PMID- 16115354
OWN - NLM
STAT- MEDLINE
DCOM- 20051011
LR  - 20190719
IS  - 0007-1145 (Print)
IS  - 0007-1145 (Linking)
VI  - 94
IP  - 2
DP  - 2005 Aug
TI  - Hyperhomocysteinaemia induced by dietary folate restriction causes kidney 
      oxidative stress in rats.
PG  - 204-10
AB  - Diet is the most common cause of mild hyperhomocysteinaemia (HHcy), which occurs 
      in approximately 5-7 % of the general population. Since HHcy causes endothelial 
      damage by oxidative stress in different organs, the present study was designed to 
      examine whether HHcy might be involved in renal oxidative stress. Twenty-five 
      male Wistar rats were randomly divided into two groups: one (n 13) was fed ad 
      libitum a folate-free diet (FF) and the other (n 12) was fed the same diet 
      supplemented with folic acid (control, CO). After 8 weeks the animals were killed 
      and kidneys removed. Malondialdehyde (MDA), superoxide dismutase (SOD) and 
      glutathione peroxidase (GPx) activities were measured in plasma and kidney 
      homogenates. Renal tissue sections were analysed by indirect immunostaining with 
      the primary antibody against oxidatively modified LDL receptor (LOX-1). A marked 
      HHcy was confirmed in the FF group. As compared with CO animals, MDA levels in 
      plasma and kidney homogenate were significantly higher in FF rats (P < 0.05). 
      Similarly, renal GPx and SOD activities were significantly higher in the FF group 
      (P < 0.001). No differences were found in LOX-1 immunohistochemical expression, 
      which in the two groups was displayed in tubular cells. The present study 
      provides evidence that HHcy does produce renal oxidative stress mediated by lipid 
      peroxidation, and that the increased kidney MDA displayed by FF animals may 
      enhance kidney antioxidant activity and thereby attenuate both kidney damage and 
      expression of LOX-1.
FAU - Diez, Nieves
AU  - Diez N
AD  - Department of Human Physiology, School of Medicine, University of Navarra, 31080 
      Pamplona, Spain.
FAU - Perez, Raquel
AU  - Perez R
FAU - Hurtado, Veronica
AU  - Hurtado V
FAU - Santidrian, Santiago
AU  - Santidrian S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Nutr
JT  - The British journal of nutrition
JID - 0372547
RN  - 0 (Antioxidants)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Free Radical Scavengers)
RN  - 0 (Proteins)
RN  - 0 (Receptors, LDL)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 935E97BOY8 (Folic Acid)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Animals
MH  - Antioxidants/metabolism
MH  - Chemokine CCL2/metabolism
MH  - Folic Acid/*administration & dosage/blood
MH  - Free Radical Scavengers/metabolism
MH  - Glutathione Peroxidase/metabolism
MH  - Homocysteine/blood
MH  - Hyperhomocysteinemia/etiology/*metabolism
MH  - Kidney/*metabolism
MH  - Lipid Peroxidation/physiology
MH  - Male
MH  - Oxidative Stress/*physiology
MH  - Proteins/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, LDL/metabolism
MH  - Superoxide Dismutase/metabolism
MH  - Vitamin B Deficiency/complications/*metabolism
MH  - Weight Loss/physiology
EDAT- 2005/08/24 09:00
MHDA- 2005/10/12 09:00
CRDT- 2005/08/24 09:00
PHST- 2005/08/24 09:00 [pubmed]
PHST- 2005/10/12 09:00 [medline]
PHST- 2005/08/24 09:00 [entrez]
AID - 10.1079/bjn20051468 [doi]
PST - ppublish
SO  - Br J Nutr. 2005 Aug;94(2):204-10. doi: 10.1079/bjn20051468.