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433slightly. Ethanolamine in the presence of added betaine is quite able to overcome the action of 2-amino-2-methylpropanol but in the presence of added methionine is unable to do so. Even though the inhibitory actions of 3AP and 2A2MP are quite similar in the rat, the latter substance appears to be the stronger inhibitor. An action difficult to explain is the decrease of liver fat when the level of 2A2MP is increased in the diet. Such is not observed when 3AP is increased.Radioactive isotope studies (5) indicate that 2A2MP inhibits the incorporation of ethanolamine and dimethylethanolamine into rat liver phospholipids, Choline incorporation on the other hand is only slightly inhibited. Additional observations (6) indicate that 2A2MP itself is incorporated into liver phospholipid. It is suggested that ethanolamine and its N-methyl derivatives must first be incorporated into phospholipid before they are methylated to choline ( 7,8,9). It is postulated that ZA2MP and 3AP increase the severity of choline deficiency by inhibiting the incorporation of ethanolamine into phospholipid thus preventing its methylation to choline.If it is demonstrated that 3AP is incorporated into phospholipid and is also an inhibitor of natural amino alcohol incorporation into phospholipid and thus methylation to choline (lecithin), it with 2A2MP should be of value in the study of phospholipid synthesis and metabolism. Further, they should be of value in studies involving the role of phospholipids in other biological mechanisms or systems.Summary. 3-Aminopropanol, like Z-amino-2-methylpropanol, increased the incidence of hemorrhagic kidneys and the level of liver fat of weanling male rats consuming a lowcholine diet. Choline, dimethylethanolamine and monomethylethanolamine prevented the antilipotropic action of 3-aminopropanol. In the presence of 3AP betaine and methionine prevented the Occurrence of kidney hemorrhages but only partially reduced the liver fat. Ethanolamine had little influence on the occurrence of hemorrhagic kidneys and only partially reduced the liver fat. Betaine and ethanolamine together in the diet were quite effective, whereas, methionine and ethanolamine together were only moderately effective. The inhibitory action of 3-aminopropanol was not as great as that of 2-amino-2-methylpropanol.

In order to determine if the correlated expression of transformation and tumorigenicity is affected by the agents used to induce transformants or by the immune status of the host used to test the tumorigenicity of transformants, we derived a series of cloned cell lines from foci of transformed cells induced by treatment of the contact-inhibited mouse cell line B/C-N7.ICI with the DNA demethylating agent 5-azacytidine (5-AZC) or the DNA demethylating and mutating agent benzo(a)pyrene dihydrodiol epoxide (BPDE). The transformed cell lines were injected into syngeneic nude and normal mice to determine their tumorigenicity. The results of this analysis showed that 93% of the transformants induced by 5-AZC treatment grew as tumors when injected into nude mice. Of those lines capable of growing as tumors in nude mice, 86% were also tumorigenic when injected into normal mice. In contrast, only 64% of BPDE-induced transformants grew as tumors in nude mice, and of those, only 44% were also tumorigenic in normal mice. The existence of non-contact-inhibited transformants that are tumorigenic only in nude mice indicates that host anti-tumor immune surveillance mechanisms are operative in normal mice. Further, the difference in both the percentage of transformed cell lines that are tumorigenic and the percentage of tumorigenic transformants that are susceptible to immune surveillance when transformants are induced by BPDE as compared to 5-AZC indicates that the transforming agent can affect both the correlation between the expression of transformation and tumorigenicity, and the interaction between the immune system and tumorigenic transformants.