The fatty acid specificity of purified human milk lipoprotein lipase was studied using the C18 to C54 (total acyl carbon number) saturated and the C54 mono-, di- and triunsaturated monoacid triacylglycerols. Kinetic determinations indicated that the medium-chain triacylglycerols were better substrates than long- or very short-chain saturated triacylglycerols. The unsaturated triacylglycerols were hydrolyzed at rates comparable to that of tricaprylin with triolein having the highest rate of hydrolysis of the unsaturated species tested. The enzyme attacked the primary ester bond much more readily than the secondary ester bond. The purified human milk lipoprotein lipase showed a preferential stereospecific lipolysis of the sn-1-position of the triacylglycerol molecule.

The mechanisms responsible for the accumulation of redox‐active brain iron in normal senescence and in Parkinson's disease remain poorly understood. The aminothiol compound cysteamine (CSH) induces the appearance of autofluorescent, iron‐rich cytoplasmic granules in cultured astroglia that are identical to glial inclusions that progressively accumulate in the aging periventricular brain. Both in situ and in culture, these glial inclusions appear to arise in the context of a generalized cellular stress (heat shock) response. Several laboratories have previously concluded that porphyrins and heme ferrous iron are responsible, respectively, for red‐orange autofluorescence and nonenzymatic peroxidase activity in the glial inclusions. In the present study we found that, contrary to hypothesis, CSH suppresses the incorporation of the heme precursors δ‐amino[14C]levulinic acid and [14C]glycine into astroglial porphyrin and heme in primary culture. Similar results were obtained when the cells were preloaded with radiolabeled heme precursors for 24 h before CSH treatment, suggesting that the latter directly inhibits porphyrin‐heme biosynthesis rather than limiting precursor uptake by these cells. We also demonstrated that CSH exposure results in the sequestration of iron‐59 by astroglial mitochondria (granule precursors). The results of this study suggest that stress‐related trapping of nonheme iron by astroglial mitochondria may be an important mechanism underlying the pathological accumulation of redox‐active iron in the basal ganglia of subjects with Parkinson's disease. CSH‐treated astrocytes provide a useful model to investigate the role of stress‐related dysregulation of neuroglial iron metabolism in the aging and degenerating nervous system.

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