Mouse brain uptake and metabolism of stearic acid.

After injection, labelled stearic acid is transported directly into the brain and incorporated into brain lipids without prior oxydation to acetate and resynthesis of fatty acids. Contamination by blood can be excluded. (The preparation contains all subcellular fraction except cytosol).

[Biosynthesis of lignoceric acid in two organelles (mitochondria and microsomes) during the development of the brain in normal and pathologic (Quaking and Jimpy) mice].

In microsomes, biosynthesis of lignoceric acid from its direct precursor (behenyl-CoA) is largely increased during myelination. The peak is hardly detectable in Quaking; in Jimpy, the synthesis is nearly absent (3% of normal value); in the adult Quaking, the synthesis is normal. Mitochondria are capable of synthesizing lignoceric acid.

[Study of the passage of stearic acid through blood-brain barrier and its incorporation in cerebral membranes (especially in myelin)].

Subcutaneously injected stearic acid is uptaken by brain and is further incorporated into membrane lipids (especially myelin). The uptake increases regularly up to 20 hrs. in total membranes as in myelin.

[Comparative biosynthesis of fatty acids, particularly lignoceric acid, in the kidney and brain of normal and "quaking" mice].

Palmityl-CoA elongation is normal in kidney and brain from Quaking mice. However elongation of stearyl-CoA and behenyl-CoA is disturbed in the mutant brain, but not in kidney. Moreove in both organs, the reaction products are the same in normal and Quaking animals.

Nervonic acid biosynthesis by erucyl-CoA elongation in normal and quaking mouse brain microsomes. Elongation of other unsaturated fatty acyl-CoAs (mono and poly-unsaturated).

Biosynthesis of nervonic acid by enzymatic elongation of erucyl-CoA has been studied in mouse brain microsomes. The substrate and cofactor requirements have been measured. Malonyl-CoA and reduced nicotine-adenine-dinucleotide phosphate are required, but not FMN, FAD or NADH.

[Biosynthesis of fatty acids in mouse brain mitochondria in the presence of malonyl-CoA or acetyl-CoA].

Incorporation of malonyl-CoA or acetyl-CoA is studied in mouse brain mitochondrial fatty acids. Rupture of mitochondria is necessary ; Triton X-100 gives the best result. Other detergents or sonication are of lesser efficiency.

[Substrates and products of fatty acid elongation in mouse brain microsomes].

In brain microsomes, palmitate and stearate elongation involve a membrane lipid-bound substrate. After elongation by malonyl-CoA, acyl-products are partially bound to proteins. Acyl-proteins are not found when endogenous fatty acid elongation takes place.