PMID- 8579366
OWN - NLM
STAT- MEDLINE
DCOM- 19960308
LR  - 20131121
IS  - 0003-9861 (Print)
IS  - 0003-9861 (Linking)
VI  - 326
IP  - 1
DP  - 1996 Feb 1
TI  - Modulation of the rat alveolar macrophage respiratory burst by hydroperoxides is 
      calcium dependent.
PG  - 166-71
AB  - Sublethal concentrations of hydroperoxides (H2O2 or tert-butylhydroperoxide) 
      produce a dual effect upon the respiratory burst of rat alveolar macrophages in 
      which low concentrations (< 50 microM) enhance and higher concentrations (> 50 
      microM) produce inhibition (J. K. Murphy, et al., Free Radical. Biol. Med. 18, 
      37-45, 1995). These effects correlate with transient versus sustained elevation 
      of [Ca2+]i caused by exposure to hydroperoxides prior to stimulation of the 
      respiratory burst. In the present study changes in [Ca2+]i caused by exposure to 
      sublethal levels of hydroperoxide were buffered by incubating macrophages with 
      the acetoxy-methyl ester of BAPTA, an intracellular Ca2+ chelator. The 
      enhancement of the phorbol ester-stimulated respiratory burst by tBOOH was 
      abolished by BAPTA, while the inhibition was attenuated. Thus, the modulation by 
      tBOOH appears to be largely dependent upon the changes in [Ca2+]i. Receptor 
      mediated stimulation of the respiratory burst (ADP stimulation) involves release 
      of Ca2+ from the inositol-1,4,5-triphosphate (IP3)-sensitive pool in the 
      endoplasmic reticulum. Comparisons were made of the effects of thapsigargin (TG), 
      an endoplasmic reticulum Ca-ATPase inhibitor, with tBOOH on release of 
      intracellular Ca2+ and the respiratory burst. Treatment with TG did not affect 
      changes in [Ca2+]i caused by tBOOH or vice versa. Although TG decreased the 
      ADP-stimulated respiratory burst, it had no effect upon tBOOH modulation. Thus, 
      the effect of tBOOH upon the respiratory burst is dependent upon the release of 
      Ca2+ and the release of Ca2+ occurs from a non-IP3-dependent pool. This aberrant 
      mimicry of normal signal transduction underlies oxidative modulation of the 
      respiratory burst.
FAU - Hoyal, C R
AU  - Hoyal CR
AD  - Department of Molecular Pharmacology and Toxicology, University of Southern 
      California, Los Angeles 90033, USA.
FAU - Gozal, E
AU  - Gozal E
FAU - Zhou, H
AU  - Zhou H
FAU - Foldenauer, K
AU  - Foldenauer K
FAU - Forman, H J
AU  - Forman HJ
LA  - eng
GR  - HL37556/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Arch Biochem Biophys
JT  - Archives of biochemistry and biophysics
JID - 0372430
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Oxidants)
RN  - 0 (Terpenes)
RN  - 67526-95-8 (Thapsigargin)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Calcium/*metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Hydrogen Peroxide/metabolism/*pharmacology
MH  - Macrophages, Alveolar/*metabolism
MH  - Male
MH  - Oxidants/metabolism/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Respiratory Burst/*drug effects
MH  - Terpenes/pharmacology
MH  - Thapsigargin
EDAT- 1996/02/01 00:00
MHDA- 1996/02/01 00:01
CRDT- 1996/02/01 00:00
PHST- 1996/02/01 00:00 [pubmed]
PHST- 1996/02/01 00:01 [medline]
PHST- 1996/02/01 00:00 [entrez]
AID - S0003-9861(96)90061-2 [pii]
AID - 10.1006/abbi.1996.0061 [doi]
PST - ppublish
SO  - Arch Biochem Biophys. 1996 Feb 1;326(1):166-71. doi: 10.1006/abbi.1996.0061.