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| 1 | Molecular aspects of intestinal calcium absorption显示文摘Intestinal Ca2+ absorption is a crucial physiological process for maintaining bone mineralization and Ca2+ homeostasis. It occurs through the transcellular and paracellular pathways. The first route comprises 3steps: the entrance of Ca2+ across the brush border membranes(BBM) of enterocytes through epithelial Ca2+ channels TRPV6, TRPV5, and Cav1.3; Ca2+ movement from the BBM to the basolateral membranes by binding proteins with high Ca2+ affinity(such as CB9k); and Ca2+ extrusion into the blood. Plasma membrane Ca2+ ATPase(PMCA1b) and sodium calcium exchanger(NCX1) are mainly involved in the exit of Ca2+ from enterocytes. A novel molecule, the 4.1R protein, seems to be a partner of PMCA1 b, since both molecules colocalize and interact. The paracellular pathway consists of Ca2+ transport through transmembrane proteins of tight junction structures, such as claudins 2, 12, and 15. There is evidence of crosstalk between the transcellular and paracellular pathways in intestinal Ca2+ transport. When intestinal oxidative stress is triggered, there is a decrease in the expression of several molecules of both pathways that inhibit intestinal Ca2+ absorption. Normalization of redox status in the intestine with drugs such as quercetin, ursodeoxycholic acid, or melatonin return intestinal Ca2+ transport to control values. Calcitriol [1,25(OH)2D3] is the major controlling hormone of intestinal Ca2+ transport. It increases the gene and protein expression of most of the molecules involved in both pathways. PTH, thyroid hormones, estrogens, p ro l a c t i n, g ro w t h h o r m o n e, a n d g l u c o c o r t i c o i d s apparently also regulate Ca2+ transport by direct action, indirect mechanism mediated by the increase of renal 1,25(OH)2D3 production, or both. Different physiological conditions, such as growth, pregnancy, lactation, and aging, adjust intestinal Ca2+ absorption according to Ca2+ demands. Better knowledge of the molecular details of intestinal Ca2+ absorption could lead to the development of nutritional and medical strategies for optimizing the efficiency of intestinal Ca2+ absorption and preventing osteoporosis and other pathologies related to Ca2+ metabolism. | Gabriela Diaz de Barboza Solange Guizzardi Nori Tolosa de Talamoni | 2015 | World Journal of Gastroenterology2015，21，23： | 20 |
| 2 | Oxidative stress, antioxidants and intestinal calcium absorption显示文摘The disequilibrium between the production of reactive oxygen(ROS) and nitrogen(RNS) species and their elimination by protective mechanisms leads to oxidative stress. Mitochondria are the main source of ROS as by-products of electron transport chain. Most of the time the intestine responds adequately against the oxidative stress, but with aging or under conditions that exacerbate the ROS and/or RNS production, the defenses are not enough and contribute to developing intestinal pathologies. The endogenous antioxidant defense system in gut includes glutathione(GSH) and GSH-dependent enzymes as major components. When the ROS and/or RNS production is exacerbated, oxidative stress occurs and the intestinal Ca2+ absorption is inhibited. GSH depleting drugs such as DLbuthionine-S,R-sulfoximine, menadione and sodium deoxycholate inhibit the Ca2+ transport from lumen to blood by alteration in the protein expression and/or activity of molecules involved in the Ca2+ transcellular and paracellular pathways through mechanisms of oxidative stress, apoptosis and/or autophagy. Quercetin, melatonin, lithocholic and ursodeoxycholic acids block the effect of those drugs in experimental animals by their antioxidant, anti-apoptotic and/or anti-autophagic properties. Therefore, they may become drugs of choice for treatment of deteriorated intestinal Ca2+ absorption under oxidant conditions such as aging, diabetes, gut inflammation and other intestinal disorders. | Gabriela Diaz de Barboza Solange Guizzardi Luciana Moine Nori Tolosa de Talamoni | 2017 | World Journal of Gastroenterology2017，23，16： | 18 |
| 3 | Glutathione depleting drugs, antioxidants and intestinal calcium absorption显示文摘Glutathione(GSH) is a tripeptide that constitutes one of the main intracellular reducing compounds. The normal content of GSH in the intestine is essential to optimize the intestinal Ca2+ absorption. The use of GSH depleting drugs such as DL-buthionine-S,R-sulfoximine, menadione or vitamin K3, sodium deoxycholate or diets enriched in fructose, which induce several features of the metabolic syndrome, produce inhibition of the intestinal Ca2+ absorption. The GSH depleting drugs switch the redox state towards an oxidant condition provoking oxidative/nitrosative stress and inflammation, which lead to apoptosis and/or autophagy of the enterocytes. Either the transcellular Ca2+ transport or the paracellular Ca2+ route are altered by GSH depleting drugs. The gene and/or protein expression of transporters involved in the transcellular Ca2+ pathway are decreased. The flavonoids quercetin and naringin highly abrogate the inhibition of intestinal Ca2+ absorption, not only by restoration of the GSH levels in the intestine but also by their anti-apoptotic properties. Ursodeoxycholic acid, melatonin and glutamine also block the inhibition of Ca2+ transport caused by GSH depleting drugs. The use of any of these antioxidants to ameliorate the intestinal Ca2+ absorption under oxidant conditions associated with different pathologies in humans requires more investigation with regards to the safety, pharmacokinetics and pharmacodynamics of them. | Luciana Moine María Rivoira Gabriela Díaz de Barboza Adriana Pérez Nori Tolosa de Talamoni | 2018 | World Journal of Gastroenterology2018，24，44： | 5 |
| 4 | Cerebral Microdialysis in Traumatic Brain Injury and Subarachnoid Hemorrhage: State of the Art显示文摘 | Marcelo Lima Oliveira Ana Carolina Kairalla Erich Talamoni Fonoff Raquel Chacon Ruiz Martinez Manoel Jacobsen Teixeira Edson Bor-Seng-Shu | 2014 | Neurocritical Care2014，，1： | 1 |
| 5 | Decompressive craniectomy and head injury: brain morphometry, ICP, cerebral hemodynamics, cerebral microvascular reactivity, and neurochemistry显示文摘 | Edson Bor-Seng-Shu Eberval G. Figueiredo Erich Talamoni Fonoff Yasunori Fujimoto Ronney B. Panerai Manoel Jacobsen Teixeira | 2013 | Neurosurgical Review2013，，3： | 1 |
| 6 | Menadione alters calcium intestinal absorption and associated variables by producing hydroxyl free radicals显示文摘 | Tolosa de Talamoni N Marchionatti A Alisio A | 2001 | Bone2001，29，： | 1 |
| 7 | Surgical management of pancreatic- cancer显示文摘 | UJIKI MB TALAMONI MS | 2005 | Semin Radiat Oncol2005，15，4： | 1 |
| 8 | Stereotactic disconnection of hypothalamic hamartoma to control seizure and behavior disturbance: case report and literature review显示文摘 | Antonio Nogueira Almeida Erich Talamoni Fonoff Gerson Ballester Manoel Jacobsen Teixeira Raul Marino | 2008 | Neurosurgical Review2008，，3： | 1 |
| 9 | Molecular Aspects of Vitamin D Anticancer Activity显示文摘 | Gabriela Picotto Ana C. Liaudat Luciana Bohl Nori Tolosa de Talamoni | 2012 | Cancer Investigation2012，，8： | 1 |
| 10 | Effects of quercetin and menadione on intestinal calcium absorption and the underlying mechanisms显示文摘 | Marchionatti A M Pacciaroni A de Talamoni N G T | 2013 | Comparative Biochemistry and Physiology Part A:Molecular & Integrative Physiology2013，164，1： | 1 |
| 11 | Temperature effect on positronium formation inhibition a contribution to the elucidation of early spur process显示文摘 | Talamoni J Abbe J C Duplate G et a1 | 1981 | Chem Phys1981，58，1： | 1 |
| 12 | Positronium quenching and inhibiting properties of the CN-, Fe(CN)6^4- and Fe(CN)6^3- ions in aqueous solutions 显示文摘 | Duplatre G Talamoni J Abbe J Ch | 1984 | Radiat Phys Chem1984，23，： | 1 |
| 13 | New perspectives in melatonin uses显示文摘 | A. Carpentieri G. Díaz de Barboza V. Areco M. Peralta López N. Tolosa de Talamoni | 2012 | Pharmacological Research2012，，4： | 1 |
| 14 | Intestinal Ca2+ absorption revisited: A molecular and clinical approach显示文摘Ca2+has an important role in the maintenance of the skeleton and is involved in the main physiological processes.Its homeostasis is controlled by the intestine,kidney,bone and parathyroid glands.The intestinal Ca2+absorption occurs mainly via the paracellular and the transcellular pathways.The proteins involved in both ways are regulated by calcitriol and other hormones as well as dietary factors.Fibroblast growth factor 23(FGF-23)is a strong antagonist of vitamin D action.Part of the intestinal Ca2+movement seems to be vitamin D independent.Intestinal Ca2+absorption changes according to different physiological conditions.It is promoted under high Ca2+demands such as growth,pregnancy,lactation,dietary Ca2+deficiency and high physical activity.In contrast,the intestinal Ca2+transport decreases with aging.Oxidative stress inhibits the intestinal Ca2+absorption whereas the antioxidants counteract the effects of prooxidants leading to the normalization of this physiological process.Several pathologies such as celiac disease,inflammatory bowel diseases,Turner syndrome and others occur with inhibition of intestinal Ca2+absorption,some hypercalciurias show Ca2+hyperabsorption,most of these alterations are related to the vitamin D endocrine system.Further research work should be accomplished in order not only to know more molecular details but also to detect possible therapeutic targets to ameliorate or avoid the consequences of altered intestinal Ca2+absorption. | Vanessa A Areco Romina Kohan Germán Talamoni Nori G Tolosa de Talamoni María E Peralta López | 2020 | World Journal of Gastroenterology2020，26，24： | 0 |
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