PMID- 7864645
OWN - NLM
STAT- MEDLINE
DCOM- 19950317
LR  - 20131121
IS  - 0003-9861 (Print)
IS  - 0003-9861 (Linking)
VI  - 316
IP  - 2
DP  - 1995 Feb 1
TI  - Hemoglobin-induced lipid peroxidation in the retina: a possible mechanism for 
      macular degeneration.
PG  - 864-72
AB  - To investigate a possible link between subretinal hemorrhage and macular 
      degeneration, oxyhemoglobin (HbO2) or methemoglobin (metHb) was incubated with 
      retinal homogenate and unsaturated phospholipid peroxidation was monitored by (a) 
      assay of thiobarbituric acid-reactive substances (TBARS), (b) luminescence 
      originating from an energy transfer of lipid-degraded products to rose bengal, 
      and (c) the decrease in composition of highly unsaturated fatty acids of 
      phospholipids. TBARS formation and rose bengal luminescence in the case of 
      metHb-induced lipid peroxidation were about 1.5 times greater than those in 
      HbO2-induced lipid peroxidation. alpha-Tocopherol, a lipid-soluble antioxidant, 
      and docosahexaenoic acid, a major unsaturated fatty acid, were slightly more 
      rapidly decomposed after a 60-min incubation with metHb than with HbO2 at the 
      same concentration. Atomic absorption analysis revealed that an equal 
      concentration of iron was released from both HbO2 and metHb during incubation 
      with retinal homogenates. The released iron may promote microsomal phospholipid 
      peroxidation in the presence of endogenous ascorbate or NADPH-dependent 
      cytochrome P-450 reductase because ascorbate oxidase and p-chloromercuribenzoic 
      acid (an inhibitor of sulfhydryl enzymes) inhibited metHb- or HbO2-induced lipid 
      peroxidation. MetHb-induced lipid peroxidation in retina was inhibited by KCN or 
      NaN3, which binds to FeIII of metHb. KCN or NaN3 had no effect on HbO2-induced 
      lipid peroxidation, because conversion of HbO2 to metHb, which can proceed in 
      HbO2 incubated with phospholipid liposome, did not occur in retinal homogenates. 
      It is concluded that metHb induces peroxidation of retinal unsaturated 
      phospholipids (1) directly and (2) by releasing iron.
FAU - Ito, T
AU  - Ito T
AD  - Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
FAU - Nakano, M
AU  - Nakano M
FAU - Yamamoto, Y
AU  - Yamamoto Y
FAU - Hiramitsu, T
AU  - Hiramitsu T
FAU - Mizuno, Y
AU  - Mizuno Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arch Biochem Biophys
JT  - Archives of biochemistry and biophysics
JID - 0372430
RN  - 0 (Azides)
RN  - 0 (Cyanides)
RN  - 0 (Fatty Acids)
RN  - 0 (Ferric Compounds)
RN  - 0 (Hemoglobins)
RN  - 0 (Oxyhemoglobins)
RN  - 0 (Phospholipids)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 1406-18-4 (Vitamin E)
RN  - 7A314HQM0I (Pentetic Acid)
RN  - 9008-37-1 (Methemoglobin)
RN  - 968JJ8C9DV (Sodium Azide)
SB  - IM
MH  - Animals
MH  - Azides/pharmacology
MH  - Cyanides/pharmacology
MH  - Fatty Acids/analysis
MH  - Ferric Compounds/*pharmacology
MH  - Hemoglobins/*pharmacology
MH  - Lipid Peroxidation/*physiology
MH  - Macular Degeneration/*metabolism
MH  - Male
MH  - Methemoglobin/pharmacology
MH  - Oxyhemoglobins/pharmacology
MH  - Pentetic Acid/pharmacology
MH  - Phospholipids/chemistry
MH  - Rats
MH  - Rats, Wistar
MH  - Retinal Hemorrhage/metabolism
MH  - Rod Cell Outer Segment/*drug effects
MH  - Sodium Azide
MH  - Swine
MH  - Thiobarbituric Acid Reactive Substances/analysis
MH  - Vitamin E/metabolism
EDAT- 1995/02/01 00:00
MHDA- 1995/02/01 00:01
CRDT- 1995/02/01 00:00
PHST- 1995/02/01 00:00 [pubmed]
PHST- 1995/02/01 00:01 [medline]
PHST- 1995/02/01 00:00 [entrez]
AID - S0003-9861(85)71116-2 [pii]
AID - 10.1006/abbi.1995.1116 [doi]
PST - ppublish
SO  - Arch Biochem Biophys. 1995 Feb 1;316(2):864-72. doi: 10.1006/abbi.1995.1116.