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F S Liotti

Publications and source records attributed to F S Liotti.

At least 37 records · Page 2Linked to original sources
PubMed1983

Stimulating effect of ascorbic acid on ascites tumor cell multiplication in vitro.

In a preceding report evidence has been presented that ascorbic acid (AA) accelerated solid tumor growth obtained by inoculating tumor ascites cells into the subcutaneous dorsal region of inbred Balb/cf/Had/Se substrain mice. The present work investigates whether this effect is the result of a direct action of AA on neoplastic cell multiplication or of an indirect action on the tumor cells mediated by changes induced by AA in the organism bearing the tumor. The results obtained demonstrate that AA at low doses (microgram 10-30/ml) stimulates ascites tumor cell multiplication in vitro, while at high doses (microgram 60-120/ml) the opposite occurs. These results suggest that the major growth of solid tumors observed in mice treated with AA may be attribute to the capacity of this substance to favor the multiplication of ATP cells which were used to induce the tumors.

Animals↗
PubMed1983

Absence of accumulation phenomena in normal and tumoral tissues of mice treated with ascorbic acid.

The authors studied the effects of an energetic and prolonged ascorbic acid (AA) treatment on AA concentration in a solid tumor obtained by transplanting ascites tumor cells in the dorsal subcutaneous region of Balb/C1/Had/Se substrain mice. The results demonstrate that this tumor, whose growth is favored by AA, not only is incapable of accumulating AA, but surprisingly presents a lowering of its concentration as the result of treatment with very high doses of AA. The levels of AA in various organs and tissues of mice bearing the aforesaid tumor show no significant difference to those observed in organs and tissues of healthy mice. An energetic and prolonged treatment with AA not only is incapable of favoring accumulation, but also causes a lowering of its concentration in the liver and kidney, similar to that observed in tumors. Therefore, the hypothesis may be advanced that this decrease is caused by the adaptation of some enzymatic system, which results in a greater utilization of AA. This greater consumption could be the cause of the decreased AA levels once esogenous administration is arrested.

Animals↗