No abstract

Pregnant rats were maintained on a fat-free diet, starting at 10-12 days after impregnation and the offspring continued on the diet during a developmental period of 120 days. Brain fatty acids showed decreases in the level of (n-3) and (n-6) fatty acids of brain phophoglycerides, except for 22:5 (n-6) which increased. These changes preceded an increase in the (n-9) fatty acids (20:3 and 22:3). Supplementation with either linoleic or linolenic acid for 10 or 30 days after induction of the deficiency state caused an increase in the (n-6) and (n-3) fatty acids respectively, to control levels. The level of 22: 5 (n-6) was increased additionally by linoleic supplementation while linolenic refeeding to deficient animals decreased 22:5 (n-6) to near control levels. The anomalous results obtained on 22:5 (n-6) with 18: 3 (n-3) supplementation is attributed to competitive inhibition of linoleate desaturation by linolenate. Linoleic and linolenic acid were equally effective in reducing the elevated levels of the (n-9) fatty acids toward control levels, although control levels with either fatty acid was not reached after 30 days supplementation. The increase of the (n-6) and (n-3) fatty acids to normal values precedes the decrease of (n-9) fatty acids following supplementation of linoleic or linolenic acid to fat-deficient rats. No change in fatty acid composition in control animals between 30 and 120 days was observed.In fat deficient as well as supplemented animals the total saturated, monounsaturated and polyunsaturated fatty acid composition was constant as was the unsaturation index. 911-917. 241. 5213-5219. M. E. (1969) Biochim. biophys. Acta. 176. 420422. Nutr. 102, 87-92. 37,

No abstract

The free and bound nonspecific esterases occurring in, respectively, the saline and triton X‐100 extracts of adult and developing human brain were studied by starch gel electrophoresis (zymograms). Zymograms of the free esterase fraction visualized with NA as substrate were qualitatively similar at 5‐12 days of age to the electrophoretic patterns observed in adult material. In both adult and developing brain, zymograms of bound esterase resembled those of the free enzyme, the major difference being the presence in the former of a slow, broad, anodic zone of diethyl‐p‐nitrophenyl phosphate‐inhibited enzyme. Esterases characteristic of adult white matter and having preferential affinity for alpha‐naphthylpropionate, alpha‐naphthyl butyrate and alpha‐naphthyl valerate were not identified in infant brain until about 4 months postnatal age. A far‐moving, anodic enzyme was distinctly evident in zymograms of brains of less than 1 month of age. This enzyme hydrolysed NP, NB, and NV more actively than alpha‐naphthyl acetate. It was present in the adult brain but, in contrast to the infant, was no longer electrophoretically‐separable from another enzyme which had greater affinity for NA and had previously been designated the A10 band. Quantitative assays demonstrated that the bound esterase increased in cerebral and cerebellar cortex during development. In contrast, the proportion of free to bound esterase showed little change in white matter. Acetylcholinesterase and butyrylcholinesterase zymograms became identical to adult patterns from 1 to 4 months of age. Thiolacetic acid esterase was present at 38 weeks gestation. Some functional and anatomical correlations were attempted in explanation of the biochemical observations.