Abstract

1. 1. Chain-elongation of [1- 14 C]16:1( n−7) to 18:1( n−7) in rat brain homogenates was dependent on exogenous NADPH and malonyl-CoA; slight additive stimulation occurred when NADH and acetyl CoA were added. Activity was greatest in developing brain and lower in the adult. 2. 2. Chain-elongation of [1- 14 C]16:0, 18:0, and 18:1 showed a similar trend. 16:0 exceeded 18:0 elongation 5–20-fold at all ages examined; 18:1 elongation was even less. 3. 3. The formation of 18:1 from [1- 14 C]16:0 by desaturation and chain-elongation was higher in developing than in adult brain, and was stimulated 2-fold (adult) to 20–30-fold (fetal to 20 days) by NADPH and malonyl CoA. 18:1( n−7) accounted for 12–19% of total 18:1 formed at all ages. Thus, in rat brain the major pathway of 18:1 formation appears to be 16:0 → 18:0 → 18:1( n−9), and the minor pathway 16:0 → 16:1 → 18: l( n−7). 4. 4. Δ6 desaturation of exogenous [1- 14 C]16:0 and 18:0, and of 18:0 formed endogenously from exogenous 16:0, occurred between fetal stage and 20 days of age only. At birth, this activity accounted for 62% of the 16:1 formed from 16:0, and 28% of the 18:1 formed from 18:0. 5. 5. The previous demonstration of Δ9 desaturating activity, and the present findings of (a) chain-elongation of 16- and 18-carbon saturates and monoenes and (b) Δ6 desaturation of 16:0 and 18:0, show that developing rat brain has the necessary enzymes for forming all the major 16:1 and 18:1 monoenoic fatty-acid isomers.

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