The effect of vitamin E on mitogenesis by polyclonal activators was studied and the vitamin was found to be stimulatory but selective in its action. Vitamin E itself is a mitogen for murine spleen cells. At suboptimal vitamin concentrations, it was capable of stimulating the response to low levels of the thymus-dependent lymphocyte (T cell) mitogen, concanavalin A (conA), but not when conA was itself at optimal levels. When vitamin E was added to the diet at normal levels, it was not as effective in stimulating mitogenesis as it was at much higher levels. The effect of the vitamin on T cell mitogenesis could be modified by the degree of unsaturation of the dietary fat; it was more effective when dietary polyunsaturated fatty acids (PUFA) were low. Under several conditions, it was shown that vitamin E can increase the phytohemagglutinin (PHA)/conA response ratio, which may suggest an effect of the vitamin on the maturation of T cells. In normal mice, vitamin E also stimulated the response to lipopolysaccharide (LPS), a "bursa-equivalent" lymphocyte (B cell) mitogen, but it was unable to do so when spleen cells from athymic, nude mice were used. This suggests a requirement for thymic factors in order for vitamin E to stimulate mitogenesis of B cells.

No abstract

Certain deletion mutants including the tryptophan operon in Salmonella typhimurium are unable to utilize several sugars as carbon sources in solid media, although they are able to grow in liquid media with these sugars. The addition of citrate or washing the agar with ethylenediaminetetraacetic acid permits growth on solid media. Analysis of the agar revealed that Fe'+ and Cr3+ were present at concentrations of 22 and 75 ,UM, respectively. The addition of Fe3+ to liquid media in 0.5 mm concentrations did not inhibit the wild type or the mutants. A similar concentration of Cr3* did not inhibit the wild type, but concentrations as low as 0.01 to 0.05 mm inhibited the deletion mutants. Other metals were inhibitory at various concentrations, but none showed any significant differential effects on the mutants and the wild type. The increased sensitivity of the mutants to chromium may be due either to an increased permeability to Cr3+, resulting in higher effective intracellular concentrations and inhibition of one or more metabolic functions, or to a binding of Cr34 to an altered cell wall, resulting in decreased permeability of required substrates. An investigation of deletion mutations of the

The sensitivity to sodium lauryl sulfate (SLS) of Shigella flexneri and Escherichia coli is determined by at least three genes. One site is located near the lactose operon, and two loci are cotransducible with the arabinose operon. Calcium ions protect against SLS lysis. One gene is concerned with the relative ability of the bacterium to retain calcium against such chelating agents as ethylenediaminetetraacetic acid or phosphate buffer. This was first observed in a mutation from virulence to avirulence in S. flexneri with a concomitant loss of ability to penetrate the intestinal epithelium. The avirulent strain is far less sensitive to lysis by SLS in the presence of phosphate buffer than its virulent parent. The avirulent strain is also less sensitive to lysozyme and ethylenediaminetetraacetic acid. E. coli K-12 is much more sensitive to SLS than both of these Shigella strains. An E. coli-S. flexneri hybrid, which is unable to survive well in the gut and thus only produces an abortive infection, has inherited this extreme sensitivity to SLS.