Normal and simian virus 40-transformed WI-38 cells exhibited a differential sensitivity to infection with type 3 reovirus. A progressive decrease in viability began 24 to 36 h after infection of transformed cells terminating in complete lysis of cultures by 96 h. Normal cells were productively infected and continued to produce and release virus for as long as 14 days after infection, but exhibited no detectable cytopathology. Inhibition of cellular DNA synthesis began 15 to 18 h after infection in transformed cells before development of cytopathology. No inhibition of DNA synthesis was detected in infected normal cells. No significant differences were noted in the adsorption or early replication characteristics of reovirus in normal and transformed cells. Virus replication and host cell DNA synthesis in normal and transformed human cells were compared to reovirusinfected L-929 mouse fibroblast cells.

It has been postulated that superoxide dismutase (SOD) protects cells from free radical-induced damage. In these experiments SOD specific activity was measured as established human diploid cell lines from various donor ages progressed through their in vitro lifespan. Significant elevations in activity occurred during the in vitro lifespans of cells from fetal and newborn donors, but no change in activity was detected during the lifespan of cells from an adult donor. In addition, a direct relationship between enzyme activity and donor age was detected with the following relative activities: adult greater than newborn greater than fetal. The possible relationship between these findings and the free radical theory of aging is discussed.

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Human fibroblasts derived from newborn foreskin and designated CF-3 were assayed for heat labile glucose-6-phosphate dehydrogenase (G6PD) when they had grown to confluency, as well as when they were arrested in an essentially nonmitotic state. Under both culture conditions there was an increase in heat labile G6PD (up to 25% of the total activity) as cells progressed through their in vitro lifespan; however, arrested cells exhibited less heat labile G6PD than did comparable growth controls (5-10% decrease). Acrylamide gel electrophoresis of crude G6PD preparations revealed three distinct bands of enzymatic activity. One of the bands was tentatively identified as the dimeric form of the enzyme and another as the tetrameric form. The tetrameric form was more heat sensitive, and the percent of the total activity of this form increased as the cells became senescent. The percent of total activity of the tetrameric form was comparable to the percent heat labile enzyme assayed at a given population doubling level. These results indicated that the observed increase in heat lability of G6PD with age may be due to a shift in equilibrium to the tetrameric form of the enzyme rather than the synthesis of aberrant enzyme molecules.

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