PMID- 16823605
OWN - NLM
STAT- MEDLINE
DCOM- 20071011
LR  - 20131121
IS  - 1389-5729 (Print)
IS  - 1389-5729 (Linking)
VI  - 8
IP  - 1
DP  - 2007 Feb
TI  - Effect of graded corticosterone treatment on aging-related markers of oxidative 
      stress in rat liver mitochondria.
PG  - 1-11
AB  - Caloric restriction (CR) decreases aging rate and lowers the rate of reactive 
      oxygen species (ROS) production at mitochondria in different organs, but the 
      signal responsible for this last change is unknown. Glucocorticoids could 
      constitute such a signal since it is well known that their levels increase during 
      CR, and available studies failed to find consistent effects of insulin, the other 
      better described hormone that varies during CR, on mitochondrial oxidative 
      stress. In addition, there is almost no information on the possible in vivo 
      effects of glucocorticoids on specific markers of mitochondrial and tissue 
      oxidative stress. In this investigation, male Wistar rats were treated with 
      corticosterone at doses of 150 and 400 mg/kg of diet during 4 weeks. After that 
      time, oxidative stress-related parameters were measured in the liver. The 
      corticosterone treatments did not change the rate of ROS production or the rate 
      of oxygen consumption of rat liver mitochondria. The two lipoxidation protein 
      markers measured (malondialdehyde-lysine and carboxymethyllysine) were decreased 
      by both corticosterone treatments. These changes were associated with decreases 
      in fatty acid unsaturation, especially with lowered levels of the highly 
      unsaturated araquidonic and docosahexaenoic acids, which decrease the sensitivity 
      to lipid peroxidation processes. The specific protein carbonyl glutamic 
      semialdehyde, a marker of protein oxidation, was also lowered at 400 mg/kg 
      corticosterone. The protein glycoxydation marker carboxyethyllysine and the level 
      of oxidative damage to mtDNA (8-oxo-7,8-dihydro-2 9-deoxyguanosine) were 
      increased by corticosterone. The results do not support the idea that 
      corticosterone is the signal responsible for the decrease in mitochondrial ROS 
      generation during CR. However, they show that this hormone modulates the level of 
      oxidative stress both in proteins and in mtDNA. Some of these changes can 
      contribute to the chronic effects of the hormone at tissue level.
FAU - Caro, Pilar
AU  - Caro P
AD  - Department of Animal Physiology-II, Facultad de Ciencias Biologicas, Complutense 
      University, c/Antonio Novais-2, Madrid 28040, Spain.
FAU - Gomez, Jose
AU  - Gomez J
FAU - Sanz, Alberto
AU  - Sanz A
FAU - Portero-Otin, Manel
AU  - Portero-Otin M
FAU - Pamplona, Reinald
AU  - Pamplona R
FAU - Barja, Gustavo
AU  - Barja G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060705
PL  - Netherlands
TA  - Biogerontology
JT  - Biogerontology
JID - 100930043
RN  - 0 (DNA, Mitochondrial)
RN  - 0 (Fatty Acids)
RN  - 0 (Lipids)
RN  - 0 (Reactive Oxygen Species)
RN  - 12133JR80S (Guanosine)
RN  - 3868-31-3 (8-hydroxyguanosine)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Aging/*metabolism
MH  - Animals
MH  - Corticosterone/*administration & dosage
MH  - DNA, Mitochondrial/chemistry
MH  - Dose-Response Relationship, Drug
MH  - Fatty Acids/analysis
MH  - Guanosine/analogs & derivatives/analysis
MH  - Hydrogen Peroxide/metabolism
MH  - Lipid Peroxidation/drug effects
MH  - Lipids/chemistry
MH  - Male
MH  - Mitochondria, Liver/*drug effects/*metabolism
MH  - Oxidative Stress/*drug effects
MH  - Oxygen Consumption/drug effects
MH  - Rats
MH  - Rats, Wistar
MH  - Reactive Oxygen Species/metabolism
EDAT- 2006/07/11 09:00
MHDA- 2007/10/12 09:00
CRDT- 2006/07/11 09:00
PHST- 2006/02/17 00:00 [received]
PHST- 2006/04/01 00:00 [accepted]
PHST- 2006/07/11 09:00 [pubmed]
PHST- 2007/10/12 09:00 [medline]
PHST- 2006/07/11 09:00 [entrez]
AID - 10.1007/s10522-006-9026-x [doi]
PST - ppublish
SO  - Biogerontology. 2007 Feb;8(1):1-11. doi: 10.1007/s10522-006-9026-x. Epub 2006 Jul 
      5.