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L Ginsberg

Publications and source records attributed to L Ginsberg.

61 records · Page 4Linked to original sources

Shifts in ATP synthesis during preimplantation stages of mouse embryos.

The actual and potential activities of the cyochrome system were studied in cleavage-stage mouse embroys. Activities were determined by assaying embroys for total ATP and the rates of [32-P]ATP synthesis both before and after their incubation in medium supplemented either with an energy coupling site inhibitor (antimycin, amytal or cyanide) or with the FADH-linked substrate, succinate. The data indicate that there are three major shifts in the mode of ATP production during preimplantation stages: the first, between the two-cell and late four-cell stages; the second, between the eight-celland late morula stages; and the third, between the late morula and late blastocyst stages. These data are discussed in relation to studies on the energy metabolism of cleavage and blastocyst stage mouse embryos.

Adenosine Triphosphate↗

ATP metabolism in tn/tn mouse embryos.

Total ATP, ATP/ADP ratios, and the rates of synthesis and turnover of ATP were determined for t12-, tw32- and T+/T+-litters at the 2-cell, 4-cell, 8-cell, early morula, late morula and late blastocyst stages. The results show that tn-litters have excessive rates of ATP metabolism up to the cleavage stage immediately before the stage of lethality for most tw32/tw32 embryos (early morula) and most t12/t12 embryos (late morula); mutant ATP metabolism then falls below control levels. After the death of the tn homozygotes, ATP metabolism in the tn-litters (composed of only T+/T+ and T+/tn embryos) returns to control levels. These data are discussed in relation to the phenotypes of the homozygous tn embryos.

Adenosine Diphosphate↗

Evidence for a membrane lipid defect in Alzheimer disease.

We have previously shown that cells normally maintain their lipid metabolic pools at a critical composition, appropriate for spontaneous assembly of a stable membrane bilayer at their physiological temperature. When disease affects membrane lipids such that the new composition will only form a stable bilayer at a critical temperature (T*), which differs from the physiological value, membrane destabilization and hence cellular damage will necessarily ensue. We have previously tested this pathogenetic mechanism in metachromatic leukodystrophy, a disorder with a known primary lipid metabolic defect. In the present study, we found T* for cerebral cortex lipids from three Alzheimer disease (AD) patients ranged between 19 and 28 degrees C, independent of membrane protein composition. Control cortex lipids yielded a normal value for T* of 37 degrees C. Thus, one possible mechanism for neurodegeneration in AD is membrane destabilization secondary to a lipid compositional aberration, which shifts T* away from 37 degrees C. This lipid defect is brain region-specific as cerebellar lipids from the AD patients gave a normal value for T*. Studies aimed at delineating the nature of the biochemical anomaly are in progress.

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