[Defects in peroxidation of erythrocyte phospholipids in sickle cell trait].
The sickle cell disease pathophysiology is provided by several events including deoxyhemoglobin S polymerization and hemorrheological troubles. Classically, such disorders have been known to concern only the homozygous SS and heterozygous SC profiles. However, troubles are more and more described since early years in the sickle cell trait patients and the pathogenesis factors are unknown. Our study focussed on phospholipids which are the basic and functional constituent elements of erythrocyte plasmic membrane. Assaying the membrane lipids extracted by Folch method and lipid standards (cholesterol, phosphatidic acid, lysophosphatidyl-choline, phosphatidyl-choline, lysophosphatidyl-ethanolamine, phosphatidyl-ethanolamine, sphingomyelin) was carried out by HPLC among 91 sickle cell trait patients as compared to 78 healthy subjects. The main abnormalities observed were an empoverishement in phosphatidyl-choline contrasting with an accumulation of membrane lysophosphatidyl-choline, lysophosphatidyl-ethanolamine, phosphatidic acid and sphingomyelin in sickle cell patients. These results suggest that sickle cell trait harmlessness is not actual. The accumulation of lysophosphatidyl-choline, by its cytolytic biomembrane perturbing properties, predispose therefore the sickled red cell to the haemolysis phenomena and allow to forecast deeper disturbances among homozygous subjects. These morbid disorders attributable to lipid peroxidation would justify an antioxidant treatment during the sickle cell disease.
Diatta
A
A
Laboratoire de Biochimie Médicale, Faculté de Médecine, UCAD Dakar, Sénégal. adiatta@refer.sn
Diallo
F
F
Sarr
N G
NG
Traore
S
S
Diagne
I
I
Lopez-Sall
P
P
Sall
N D
ND
Toure
M
M
D004912:Erythrocytes / Q000378:metabolism*; D006801:Humans; D015227:Lipid Peroxidation; D008659:Metabolic Diseases / Q000097:blood; D010743:Phospholipids / Q000378:metabolism*; D012805:Sickle Cell Trait / Q000097:blood / Q000378:metabolism*
D010743:Phospholipids