PMID- 10828450
OWN - NLM
STAT- MEDLINE
DCOM- 20000706
LR  - 20240109
IS  - 0014-5793 (Print)
IS  - 0014-5793 (Linking)
VI  - 474
IP  - 1
DP  - 2000 May 26
TI  - The role of mild uncoupling and non-coupled respiration in the regulation of 
      hydrogen peroxide generation by plant mitochondria.
PG  - 53-7
AB  - The roles of mild uncoupling caused by free fatty acids (mediated by plant 
      uncoupling mitochondrial protein (PUMP) and ATP/ADP carrier (AAC)) and 
      non-coupled respiration (alternative oxidase (AO)) on H(2)O(2) formation by plant 
      mitochondria were examined. Both laurate and oleate prevent H(2)O(2) formation 
      dependent on the oxidation of succinate. Conversely, these free fatty acids (FFA) 
      only slightly affect that dependent on malate plus glutamate oxidation. 
      Carboxyatractylate (CAtr), an inhibitor of AAC, completely inhibits oleate- or 
      laurate-stimulated oxygen consumption linked to succinate oxidation, while GDP, 
      an inhibitor of PUMP, caused only a 30% inhibition. In agreement, CAtr completely 
      restores the oleate-inhibited H(2)O(2) formation, while GDP induces only a 30% 
      restoration. Both oleate and laurate cause a mild uncoupling of the electrical 
      potential (generated by succinate), which is then followed by a complete collapse 
      with a sigmoidal kinetic. FFA also inhibit the succinate-dependent reverse 
      electron transfer. Diamide, an inhibitor of AO, favors the malate plus 
      glutamate-dependent H(2)O(2) formation, while pyruvate (a stimulator of AO) 
      inhibits it. These results show that the succinate-dependent H(2)O(2) formation 
      occurs at the level of Complex I by a reverse electron transport. This generation 
      appears to be prevented by mild uncoupling mediated by FFA. The anionic form of 
      FFA appears to be shuttled by AAC rather than PUMP. The malate plus 
      glutamate-dependent H(2)O(2) formation is, conversely, mainly prevented by 
      non-coupled respiration (AO).
FAU - Casolo, V
AU  - Casolo V
AD  - Department of Biology and Agro-Industrial Economics, Section of Plant Biology, 
      University of Udine, via Cotonificio 108, I-33100, Udine, Italy.
FAU - Braidot, E
AU  - Braidot E
FAU - Chiandussi, E
AU  - Chiandussi E
FAU - Macri, F
AU  - Macri F
FAU - Vianello, A
AU  - Vianello A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - FEBS Lett
JT  - FEBS letters
JID - 0155157
RN  - 0 (Carrier Proteins)
RN  - 0 (Ion Channels)
RN  - 0 (Lauric Acids)
RN  - 0 (Malates)
RN  - 0 (Membrane Proteins)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (Uncoupling Agents)
RN  - 0 (Uncoupling Protein 1)
RN  - 1160N9NU9U (lauric acid)
RN  - 146-91-8 (Guanosine Diphosphate)
RN  - 17754-44-8 (Atractyloside)
RN  - 2UMI9U37CP (Oleic Acid)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 817L1N4CKP (malic acid)
RN  - 9068-80-8 (Mitochondrial ADP, ATP Translocases)
RN  - AB6MNQ6J6L (Succinic Acid)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - SNP1XL23E6 (carboxyatractyloside)
SB  - IM
MH  - Atractyloside/analogs & derivatives/pharmacology
MH  - Carrier Proteins/metabolism
MH  - Glutamic Acid/pharmacology
MH  - Guanosine Diphosphate/pharmacology
MH  - Hydrogen Peroxide/*metabolism
MH  - Ion Channels
MH  - Lauric Acids/pharmacology
MH  - Malates/pharmacology
MH  - Membrane Proteins/metabolism
MH  - Mitochondria/*metabolism
MH  - Mitochondrial ADP, ATP Translocases/antagonists & inhibitors/metabolism
MH  - Mitochondrial Proteins
MH  - Oleic Acid/pharmacology
MH  - Oxidation-Reduction
MH  - Oxidative Phosphorylation
MH  - *Oxygen Consumption
MH  - Pisum sativum/*ultrastructure
MH  - Succinic Acid/metabolism/pharmacology
MH  - Uncoupling Agents/metabolism
MH  - Uncoupling Protein 1
EDAT- 2000/06/01 09:00
MHDA- 2000/07/08 11:00
CRDT- 2000/06/01 09:00
PHST- 2000/06/01 09:00 [pubmed]
PHST- 2000/07/08 11:00 [medline]
PHST- 2000/06/01 09:00 [entrez]
AID - S0014-5793(00)01576-3 [pii]
AID - 10.1016/s0014-5793(00)01576-3 [doi]
PST - ppublish
SO  - FEBS Lett. 2000 May 26;474(1):53-7. doi: 10.1016/s0014-5793(00)01576-3.