supply is also deficient, then the condition may become severe because of increased risks of high blood pressure and bowel cancer (7). Other consequences of P deficiency are rickets in children, osteomalacia in adults, hyperparathyroidism, anorexia, anemia, muscle weakness, De Toni-Fanconi syndrome, general debility, increased susceptibility to infection, paresthesia, ataxia, confusion, and even death (3, 7–8). Ingesting dosages of P exceeding 3–4 g/day may be harmful as it can interfere with Ca absorption (7). Hyperphosphatemia or increased phosphate level in blood is found in chronic nephritis and hypoparathyroidism. It may also lead to bone loss due to hypocalcemia (8). In addition, high phosphorus intakes could decrease calcium absorption by complexing calcium in the chyme, and may be due to high levels of food phosphate additives and cola beverages in the Western diet (3).
Impairment of Lipid Metabolism in Ischemic and Reperfused Myocardial Tissue
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
Ger J. van der Vusse, Marc van Bilsen, Robert S. Reneman
During the initial stage of ischemia, notable chemical changes have been observed in the oxygen-deprived tissue. Tissue pH drops and lactate accumulates. The cellular content of inorganic phosphate rapidly increases mainly due to the depletion of the creatine phosphate store.13,20,23 The decrease in ATP content follows slowly, since a shift from aerobic to anaeorbic ATP formation has taken place. Intracellular glycogen and extracellular glucose are catabolyzed to lactate (Figure 1). The ratio of NADH/NAD+ increases in the cells affected. Due to its obligate oxygen-requiring nature, fatty acid oxidation is severely hampered under ischemic conditions. In low-flow ischemic hearts in the presence of extracellular NEFA intermediates like hydroxy fatty acids, fatty acyl CoA, and fatty acylcamitine accumulate (Figure 2).
The Basal Cell Nevus Syndrome
Published in Roger M. Browne, Investigative Pathology of the Odontogenic Cysts, 2019
Julia A. Woolgar, J. W. Rippin
The need is emphasized by the fact that a number of other studies have suggested the possibility of abnormalities in calcium metabolism. For example, raised serum alkaline phosphatase levels have been reported in some patients,40,68 and elevated serum calcitonin levels in some others;40,65 Totten40 found that in two of his four patients (father and daughter) there was both raised alkaline phosphatase and raised calcitonin, though in both calcium and phosphorus levels were within normal limits. However, four of the seven patients reported by Tasanen et al.61 had depressed serum inorganic phosphate levels as well as increased alkaline phosphatase. Lindeberg et al.7 perhaps went some way towards resolving these contradictory results by suggesting that raised alkaline phosphatase levels occur only in those patients who have actively growing odontogenic keratocysts — for their study showed that at the time of their report one out of eight patients had an increased beta1-fraction of alkaline phosphatase (the bone-related fraction), but that a small number of other patients had shown a similar increase when it was supposed that their odontogenic keratocysts were expanding; even then, all of their patients had normal serum calcium and inorganic phosphorus levels.
An update on phosphate binders for the treatment of hyperphosphatemia in chronic kidney disease patients on dialysis: a review of safety profiles
Published in Expert Opinion on Drug Safety, 2022
Hiroaki Ogata, Akiko Takeshima, Hidetoshi Ito
Hyperphosphatemia is an inevitable complication among patients with advanced chronic kidney disease (CKD) because impaired kidneys cannot excrete urinary phosphate commensurate to the dietary load [1,2]. Hyperphosphatemia is associated with various complications; therefore, nephrologists manage serum phosphate concentrations using restriction of dietary phosphorus intake, phosphate removal by dialysis, and drug therapy to ensure they stay within the optimal range. There is little evidence based on large-scale prospective cohorts or randomized control trials to know whether dietary intervention can improve clinical outcomes in CKD patients [3]. Strict restriction of dietary phosphate intake should not always be applied to all hyperphosphatemic patients [4]. Most foods inevitably contain phosphate; particularly, high-protein foods are rich in phosphate. Interestingly, the bioavailability of phosphate varies widely depending on foods [5]. In general, phosphate derived from meat, fish, and dairy products is likely to be absorbed in the gastrointestinal tract as compared with that from plants. Inorganic phosphate derived from food additives is thought to be absorbed almost completely. Therefore, in contrast to simply restricting the intake of phosphate or protein, the type of food might be more important in CKD patients with hyperphosphatemia.
Prevalence and management of vitamin D deficiency in children with newly diagnosed coeliac disease: cohort study
Published in Paediatrics and International Child Health, 2021
Akhshayaa G, Anju Seth, Praveen Kumar, Anju Jain
The 38 children with CD with serum 25(OH)D ≤ 20 ng/ml were treated with oral vitamin D and calcium and followed up as described above. Except for two children with occasional dietary transgressions, all others were compliant with a GFD and vitamin D and calcium intake. On reassessment of biochemical parameters 1 week after vitamin D therapy, there was a significant rise in the serum 25(OH)D from a pre- treatment median of 12.55 ng/ml (IQR 9.05–17.1) to 64.93 ng/ml (IQR 57.54–72.4). This was associated with a significant rise in serum calcium (total and ionised) and inorganic phosphate and a fall in PTH and ALP (Table 3). In all cases, the hypocalcaemia, hypophosphataemia and elevated ALP and PTH levels normalised after treatment. The seven cases who had radiologically confirmed rickets showed signs of complete healing. Two of the 38 children (5%) had serum 25(OH)D levels >100 ng/ml after treatment. However, none of them had hypercalcaemia, hypercalciuria or nephrocalcinois, and, on further follow-up 4–7 weeks after treatment, their vitamin D levels had fallen to the normal range.
Chemotherapeutic and prophylactic antimalarial drugs induce cell death through mitochondrial-mediated apoptosis in murine models
Published in Drug and Chemical Toxicology, 2021
John Oludele Olanlokun, Folashade Abimbola Balogun, Olufunso Olabode Olorunsogo
The method of Lardy and Wellman (1953) was used. To each test tube in duplicate, 0.25 M sucrose, 5 mM KCl, 0.1 M Tris-HCl (pH 7.4) were added to all test tubes containing mitochondria (1 mg/mL protein) and the volumes were made up to 2 mL. Uncoupler (25 µM 2, 4 dinitrophenol) was added to the designated tubes followed by 0.01 M ATP. Sodium dodecylsulphate (SDS, 10% w/v) was added to the tubes designated zero time tubes after the addition of mitochondria. After adding ATP, mitochondria were added to each test tube at 30 seconds interval in a shaking water bath at 27 °C. The mixture was incubated for 30 minutes. After incubation, 1 mL of SDS was added to each test tube (except zero time) at 30 seconds interval in the order mitochondria were added to terminate the reaction. Ammonium molybdate (1 mL of 1.25% (w/v) in 6.25% H2SO4 preparation) was added to each test tube followed by 1 mL (9% w/v) of ascorbate. The solutions were allowed to stand for 30 minutes and absorbance was read at 680 nm. The inorganic phosphate (Pi) concentration was obtained from a phosphate standard curve.