PMID- 10484461
OWN - NLM
STAT- MEDLINE
DCOM- 19991028
LR  - 20181011
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 277
IP  - 3
DP  - 1999 Sep
TI  - Effects of reactive oxygen and nitrogen metabolites on MCP-1-induced monocyte 
      chemotactic activity in vitro.
PG  - L543-9
LID - 10.1152/ajplung.1999.277.3.L543 [doi]
AB  - Peroxynitrite, an oxidant generated by the interaction between superoxide and 
      nitric oxide (NO), can nitrate tyrosine residues, resulting in compromised 
      protein function. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that 
      attracts monocytes and has a tyrosine residue critical for function. We 
      hypothesized that peroxynitrite would alter MCP-1 activity. Peroxynitrite 
      attenuated MCP-1-induced monocyte chemotactic activity (MCA) in a dose-dependent 
      manner (P < 0.05) but did not attenuate leukotriene B4 or complement-activated 
      serum MCA. The reducing agents dithionite, deferoxamine, and dithiothreitol 
      reversed the MCA inhibition by peroxynitrite, and exogenous L-tyrosine abrogated 
      the inhibition by peroxynitrite. PAPA-NONOate, an NO donor, or superoxide 
      generated by xanthine and xanthine oxidase did not show an inhibitory effect on 
      MCA induced by MCP-1. The peroxynitrite generator 3-morpholinosydnonimine caused 
      a concentration-dependent inhibition of MCA by MCP-1. Peroxynitrite reduced MCP-1 
      binding to monocytes and resulted in nitrotyrosine formation. These findings are 
      consistent with nitration of tyrosine by peroxynitrite, with subsequent 
      inhibition of MCP-1 binding to monocytes, and suggest that peroxynitrite may play 
      a role in regulation of MCP-1-induced monocyte chemotaxis.
FAU - Sato, E
AU  - Sato E
AD  - Research Services, Tucson and Overton Brooks Veterans Affairs Medical Centers, 
      and Department of Medicine, University of Arizona, Tucson, Arizona 85723, USA.
FAU - Simpson, K L
AU  - Simpson KL
FAU - Grisham, M B
AU  - Grisham MB
FAU - Koyama, S
AU  - Koyama S
FAU - Robbins, R A
AU  - Robbins RA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Chemokine CCL2)
RN  - 0 (Nitrates)
RN  - 0 (Oxidants)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Reducing Agents)
RN  - 11062-77-4 (Superoxides)
RN  - 1HGW4DR56D (Leukotriene B4)
RN  - 26404-66-0 (peroxynitric acid)
RN  - 3604-79-3 (3-nitrotyrosine)
RN  - 42HK56048U (Tyrosine)
RN  - N762921K75 (Nitrogen)
SB  - IM
MH  - Blood Physiological Phenomena
MH  - Cells, Cultured
MH  - Chemokine CCL2/*pharmacology
MH  - Chemotaxis, Leukocyte/drug effects/*physiology
MH  - Dose-Response Relationship, Drug
MH  - Humans
MH  - Leukotriene B4/pharmacology
MH  - Monocytes/*drug effects/*physiology
MH  - Nitrates/pharmacology
MH  - Nitrogen/*metabolism
MH  - Oxidants/pharmacology
MH  - Reactive Oxygen Species/*metabolism
MH  - Reducing Agents/pharmacology
MH  - Superoxides/pharmacology
MH  - Tyrosine/analogs & derivatives/biosynthesis/pharmacology
EDAT- 1999/09/14 00:00
MHDA- 1999/09/14 00:01
CRDT- 1999/09/14 00:00
PHST- 1999/09/14 00:00 [pubmed]
PHST- 1999/09/14 00:01 [medline]
PHST- 1999/09/14 00:00 [entrez]
AID - 10.1152/ajplung.1999.277.3.L543 [doi]
PST - ppublish
SO  - Am J Physiol. 1999 Sep;277(3):L543-9. doi: 10.1152/ajplung.1999.277.3.L543.