Thiamine and Oxidants Interact to Modify Cellular Calcium Stores
- 24 August 2010
- journal article
- research article
- Published by Springer Science and Business Media LLC in Neurochemical Research
- Vol. 35 (12), 2107-2116
- https://doi.org/10.1007/s11064-010-0242-z
Abstract
Diminished thiamine (vitamin B1) dependent processes and oxidative stress accompany Alzheimer’s disease (AD). Thiamine deficiency in animals leads to oxidative stress. These observations suggest that thiamin may act as an antioxidant. The current experiments first tested directly whether thiamin could act as an antioxidant, and then examined the physiological relevance of the antioxidant properties on oxidant sensitive, calcium dependent processes that are altered in AD. The first group of experiments examined whether thiamin could diminish reactive oxygen species (ROS) or reactive nitrogen species (RNS) produced by two very divergent paradigms. Dose response curves determined the concentrations of t-butyl-hydroperoxide (t-BHP) (ROS production) or 3-morpholinosydnonimine ((SIN-1) (RNS production) to induce oxidative stress within cells. Concentrations of thiamine that reduced the RNS in cells did not diminish the ROS. The second group of experiments tested whether thiamine alters oxidant sensitive aspects of calcium regulation including endoplasmic reticulum (ER) calcium stores and capacitative calcium entry (CCE). Thiamin diminished ER calcium considerably, but did not alter CCE. Thiamine did not alter the actions of ROS on ER calcium or CCE. On the other hand, thiamine diminished the effect of RNS on CCE. These data are consistent with thiamine diminishing the actions of the RNS, but not ROS, on physiological targets. Thus, both experimental approaches suggest that thiamine selectively alters RNS. Additional experiments are required to determine whether diminished thiamine availability promotes oxidative stress in AD or whether the oxidative stress in AD brain diminishes thiamine availability to thiamine dependent processes.Keywords
This publication has 45 references indexed in Scilit:
- Potent Radical-Scavenging Activities of Thiamin and Thiamin DiphosphateJournal of Clinical Biochemistry and Nutrition, 2007
- Increased brain endothelial nitric oxide synthase expression in thiamine deficiency: relationship to selective vulnerabilityNeurochemistry International, 2004
- Nitric oxide inhibits capacitative Ca2+ entry by suppression of mitochondrial Ca2+ handlingBritish Journal of Pharmacology, 2002
- Abnormalities of mitochondrial enzymes in Alzheimer diseaseJournal of Neural Transmission, 1998
- Effects of Hydroxyl Radical and Sulfhydryl Reagents on the Open Probability of the Purified Cardiac Ryanodine Receptor Channel Incorporated into Planar Lipid BilayersBiochemical and Biophysical Research Communications, 1998
- Immunochemical Characterization of the Deficiency of the α‐Ketoglutarate Dehydrogenase Complex in Thiamine‐Deficient Rat BrainJournal of Neurochemistry, 1998
- Radical chemistry of tert-butyl hydroperoxide (TBHP). Part 1. Studies of the FeIII–TBHP mechanismNew Journal of Chemistry, 1998
- Brain thiamine, its phosphate esters, and its metabolizing enzymes in alzheimer's diseaseAnnals of Neurology, 1996
- Possible regulation of capacitative Ca2+ entry into colonic epithelial cells by NO and cGMPCell Calcium, 1995
- Cytotoxicity of an organic hydroperoxide and cellular antioxidant defense system against hydroperoxides in cultured mammalian cellsToxicology, 1989