[The level of lipoprotein(a) in human cataractous lens]

Molecular features of lipoprotein(a) [Lp (a)] associated with membranes of the lens were examined with respect to the pathogenesis and progression of cataract.

Lenses were homogenized and separated into urea-soluble (US) and water-soluble (WS) fractions. Then low density lipoprotein (LDL) and high density lipoprotein (HDL) fractions were separated from US & WS fractions by flotation density gradient ultracentrifugation. LDL and HDL fractions were prepared from 14 and 54 lenses, respectively, of a group of diabetic patients with senile cataract (DM group) or a group of non-diabetic patients with senile cataract (non-DM group). Lp(a) in each fraction and in human aqueous humor was immunochemically assayed using the latex agglutination method. Molecular phenotypes of Lp(a) were identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) followed by western blotting.

Lp (a) contents in LDL fractions were significantly higher (p < 0.05) in the DM group [11.14 +/- 0.88(mean +/- standard deviation) micrograms/lens] than in the non-DM group [5.77 +/- 2.75 micrograms/lens]. Lp(a) values in HDL fractions were higher in the DM group than in the non-DM group, although the values did not differ significantly between the two groups. Lp (a) concentration in aqueous humor was slightly higher in the DM group than in the non-DM group. Lp (a) components examined by SDS-PAGE were detected only at the origin using immunoblotting.

The Lp(a) content in cataractous lenses was higher in the DM group than in the non-DM group. In contrast to the molecular features of Lp(a) in blood, those of Lp(a) in cataractous lens seemed to be high molecular weight complexes. These results suggests that impairment of LDL receptors in DM is associated with disturbance in lipid metabolism which leads to accumulation of degenerated lipoproteins and altered membrane structure.