PMID- 11500180
OWN - NLM
STAT- MEDLINE
DCOM- 20011025
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 158
IP  - 1
DP  - 2001 Sep
TI  - Intravascular hemolysis increases atherogenicity of diet-induced 
      hypercholesterolemia in rabbits in spite of heme oxygenase-1 gene and protein 
      induction.
PG  - 103-11
AB  - Free radical mediated oxidation of apoB lipoproteins in the arterial intima 
      appears to contribute to atherogenicity of the entrapped particles. A plausible 
      pathogenic mechanism for oxidation is the one induced by heme leaking from 
      erythrocytes that is then carried into the arterial wall by its high affinity for 
      lipoproteins. In the intima, in the presence of H(2)O(2) secreted by macrophages, 
      heme can be a potent oxidant. To study the role of heme as a promoter of 
      oxidative stress damage in vivo we used a model of intravascular hemolysis (IVH) 
      caused by phenylhydrazine in rabbits with and without diet-induced moderate 
      hypercholesterolemia (MHC). Evaluation of the antioxidant status of plasma 
      indicated that at the end of the treatment period this was compromised by the 
      MHC-IVH. After 10 weeks the animals with combined MHC-IVH showed more of the 
      aorta surface covered by lesions (27%+/-8, mean (SD) than the animals with only 
      MHC (11%+/-7), in spite of having similar plasma levels of VLDL+LDL lipoproteins. 
      The animals with only IVH, as well as the controls, showed minimal lesions (<1%). 
      Heme oxygenase (HO-1) expression in aorta and other tissues was markedly 
      increased in the group with MHC-IVH and it was correlated with the extent of IVH. 
      The data suggest that the oxidative stress associated with IVH potentiates the 
      atherogenicity of moderate hypercholesterolemia and that in spite of a strong 
      induction of HO-1 this is not sufficient to counteract the atherogenicity of the 
      combined condition.
FAU - Fernandez, A Z
AU  - Fernandez AZ
AD  - Laboratorio de Trombosis Experimental, Centro de Biofisica y Bioquimica, 
      Instituto Venezolano de Investigaciones Cientificas (IVIC), Caracas, Venezuela.
FAU - Lopez, F
AU  - Lopez F
FAU - Tablante, A
AU  - Tablante A
FAU - Romano, E
AU  - Romano E
FAU - Hurt-Camejo, E
AU  - Hurt-Camejo E
FAU - Camejo, G
AU  - Camejo G
FAU - Apitz-Castro, R
AU  - Apitz-Castro R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Hemoglobins)
RN  - 0 (Phenylhydrazines)
RN  - 064F424C9K (phenylhydrazine)
RN  - EC 1.14.14.18 (Heme Oxygenase (Decyclizing))
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
SB  - IM
CIN - Atherosclerosis. 2002 Jul;163(1):199-201. PMID: 12048140
MH  - Animals
MH  - Aorta/pathology
MH  - Arteriosclerosis/etiology/metabolism/pathology/*physiopathology
MH  - Diet, Atherogenic
MH  - Gene Expression Regulation
MH  - Heme Oxygenase (Decyclizing)/*genetics/physiology
MH  - Heme Oxygenase-1
MH  - Hemoglobins/analysis
MH  - Hemolysis/drug effects/*physiology
MH  - Hypercholesterolemia/blood/*complications
MH  - Male
MH  - Oxidative Stress
MH  - Phenylhydrazines/pharmacology
MH  - Rabbits
EDAT- 2001/08/14 10:00
MHDA- 2001/10/26 10:01
CRDT- 2001/08/14 10:00
PHST- 2001/08/14 10:00 [pubmed]
PHST- 2001/10/26 10:01 [medline]
PHST- 2001/08/14 10:00 [entrez]
AID - S0021-9150(01)00422-1 [pii]
AID - 10.1016/s0021-9150(01)00422-1 [doi]
PST - ppublish
SO  - Atherosclerosis. 2001 Sep;158(1):103-11. doi: 10.1016/s0021-9150(01)00422-1.