M. K. Horwitt
University of Illinois at Chicago
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Featured researches published by M. K. Horwitt.
Science | 1959
M. K. Horwitt; Cecil C. Harvey; Bernard Century
Through gas-liquid chromatography it can be shown that increasing the ingestion of linoleic acid-containing fats increases the deposition of linoleic acid in erythrocytes and in brain tissue. Such changes are probably causally related to the tocopherol requirement, the incidence of chick encephalomalacia, and the peroxide hemolysis test. Whether similar mechanisms are involved in the ability of unsaturated oils to lower serum cholesterol levels remains to be determined.
The American Journal of Clinical Nutrition | 1963
Bernard Century; Lloyd A. Witting; Cecil C. Harvey; M. K. Horwitt
L IPIL) composition of braimi may be readily affected by diet.’ � Efforts to evaluate the possible relationship between an alteration in the composition of brain lipids and a disease process have stimulated studies of chick encephalomalacia. This in turn led to observations of a similar pathologic disease in the brain of a child who had been fed intravenously an emulsion which furnished a high level of linoleic acid.35
Experimental Biology and Medicine | 1959
Bernard Century; M. K. Horwitt
Summary Corn oil or lard from which tocopherol had been removed, promoted chick encephalomalacia, whereas coconut oil, butter, linseed oil, and cod liver oil did not produce symptoms, and olive oil had a questionable effect. Dietary combinations of 2% corn oil with either 8% coconut oil, lauric acid, myristic acid, or a mixture of saturated fatty acids like coconut oil significantly increased the incidence of encephalomalacia over 2% corn oil alone, while 6% linseed oil, cod liver oil, or oleic acid inhibited the effect of 4% corn oil. Olive oil, butter, fatty acids like butter, palmitic acid, and stearic acid had no net effects upon the incidence of encephalomalacia induced by corn oil. The intake of linoleic acid appears to be a primary factor in the etiology of encephalomalacia, but some of the other fatty acids may secondarily increase or decrease this effect.
Experimental Biology and Medicine | 1956
Bernard Century; M. K. Horwitt
Summary Oxidative phosphorylation by rat brain homogenates was depressed by chlorpromazine at 2.5 × 10-4 M or greater, while reserpine at 25 and 50 μg/ml only slightly depressed oxygen uptake and phosphorylation. Effective concentrations of reserpine appeared to depress phosphorylation synergistically with chlorpromazine. Oxygen uptake was slightly increased with brain homogenates from animals treated with 10 mg/kg or chlorpromazine. Reserpine up to 50 mg/1 had no effect on enzymatic ATP breakdown, while chlorpromazine, at 1.2 × 10-4 M and 1.5 × 10-4 M depressed rat brain adenosinetriphosphatase slightly.
Archives of Biochemistry and Biophysics | 1964
Bernard Century; M. K. Horwitt
Abstract Combining 8% reconstituted cod liver oil with 8% reconstituted corn oil in a tocopherol-free diet prevented the appearance of nutritional encephalomalacia in chicks. Adding 8% reconstituted cod liver oil to a diet containing 1% ethyl arachidonate enhanced the incidence of encephalomalacia in tocopherol-deficient chicks and resulted in lower tissue arachidonate levels than in the group fed 1% ethyl arachidonate alone. Adding 8% reconstituted cod liver oil, from which tocopherol was removed, to a diet containing 8% reconstituted corn oil depressed arachidonate and higher essential fatty acids in tissues, and markedly increased the levels of the nonessential unsaturated fatty acids of the linolenic series. These data are consistent with the hypothesis that fatty acids of the linolenic series, found in cod liver oil, can readily displace essential fatty acids in tissues, even in brain, and inhibit the conversion of linoleic to arachidonic acid.
Experimental Biology and Medicine | 1965
L. A. Witting; E. M. Harmon; M. K. Horwitt
Summary Rats fed a diet containing either a saturated or an unsaturated fat were depleted of α-tocopherol (whole body) at comparable rates. Upon depletion to an average tissue α-tocopherol level of 2.4 μg/g wet weight of tissue, the group fed the unsaturated fat showed a significant creatinuria. Depletion of the saturated fat-fed group to an average tissue α-tocopherol level of 0.4 μg/g did not produce creatinuria.
Experimental Biology and Medicine | 1964
Bernard Century; M. K. Horwitt
Summary Addition of 0.13 ppm of selenium as sodium selenite to a semisynthetic diet containing 4% corn oil freed of tocopherol reduced the incidence of encephalomalacia. On the other hand, when 8% corn oil was fed, selenium in levels up to 1.56 ppm had no effect on the proportion of chicks with encephalomalacia. Growth was not affected by addition of selenium.
Experimental Biology and Medicine | 1964
L. A. Witting; M. K. Horwitt
Summary The l epimer of α-tocopheryl acetate, appears to have approximately 20 0/0 of the biological activity of the d epimer in the rat by the criteria of growth and delay in onset of creatinuria as a sign of nutritional muscular dystrophy. The l epimer alone can replace d-a-tocopherol but only if sufficient is supplied. No evidence of synergism or sparing action was observed. We wish to thank Dr. Stanley Ames of Distillation Products Industries for the generous gift of l-α-tocopherol acetate and Una Barnett for performing the creatine and creatinine determinations.
Life Sciences | 1969
Bernard Century; M. K. Horwitt
Abstract The action of chlorpromazine in depressing uptake of 32 P into rat brain phospholipids was lowest in animals fed high levels of corn oil, in comparison with rats fed beef fat, or fish oils. While this response is related to hypothermia produced by chlorpromazine, the differences in body temperature did not appear to be sufficient to account for the differences in this chlorpromazine activity among the animals fed different lipids.
Journal of Nutrition | 1964
Lloyd A. Witting; M. K. Horwitt