EFFECT OF U. V. IRRADIATION ON ENZYME SYSTEMS 61 increase in rate was noted. Measurements of glucose oxidation and transaminase activity were not measured at periods of time longer than four hours after irradiation. While the mechanism for the inactivation of transaminase activity is un- known, it appears that the mechanism by which the decrease in glucose oxidation occurs is related to some malfunction in the glucose phosphory- lating system. Thus it has been shown that in the presence of glucose-6- phosphate as substrate or with the addition of exogenous hexokinase, no difference can be observed between the rate of glucose oxidation of extracts prepared from normal animal skin and those from irradiated animal skin. It is interesting to note that one of the early histological changes seen in irradiated skin is a build-up in glycogen (8). This glycogen build-up has also been observed after X-irradiation, and it is speculated to result from an enzymatic disbalance between glucose and glycogen metabolism (18). Perhaps the enzymatic changes in glucose metabolism reported herein are related to this imbalance. SUMMARY The effect ofU. V. light on enzyme systems present in the epidermis of the rat has been investigated. Exposure of rats to U. V. light has resulted in a decreased rate of glucose metabolism in homosenates prepared from the epidermis of the irradiated animals. This marked decrease in glucose oxidation can be observed within one hour after irradiation. Inactivation of the glucose phosphorylating mechanism is believed to be the cause for this decreased glucose metabolism. Complete inhibition of two trans- aminase enzyme systems was also noted in the epidermis of rats, one hour after U. V. irradiation. (Received September 18, 1962) REFERENCES (1) Bachem, A., •7. Invest. Dermatol., 25, 215 (1955). (2) Lund, H. Z., and Sommerville, R. L., din. 7. Clin. PathoL, 27, 183 (1957). (3) Wrong, H. M., and Rutton, H. R., Can. Med. dssoc. •7., 76, 899 (1957). (4) Blum, H. F., "Ultraviolet Radiation and Cancer," In Hollaender (Ed.) "Radiation Biology II." New York, McGraw-Hill Book Co., Inc. (1955). (5) Edwards, E. A., and Duntley, S. Q., Science, 90, 235 (1939). (6) Cockerell, E.G., Freeman, R. G., and Knox, J. M., d. M.d. drch. Dermatol., 84, 157 (1961). (7) Miescher, G., Dermatologica, 115, 345 (1957). (8) Daniels, F., Jr., Biophy, D., and Lobitz, W. C., Jr., •7. Invest. DermatoL, 37, 351 (1961). (9) Hershey, F. B., Ibid., 32, 1 (1959). (10) Freinkel, R. K., Ibid., 34, 37 (1960). (11) Pomerantz, S. H., and Asbornsen, M. F., drch. Biochem. Biophys., 93, 147 (1961). (12) Daniels, F., Jr., •7. Invest. Dermatol., 32, 147 (1959). (13) McLaren, A.D., dtti congr. intern.fotobiol., 2 ø, Torino, 123 (1957). (14) Schlenk, F., Fisher, A., and Snell, E. E., Proc. Soc. Exptl. Biol. Med., 61, 183 (1946). (15) Hanke, W., Z. Zellforsch. u. mikroskop. dnat., 50, 644 (1959). (16) Antonova, G. M., et aL, Shornik Trudov drkhangelsk. Med. Inst., 17, 38 (1957). (17) Smernova, M. G., Biokhimiya, 21,441 (1956). (18) Chow, D.C., and Rothman, S., Science, 135, 216 (1962).

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