TRIGLYCERIDES AND FATTY ACIDS 189 



exerts a greater antioxidant effect in the photo-oxidation of methyl Hno- 

 leate than does d-7-tocopherol. However, the carotenoid, l)ixin, enhances 

 the antioxidant capabihty of 7-tocopherol more than it does that of 

 a-toeopherol. Hence, the 7-isomer of tocopherol possesses a greater anti- 

 oxygenic acti\'ity than does the a-form in the presence of bixin, although 

 the contrary is the case in the pure system. The apparent diene con- 

 jugation of methyl linoleate per mole of absorbed oxygen was found to be 

 less in the presence of 7-tocopherol than when a-tocopherol or no tocopherol 

 was present in the system.^*^ 



In in vivo tests on deficient rats, Witten and Holman^^^ demonstrated 

 that the metabolic conversions of linoleate and linolenate by fat-deficient 

 rats are not influenced by the "oxidative or reductive status" of the 

 animals; the variations were studied by comparing the results of control 

 experiments in which linoleate or linolenate was fed with others in which 

 tocopherol or benzoyl peroxide was added. In later investigations, these 

 workers^^^ reported that pyridoxine is also required for the normal inter- 

 conversions of linoleate and linolenate. When pyridoxine and linoleate 

 were administered together to fat-deficient, pyridoxine-deficient rats, 

 growth, fat sjaithesis, and arachidonate synthesis were stimulated to a 

 much greater extent than when either supplement was given by itself. 

 Similar data were recorded for linolenate, with the exception that dermal 

 symptoms were not relieved. Hexaenoic acid synthesis was also augmented 

 when the trienoic acid was fed. 



A still further investigation of the behavior of linoleate as related to 

 oxidation was carried out by Holman and Greenberg.^*^ Whereas all 

 supplements containing linoleate with or without peroxide were able to 

 cure fat-deficiency symptoms, to reduce water consumption and to stimu- 

 late arachidonate synthesis, completely negative results were obtained in 

 all respects by the following products: linoleate peroxide, reduced lino- 

 leate peroxide, decomposed linoleate peroxide, and conjugated linoleate. 

 In fact, dermal symptoms were actually aggravated. It was suggested 

 that these substances, all of which have conjugated double bond systems, 

 actually produce toxic effects on fat-deficient rats. 



{6) The Site of Oxidation of Fats in the Animal Body 



a. The Liver as the Site of Oxidation. The liver has long been recog- 

 nized as the key organ in the oxidation of fatty acids. Thus, it is immedi- 



«"P. W. Witten and R. T. Holman, Arch. Biochem. Biophys., 37, 90-98 (1952). 

 «« P. W. Witten and R. T. Holman, Arch. Biochem. Biophys., 4I, 266-273 (1952). 

 6" R. T. Holman and S. I. Greenberg, Arch. Biochem. Biophys., 49, 49-57 (1954). 



