Lipid extracts from normal cat, chicken, and beef sciatic nerve were fractionated into their components by combinations of silicic acid, Florisil, DEAE‐cellulose, or silicic acid‐silicate column chromatography. The constitutent fatty acids of total lipid extracts and of individual lipid classes were qualitatively and quantitatively determined as their methyl esters by gas chromatography. These methods were also applied to lipid extracts from cat sciatic nerve undergoing Wallerian degeneration at 8, 16, 32, and 96 days after section and to chicken sciatic nerve undergoing demyelination due to organophosphate poisoning. All fatty acids were markedly decreased in the total lipids of cat sciatic nerve at 96 days after section and most of these were decreased at 32 days. As early as 8 days after section 16:0, 16:1, 18:2, 20:0, and 20:4 showed decreases, while 18:0, 18:1, 22:1, 22:5, 22:6, and 24:1 did not begin to show decreases until 16 days after section. The decreases in fatty acids were considered to be due to increased catabolism, decreased synthesis, or increased removal of fatty acids from nervous tissue. The fatty acid content of the total lipids of chicken nerve undergoing demyelination resembled that of cat sciatic nerve between 16 and 32 days after section. Myelin lipids, sphingomyelin, cerebrosides, and phosphatidyl ethanolamine (PE) began to decrease as early as 8 days after section in cat sciatic nerve. Phosphatidyl serine (PS) also decreased at this time. Cholesterol, lecithin, and ethanolamine plasmalogen did not begin to decrease until 16 days after section and phosphatidyl inositol (PI) did not decrease until 32 days after section. Triglycerides decreased markedly at 8 days after section gradually returning to normal by 96 days. This was accompanied by a transient increase in free fatty acids and monoglycerides. Cholesterol esters and lysolecithin increased markedly at 8 days after section and were higher than normal levels even at 96 days after section. In chicken sciatic nerve undergoing demyelination after organophosphate poisoning, cerebroside was the only myelin lipid which decreased in amt, while cholesterol esters and diglycerides increased. Sphingomyelin and cerebrosides containing 16:0, 18:0, 18:1, 18:2, 20:0, 22:0, 23:0, 24:0, 24:1 seemed to be most susceptible to degradation or interference in synthesis in degenerating nerve. For the most part, these fatty acids were observed to increase in cholesterol esters, free fatty acids, and, in some instances, triglycerides. The changes in various lipid classes and their constituent fatty acids are discussed in relation to various cellular changes which accompany degeneration.

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The effects of long‐term hyperglycaemia (5 months), through feeding high levels of dietary carbohydrates, on the non‐specific immunity parameters of rainbow trout, Oncorhynchus mykiss (Walbaum), was assessed. Fish were fed one of three diets composed of a basal diet containing ≈ 14% digestible carbohydrate which was progressively diluted with gelatinized potato starch in the following ratios of basal diet to supplemental carbohydrate (gelatinized potato starch): 65:00, 65:20, 65:35. The three diets were pair‐fed based on the feed intake of the fish fed the diet containing the highest level of starch (65:35) and representing 100% intake. The other diets were then fed at different levels in a manner that allowed all the groups of fish in the same block to receive the same amount of the basal diet [e.g. the basal diet (undiluted, 65:00) was fed at 65% of the dietary intake of the 65:35 diet]. Blood glucose concentrations and relative liver‐to‐body size increased with increased dietary carbohydrate intake. Feeding supplemental carbohydrates resulted in a small increase in weight gain of the fish at both supplemental levels. Pronephros tissue lysozyme activity and pronephros macrophage superoxide production were not affected by the dietary treatments. The results suggest the presence of advanced glycosylation end‐products in muscle tissue collagen, but were not significantly different between treatments. No substantial effect of long‐term feeding of a high carbohydrate diet on the non‐specific immunity of rainbow trout was observed. However, the results suggest that dietary carbohydrates may have a slight stimulatory effect on phagocytosis at low–moderate levels.