Hydrogen peroxide inhibits Ca 2+ efflux through plasma membrane Ca 2+ -ATPase in mouse parotid acinar cells

• Published in: The Korean journal of physiology & pharmacology 2018-03, Vol.22 (2), p.215
• Main Authors: Kim, Min Jae, Choi, Kyung Jin, Yoon, Mi Na, Oh, Sang Hwan, Kim, Dong Kwan, Kim, Se Hoon, Park, Hyung Seo
• Format: Article
• Language: English
• ISSN: 1226-4512; 2093-3827
• DOI: 10.4196/kjpp.2018.22.2.215

Intracellular Ca mobilization is closely linked with the initiation of salivary secretion in parotid acinar cells. Reactive oxygen species (ROS) are known to be related to a variety of oxidative stress-induced cellular disorders and believed to be involved in salivary impairments. In this study, we investigated the underlying mechanism of hydrogen peroxide (H O ) on cytosolic Ca accumulation in mouse parotid acinar cells. Intracellular Ca levels were slowly elevated when 1 mM H O was perfused in the presence of normal extracellular Ca . In a Ca -free medium, 1 mM H O still enhanced the intracellular Ca level. Ca entry tested using manganese quenching technique was not affected by perfusion of 1 mM H O . On the other hand, 10 mM H O induced more rapid Ca accumulation and facilitated Ca entry from extracellular fluid. Ca refill into intracellular Ca store and inositol 1,4,5-trisphosphate (1 µM)-induced Ca release from Ca store was not affected by 1 mM H O in permeabilized cells. Ca efflux through plasma membrane Ca -ATPase (PMCA) was markedly blocked by 1 mM H O in thapsigargin-treated intact acinar cells. Antioxidants, either catalase or dithiothreitol, completely protected H O -induced Ca accumulation through PMCA inactivation. From the above results, we suggest that excessive production of H O under pathological conditions may lead to cytosolic Ca accumulation and that the primary mechanism of H O -induced Ca accumulation is likely to inhibit Ca efflux through PMCA rather than mobilize Ca ions from extracellular medium or intracellular stores in mouse parotid acinar cells.