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A preparation of formaldehyde-treated casein (formol-casein) that had been shown to supply more amino acids than untreated casein for absorption when given by mouth to sheep, was fed to rats as the sole protein at 11%, 20% and 40% of the diet. The 11% formol-casein diet did not support growth and a supplement of L-lysine, L-histidine and L-tryptophan was without benefit; its protein efficiency ratio (PER) was 0, as compared to a PER of 2.8 for untreated casein. When fed at 20% of the diet it supported growth at about half the control value. Nearly normal growth and normal body weight was maintained for 13 weeks when 40% of the diet was formol-casein. The apparent protein digestibility of the formol-casein was 66% as compared with 93% for the untreated casein. A soluble lactalbumin concentrate was treated with formaldehyde at 0, 2, 4, 8 and 16 g/kg. When fed to rats to supply 6.6% protein in the diet, solubility, weight gain, PER, apparent protein digestibility and nitrogen retention progressively decreased, as did digestion by trypsin in vitro. The percentage of absorbed nitrogen retained did not decrease in the formol-lactalbumin fed rats. This indicated that the loss of nutritional value of the proteins was due to depressed digestibility only.

Graded levels of cellulose (0 to 20%) or of pectin (0 to 10%) were incorporated in purified diets with either 22 or 8.5% casein as the protein source. Weanling male rats were fed these diets for 4 weeks. Body weight gain, food consumption, feed efficiency, protein biological value, apparent digestion of food, fiber and protein, cecal weight and cecal volatile fatty acids (VFA) were recorded. Cellulose was largely an inert diet diluent causing increased weight gains when protein was limiting but not when protein was sufficient. The 25% disappearance in the gut was due, at least in part, to compaction in the ceca and in increased cecal VFA. Pectin caused progressively greater depressions in body weight gain, food intake and efficiency and protein digestion at both levels of dietary protein. At least part of the 75% disappearance of pectin during passage through the gut could be attributed to increased cecal VFA. However, a rat growth bioassay for energy showed that pectin as well as cellulose, agar and gum arabic contributed no measurable energy to young rats.

The effectiveness of cystine supplementation in improving the nutritional quality of diets deficient in sulfur amino acids was investigated by measured the weight gain and protein efficiency ratio of rats fed basal 10% protein diets and basal diets supplemented with either 2.0 g/kg DL-methionine or 4.0 g/kg L-cystine. Whereas methionine improved the weight gain of rats and the protein quality of all sources of dietary protein tested, cystine gave a positive response with diets containing lupin tops, casein, yeast and leaf protein concentrate but was ineffective for sweet lupin seed, soybean meal, broad beans and lentils. The ineffectiveness was observed as a general depression of weight gain and protein efficiency ratio. The depression was statistically significant for some diets containing lentils as the sole source of protein. The endogenous methionine and cystine contents of the diets were determined, and the ratios of cystine to methionine were correlated with the responses to supplementary cystine. Generally supplementary cystine was effective where the ratio was less than one and was ineffective where greater than one. The data are discussed in relation to the generally accepted concepts of the dietary methionine-cystine interrelationship.

Limited studies by other investigators suggested that thiamine is not a dietary essential for the rabbit. To determine whether this is true, rabbits were fed a purified diet in which the thiamine level was varied and the thiamine antagonist, neopyrithiamine, was added. In the absence of the antagonist, mild ataxia of the hindquarters occurred in about one-half of the animals that received the thiamine-free diet. All rabbits fed the thiamine-free diet showed a decreased urinary thiamine excretion; the level of thiamine in the livers and brains was reduced. However, the rabbits fed this diet gained as much weight as those fed the same diet supplemented with the vitamin. When weanling rabbits were fed a diet containing neopyrithiamine there was no reduction in rate of body weight gain prior to the appearance of symptoms. The rabbits developed neurologic symptoms between the 18th and 57th day of the experiment. They showed severe ataxia, flaccid paralysis, coma and death within 3 days of onset unless treated. These symptoms were reversed by the administration of thiamine. Neopyrithiamine increased urinary thiamine excretion 10- to 20-fold over that of the controls; it produced a very significant reduction in the level of brain thiamine but had no effect on hepatic, cecal or fecal thiamine levels. The appearance of neurologic symptoms in rabbits fed a thiamine-free diet for prolonged periods and the effects produced by neopyrithiamine suggest that dietary thiamine is required by the rabbit.

The pathological states observed in vitamin E deficiencies have been suggested to result from the action of lipid peroxides on sulfhydryl-sensitive enzyme systems. Vitamin E antagonists, such as unsaturated fat, o-cresyl esters, carbon tetrachloride, pyridine, sulfathiazole, sulfaguanidine, and sodium sulfite, may act as pro-oxidants. They promote the production of lipid peroxides in the body tissues, and thus increase the need for vitamin E.