PMID- 17018869
OWN - NLM
STAT- MEDLINE
DCOM- 20061025
LR  - 20190608
IS  - 1535-3702 (Print)
IS  - 1535-3699 (Linking)
VI  - 231
IP  - 9
DP  - 2006 Oct
TI  - Effect of soluble nickel on cellular energy metabolism in A549 cells.
PG  - 1474-80
AB  - Iron is an essential nutrient to most organisms, and is actively involved in 
      oxygen delivery, electron transport, DNA synthesis, and many other biochemical 
      reactions important for cell survival. We previously reported that nickel (Ni) 
      ion exposure decreases cellular iron level and converts cytosolic aconitase 
      (c-aconitase) to iron-regulatory protein-1 in A549 cells (Chen H, Davidson T, 
      Singleton S, Garrick MD, Costa M. Toxicol Appl Pharmacol 206:275-287, 2005). 
      Here, we further investigated the effect of Ni ion exposure on the activity of 
      mitochondrial iron-sulfur (Fe-S) enzymes and cellular energy metabolism. We found 
      that acute Ni ion treatment up to 1 mM exhibits minimal toxicity in A549 cells. 
      Ni ion treatment decreases the activity of several Fe-S enzymes related to 
      cellular energy metabolism, including mitochondrial aconitase (m-aconitase), 
      succinate dehydrogenase (SDH), and NADH:ubiquinone oxidoreductase (complex I). 
      Low doses of Ni ion for 4 weeks resulted in an increased cellular glycolysis and 
      NADH to NAD+ (NADH/NAD+) ratio, although glycolysis was inhibited at higher 
      levels. Collectively, our results show that Ni ions decrease the activity of 
      cellular iron (Fe)-containing enzymes, inhibit oxidative phosphorylation 
      (OxPhos), and increase cellular glycolytic activity. Since increased glycolysis 
      is one of the fundamental alterations of energy metabolism in cancer cells (the 
      Warburg effect), the inhibition of Fe-S enzymes and subsequent changes in 
      cellular energy metabolism caused by Ni ions may play an important role in Ni 
      carcinogenesis.
FAU - Chen, Haobin
AU  - Chen H
AD  - Nelson Institute of Environmental Medicine, New York University School of 
      Medicine, 57 Old Forge Road, Tuxedo, NY 10987, USA.
FAU - Costa, Max
AU  - Costa M
LA  - eng
PT  - Journal Article
PL  - Switzerland
TA  - Exp Biol Med (Maywood)
JT  - Experimental biology and medicine (Maywood, N.J.)
JID - 100973463
RN  - 7OV03QG267 (Nickel)
RN  - E1UOL152H7 (Iron)
SB  - IM
MH  - Cell Line, Tumor
MH  - *Energy Metabolism
MH  - Humans
MH  - Iron/metabolism
MH  - Nickel/*metabolism
MH  - Solubility
EDAT- 2006/10/05 09:00
MHDA- 2006/10/26 09:00
CRDT- 2006/10/05 09:00
PHST- 2006/10/05 09:00 [pubmed]
PHST- 2006/10/26 09:00 [medline]
PHST- 2006/10/05 09:00 [entrez]
AID - 231/9/1474 [pii]
AID - 10.1177/153537020623100905 [doi]
PST - ppublish
SO  - Exp Biol Med (Maywood). 2006 Oct;231(9):1474-80. doi: 10.1177/153537020623100905.