Der Mechanismus der Blutkörperchensenkung, XIII. Charakterisierung von Lysolecithin als Inhibitor der beschleunigten Blutkörperchensenkung im inkubierten Serum

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Abstract
Serum was incubated for 20 hr. at 37[degree]; lysolecithln (about 0.38 [mu]mol./ml serum) was released from the [alpha]1 -lipoprotein fraction (which contains the erythrocyte sedimentation rate prolnhlbltor) and became bound to albumin. After the incubation of serum for 20 hr., the albumin yielded about 0.77 mol. lysoleclthin/mol. albumin after extraction in a Soxhlet with chloroform/methanol, 2:1 (v/V), whereas albumin from non-incubated serum contained about 0.15 mol. lysolecithin/mol. The lysoleclthin was identified by comparison with authentic lysoleclthin (phosphorus and choline contents, infrared spectrum, RF value). The lysoleclthln-albumln complex is the lysoleclthln-rlch lipoproteln, density> 1.21, which has been described by several authors. In the standardised sedimentation experiment, about 23 [mu]g lysoleclthin (0.9 x 10-11 [mu]mol. lysolecithln/cell) causes a 90% inhibition of sedimentation in the absence of albumin; for each 10 mg of albumin added to the standardised experiment 30 [mu]g. of lysoleclthin were required, to obtain the same rate of inhibition. This result agrees with the interpretation, that only the free lysoleclthin not bound to albumin is responsible for the inhibition of the sedimentation rate. Low concentrations of lysolecithin cause an increased rate of sedimentation. As the concentration of lysoleclthin is raised, the effect is reversed and the erythrocyte sedimentation rate is inhibited. This explains the accelerated erythrocyte sedimentation rate, that is frequently observed in plasma incubated for a short time. Lecithin that is pure in thin layer chromatography causes no inhibition of sedimentation up to a concentration of 150 [mu]g/ml.