Although iodides have been administered for many decades to patients suffering from arteriosclerotic disorders, it was Liebig (1, 2) who first furnished experimental data possibly justifying the use of this substance in such disorders. He observed that the majority of his cholesterol fed rabbits could be protected against subsequent aortic atherosclerosis if iodide were administered.Since his initial observations, various other studies have been done concerning the possible protective effect of iodide administration against both experimentally induced hypercholesteremia and atherosclerosis. have agreed with the conclusions of Liebig but others (7,8) were unable to demonstrate any specific anti-hypercholesteremic or anti-atherogenic effect of iodide administration. Furthermore, although Turner (3) initially observed that iodide administration was protective, he and Bidwell (9, 10) later observed that at best the supposed protection by iodide administration was but a temporary phenomenon. Finally, Brown and Page (11) were unable to detect any effect of iodide administration upon the hepatic cholesterol content of the normal, cholesterol fed rabbit.In view of these sometimes conflicting reports it was decided therefore to pursue a series of studies concerning the possible effects of iodide administration both upon normo-and hypercholesteremic animals with the intent of determining the actual efficacy of this cation both as an antihypercholesteremic and antiatherogenic agent. The results clearly indicate that iodide per se possesses neither of these two effects. anesthetized with ether, the abdomen incised, the intestinal lymph duct cannulated and the lymph collected for 24 hours by methods previously described (12). This collected lymph then was analyzed for total cholesterol by the method of Saifer and Kammerer (13) and for total lipid by the method of Bragdon (14).B. Rabbits: A series of young male rabbits (average weight: 1,424 to 1,436 grams) was given 800 mg. of cholesterol dissolved in 8 ml. of olive oil by stomach tube and then divided into two groups. Group I (16 rabbits) which served as a control received only the cholesterol. Group II (10 rabbits) received in addition to the cholesterol, 1,250 mg. of KI. The animals then were caged individually and fed a cholesterol-free diet (leafy vegetables) for 72 hours. All feces excreted during this period were individually collected and analyzed for total sterol, total cholesterol, and non-cholesterol sterol according to methods previously described (12). ResultsInspection of Tables I and II will indicate that the oral administration of potassium iodide had no significant effect upon the intestinal absorption of cholesterol in either the rat or the rabbit.Regardless of whether the rat was given 25, 100 or 200 mg. of KI, the total amount of cholesterol absorbed during the 24 hours following the ingestion of 25 mg. of cholesterol did not appear to differ from that observed in the control animals (cf. A with B, C and D of Table I). Similarly, no 1015
IODIDE AND PLASMA CHOLESTEROL grees of ultraviolet sensitivity. Ultraviolet intensities which markedly reduce viability affect adaptive enzyme synthesis only slightly, and have no effect on the oxidative activity of constitutive enzymes (Fig. 2 ) . Higher intensities (30 to 90 second exposures) progressively reduce adaptive enzyme synthesis until it is inhibited completely without affecting constitutive enzyme activity. This pattern of progressive sensitivity of viability, adaptability and oxidative activity by constitutive enzymes, in that order, already has been reported for yeasts ( 7 ) and bacteria ( 5 ) . The extent to which ultraviolet irradiation inhibits adaptive enzyme synthesis by interfering with nitrogen assimilation is still under study. However, preliminary, unpublished data indicate that ultraviolet does not interfere with nitrogen assimilation a t intensities which inhibit the induction of adaptive enzyme synthesis.'Summary. Induction of adaptive enzyme synthesis is described in a phytoflagellate. The adaptation has been shown to occur in non-proliferating cell suspensions. and it is also shown to be dependent upon an exogenous source of nitrogen. The adaptive enzyme synthesis is selectively inhibited by ultraviolet irradiation without affecting the activity of pre-existing enzymes. &4t low ultraviolet intensities viability and adaptability have been partially dissxiated ; adaptation is only slightly inhibited while viability is reduced by 80%. -1.
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