Lipoperoxide levels, glutathione status and glutathione peroxidase activity in liver and tumors of mice bearing the Lewis lung carcinoma.

Lipoperoxides, glutathione status and glutathione peroxidase activity have been determined in normal and neoplastic tissues of control and tumor-bearing mice, tissues from both groups being assayed 5, 7, 9, 11, 13 and 15 days after inoculation. The ratio of hepatic reduced: oxidized glutathione increased in tumor-bearing animals as the tumor increased in size. This ratio was 2.5-fold higher at 15 days than at 10 days after tumor inoculation. In both tumor and hepatic tissue the alteration in the ratio was the result of both an increase in reduced glutathione and a decrease in oxidized glutathione levels. In tumor tissue the progressively increasing reduced glutathione content correlated closely with tumor growth. The presence of a tumor did not significantly affect hepatic glutathione peroxidase activity and there was no significant difference between tumor enzyme activity assayed at 2-day intervals between 9 and 15 days after inoculation. The livers of tumor-bearing animals had significantly higher lipoperoxides than control mice, the levels increasing progressively with tumor growth. Tumor lipoperoxides were also high, usually in excess of the hepatic level. The lungs of nontumored littermates, which were compared with the carcinoma as reference tissue, showed no significant change in either glutathione peroxidase activity or lipoperoxide levels when monitored over the same period.

Superoxide dismutase activity, caeruloplasmin activity and lipoperoxide levels in tumour and host tissues of mice bearing the Lewis lung carcinoma.

Superoxide dismutase (SOD) activity, plasma caeruloplasmin activity and the level of whole tissue and subcellular lipoperoxides have been determined in normal and neoplastic tissues from control and tumour-bearing mice, measurements being made nine, twelve and fifteen days after the inoculation of Lewis lung carcinoma cells. SOD activity of host liver and lung tissues did not vary significantly from those of the control animals. Blood SOD activity of the tumoured animals was markedly elevated on the ninth and twelfth days after inoculation, decreasing to control levels on the fifteenth day. Tumor SOD diminished from activity on the ninth day which was greater than that for control lung to a level significantly lower than that for control lung on the twelfth and fifteenth days after inoculation. The presence of a tumor did not appear to affect plasma caeruloplasmin oxidase levels. The lipoperoxide level of hepatic tissue rose significantly as the tumour progressed. In the lung tissue the lipoperoxides decreased from a level four times higher on the ninth day to one not significantly different from that of the controls. Tumour lipoperoxides were about twice the level of hepatic tissue and of the order of ten-fold greater than those of lung. The level of lipoperoxide in the plasma of tumoured mice did not differ markedly from that of control mice. Assays of lipoperoxide in subcellular fractions of liver, lung and tumour tissue revealed that the elevated lipoperoxide was principally synthesized in the endoplasmic reticulum.