Inhibition and Enhancement Effects of Hypochlorite on Ascites Tumor Cell Metabolism and Growth, and on Host Resistance

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Abstract
Hypochlorite (500 ppm) inhibited the respiration and glycolysis of Krebs-2 carcinoma mouse ascites cells over 90 percent and rendered the cells totally nonviable in inoculation tests. Hypochlorite gave much less inhibition of the metabolism of Krebs-2 carcinoma slices, and even increased the oxygen consumption of normal liver slices. A single optimal, intraperitoneal injection of inorganic sodium hypochlorite solution (Clorox) or of “organic” hypochlorite (Clorpactin XCB) gave greater than a 100 percent increase in the median survival time of mice that had been inoculated previously with Krebs-2 ascites cells. The effect was optimal when approximately 2 mg. of hypochlorite in 0.5 cc. of water was administered 15 minutes post inoculation, and diminished to about a 25 percent increase in median survival time when given 24 hours post inoculation. Supraoptimal doses of hypochlorite enhanced the rate and dissemination of tumor growth, as did repeated daily administration. Host pretreatment with hypochlorite, given intraperitoneally or subcutaneously, similarly enhanced the growth and virulence of the tumor cells. The enhancement of tumor growth was not specific for hypochlorite but was also observed upon pretreatment by either formalin, methotrexate, total-body irradiation, or host temperature stress for 24 hours at 37° C. Hydrocortisone or prednisolone pretreatments did not enhance but retarded tumor growth. Moreover, the effects observed with Krebs-2 ascites were also noted with lymphoid leukemia neoplasm P388 that had arisen in DBA mice and had been carried in ascites form in (BALB/c×DBA/2)F1 hybrids. The mechanism of tumor growth enhancement produced by a variety of chemical and physiological agents thus appears to involve more than mere loss of immune response.