4.4 Article

Reduced expressions of calmodulin genes and protein and reduced ability of calmodulin to activate plasma membrane Ca2+-ATPase in the brain of protein undernourished rats: modulatory roles of selenium and zinc supplementation

期刊

CELL BIOCHEMISTRY AND FUNCTION
卷 34, 期 2, 页码 95-103

出版社

WILEY
DOI: 10.1002/cbf.3168

关键词

calcium; calmodulin; erythrocyte ghost membrane; plasma membrane; synaptosome

资金

  1. Academy of Sciences for the Developing World, Italy
  2. Centre for International Co-operation in Science (CICS), India
  3. Department of Science and Technology (DST), New Delhi under Promotion of University Research and Scientific Excellence (PURSE) grant
  4. University Grants Commission, New Delhi under Special Assistance Programme (SAP)

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The roles of protein undernutrition as well as selenium (Se) and zinc (Zn) supplementation on the ability of calmodulin (CaM) to activate erythrocyte ghost membrane (EGM) Ca2+-ATPase and the calmodulin genes and protein expressions in rat's cortex and cerebellum were investigated. Rats on adequate protein diet and protein-undernourished (PU) rats were fed with diet containing 16% and 5% casein, respectively, for a period of 10weeks. The rats were then supplemented with Se and Zn at a concentration of 0.15 and 227mgl(-1), respectively, in drinking water for 3weeks. The results obtained from the study showed significant reductions in synaptosomal plasma membrane Ca2+-ATPase (PMCA) activity, Ca2+/CaM activated EGM Ca(2+)ATPase activity and calmodulin genes and protein expressions in PU rats. Se or Zn supplementation improved the ability of Ca2+/CaM to activate EGM Ca2+-ATPase and protein expressions. Se or Zn supplementation improved gene expression in the cerebellum but not in the cortex. Also, the activity of PMCA was significantly improved by Zn. In conclusion, it is postulated that Se and Zn might be beneficial antioxidants in protecting against neuronal dysfunction resulting from reduced level of calmodulin such as present in protein undernutrition. Copyright (c) 2016 John Wiley & Sons, Ltd.

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