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From the Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Abstract
The ascites form of a chemically induced guinea pig hepatoma, line-10, was resistant to killing in vitro by xenogeneic antibody and guinea pig complement. Pretreatment of line-10 cells with certain proteolytic enzymes rendered them susceptible to the killing action of antibody and guinea pig complement. The effects of enzyme pretreatment were dependent on enzyme concentration, temperature, and could be blocked by addition of competitive or non-competitive inhibitors. The effect of the enzyme treatment could be reversed by incubating the treated cells at 37°C (but not at 0°C), in the absence of the enzyme. Effective enzymes included ficin, bromelain, pronase, elastase, papain, trypsin, collagenase, lipases type I and type VI, and the neuraminidase preparation isolated from Clostridium perfringens. The activity of the lipase preparations and the neuraminidase preparation isolated from Clostridium perfringens appeared to be caused by proteolytic enzyme contamination. Enzyme preparations that proved ineffective in rendering the line-10 cells sensitive to killing by antibody and guinea pig complement included DNase, RNase,
-glucuronidase type 6A or type B10, hyaluronidase type V or type VI, and pectinesterase.
Enzyme pretreatments that rendered the cells sensitive to killing by antibody and guinea pig complement also enhanced the sensitivity of the cells to the killing action and human complement. In addition the neuraminidase enzyme preparations from Vibrio cholorea or influenza virus increased the sensitivity of the line-10 cells to killing by antibody and human complement, but not to killing by antibody and guinea pig complement.
Footnotes
1 National Institutes of Health Visiting Fellow.
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