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At least 217 records · Page 12Linked to original sources
PubMed2002

Arginine catabolism, liver extracts and cancer.

Although it is self evident that cells will not grow in amino acid deficient medium, an observation less well appreciated is that malignant cells are particularly vulnerable to such deprivation, which can lead to their rapid demise. Indeed, the more flagrantly malignant the phenotype (anaplastic the tumor), the more susceptible the cells seem to be to deprivation. While some attempts to employ this strategy in cancer treatment have been made, the difference between normal and malignant cells should be more fully exploited as a means of selectively eliminating tumor cell populations. To be successful, information on differences between the normal and the deranged cell cycle engine and checkpoints, especially how these are affected by deprivation, is of crucial importance. Since it is only recently that the controls at restriction points have been elucidated, it is little surprise that earlier attempts to control tumor cell growth by limiting the availability of an essential amino acid have met with limited success. Studies have been sporadic and isolated, often with little more than anecdotal descriptions as far as clinical work was concerned. This review concentrates on what has been accomplished primarily in vitro and since about 1950 with regard to arginine catabolism, while recognising that other essential amino acids have also been the focus of attention by some investigators. Treatments have included medium and plasma manipulation, dietary control, enzymatic degradation, and the use of liver extracts. On some occasions, substitution of amino acid analogues has been explored. It is argued that current knowledge, combined with past experience, calls for a much closer examination of the full potential of amino acid (and specifically arginine) deprivation as a means of controlling tumor growth, with greater attention to protocols that might be used to treat human cancers.

Animals↗
PubMed1988

The mechanisms of inhibitory effects of liver extract on lymphocyte proliferation: II. Inhibition of DNA, RNA, and protein synthesis and their relationship to the effects of metabolic inhibitors.

The inhibitory effects of liver extract (LEx) on DNA, RNA, and protein synthesis in phytohaemagglutinin (PHA)-stimulated lymphocytes were studied by measuring the incorporation of labelled precursors. DNA, RNA, and protein synthesis were all inhibited by LEx in a dose-related manner. The inhibitory effect of LEx on protein synthesis was additive to the inhibitory effect of puromycin. The inhibitory effect of LEx on DNA synthesis was antagonistic to the inhibitory effect of mitomycin C. In the case of actinomycin D for RNA synthesis, its interactions with LEx were variable, but not additive. LEx may act as an inhibitor of protein synthesis through the mechanism of arginine-depletion.

Animals↗
PubMed1987

The mechanisms of inhibitory effects of liver extract on lymphocyte proliferation. I. The extracellular mechanism of the inhibition.

Liver aqueous extract (LEx) can powerfully inhibit phytohaemagglutinin (PHA)-induced lymphocyte proliferation. The extracellular mechanism of inhibition by LEx was studied. There are three possibilities. (1) The possibility of extracellular inactivation of PHA by LEx was excluded by incubating cells with PHA first, followed by washing, and then incubating cells with LEx. The result was that LEx was still able to inhibit cell proliferation completely. (2) The possibility of competition for cell surface PHA receptors by LEx was excluded by the above experiments plus the use of N-acetyl-D-galactosamine to remove surface-bound PHA. Following this treatment, LEx was still able to inhibit cell proliferation completely. (3) The possibility of arginase-induced arginine depletion resulting in lymphocyte suppression was supported by the following experiments. Cells were incubated in media in which arginine was depleted either by reacting with LEx, and the media were afterwards bound with anti-arginase antibody, or by amino acid constituted media without arginine. The degrees of proliferation inhibition were similar in both treatments. These results indicate the important role of arginine-depletion by LEx, and may account for the LEx-induced lymphocyte inhibition.

Animals↗
PubMed1981

Effect of thiol blocking agents on the binding of T3 and T4 in rat liver nuclear extract.

Liver nuclei bind thyroid hormones (T3 and T4) with different binding affinities. In out studies it was estimated that the apparent association constant (Ka) in the liver nuclei for T3 was 8.8 X 10(10) l mol-1 and for T4 was 4.1 X 10(9) l mol-1. We have found that the binding sites for T4 are also saturated by an excess of unlabelled T4 and that saturation was dependent on the purification step of liver binding proteins. In liver nuclear extracts with 0.4 mol l-1 KCl the specific binding of T3 and T4 was blocked with a typical -SH blocking agent N-ethylmaleinimide (NEM) and by new types of -SH blocking agents such as p-bromphenylisothiocyanate (p-BPI) and 2,3 dicyano-1,4-dithio-9,10 antrachinone (Delan). NEM and p-BPI increased the non-specific binding of T4 and completely abolished specific binding. All these agents blocked the specific binding of T3. These results demonstrate that T3 and T4 binding sites in the liver nuclei may not be altogether identical and that the different effects of -SH blocking agents on the binding of T3 and T4 is probably associated with the structural configuration of these drugs.

Animals↗