PMID- 28280417
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1226-4512 (Print)
IS  - 2093-3827 (Electronic)
IS  - 1226-4512 (Linking)
VI  - 21
IP  - 2
DP  - 2017 Mar
TI  - Hydrogen peroxide attenuates refilling of intracellular calcium store in mouse 
      pancreatic acinar cells.
PG  - 233-239
LID - 10.4196/kjpp.2017.21.2.233 [doi]
AB  - Intracellular calcium (Ca(2+)) oscillation is an initial event in digestive 
      enzyme secretion of pancreatic acinar cells. Reactive oxygen species are known to 
      be associated with a variety of oxidative stress-induced cellular disorders 
      including pancreatitis. In this study, we investigated the effect of hydrogen 
      peroxide (H(2)O(2)) on intracellular Ca(2+) accumulation in mouse pancreatic 
      acinar cells. Perfusion of H(2)O(2) at 300 microM resulted in additional elevation of 
      intracellular Ca(2+) levels and termination of oscillatory Ca(2+) signals induced 
      by carbamylcholine (CCh) in the presence of normal extracellular Ca(2+). 
      Antioxidants, catalase or DTT, completely prevented H(2)O(2)-induced additional 
      Ca(2+) increase and termination of Ca(2+) oscillation. In Ca(2+)-free medium, 
      H(2)O(2) still enhanced CCh-induced intracellular Ca(2+) levels and thapsigargin 
      (TG) mimicked H(2)O(2)-induced cytosolic Ca(2+) increase. Furthermore, 
      H(2)O(2)-induced elevation of intracellular Ca(2+) levels was abolished under 
      sarco/endoplasmic reticulum Ca(2+) ATPase-inactivated condition by TG 
      pretreatment with CCh. H(2)O(2) at 300 microM failed to affect store-operated Ca(2+) 
      entry or Ca(2+) extrusion through plasma membrane. Additionally, ruthenium red, a 
      mitochondrial Ca(2+) uniporter blocker, failed to attenuate H(2)O(2)-induced 
      intracellular Ca(2+) elevation. These results provide evidence that excessive 
      generation of H(2)O(2) in pathological conditions could accumulate intracellular 
      Ca(2+) by attenuating refilling of internal Ca(2+) stores rather than by 
      inhibiting Ca(2+) extrusion to extracellular fluid or enhancing Ca(2+) 
      mobilization from extracellular medium in mouse pancreatic acinar cells.
FAU - Yoon, Mi Na
AU  - Yoon MN
AD  - Department of Physiology, College of Medicine, Konyang University, Daejeon 35365, 
      Korea.
FAU - Kim, Dong Kwan
AU  - Kim DK
AD  - Department of Physiology, College of Medicine, Konyang University, Daejeon 35365, 
      Korea.
FAU - Kim, Se Hoon
AU  - Kim SH
AD  - Department of Physiology, College of Medicine, Konyang University, Daejeon 35365, 
      Korea.
FAU - Park, Hyung Seo
AU  - Park HS
AD  - Department of Physiology, College of Medicine, Konyang University, Daejeon 35365, 
      Korea.; Myunggok Medical Research Institute, Konyang University, Daejeon 35365, 
      Korea.
LA  - eng
PT  - Journal Article
DEP - 20170221
PL  - Korea (South)
TA  - Korean J Physiol Pharmacol
JT  - The Korean journal of physiology & pharmacology : official journal of the Korean 
      Physiological Society and the Korean Society of Pharmacology
JID - 9709505
PMC - PMC5343057
OTO - NOTNLM
OT  - Hydrogen peroxide
OT  - Intracellular Ca2+ stores
OT  - Pancreatic acinar cells
OT  - Reactive oxygen species
OT  - Sarcoplasmic reticulum Ca2+ ATPase
COIS- CONFLICTS OF INTEREST: The authors declare no conflicts of interest.
EDAT- 2017/03/11 06:00
MHDA- 2017/03/11 06:01
PMCR- 2017/03/01
CRDT- 2017/03/11 06:00
PHST- 2016/11/21 00:00 [received]
PHST- 2016/12/12 00:00 [revised]
PHST- 2016/12/13 00:00 [accepted]
PHST- 2017/03/11 06:00 [entrez]
PHST- 2017/03/11 06:00 [pubmed]
PHST- 2017/03/11 06:01 [medline]
PHST- 2017/03/01 00:00 [pmc-release]
AID - 10.4196/kjpp.2017.21.2.233 [doi]
PST - ppublish
SO  - Korean J Physiol Pharmacol. 2017 Mar;21(2):233-239. doi: 
      10.4196/kjpp.2017.21.2.233. Epub 2017 Feb 21.