重合油の構造と栄養価に関する研究 (第11報) : 熱重合油の毒性発生機構 (1)

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In a previous paper, we reported that linseed oil heated in an inert gas showed toxicity to mice and the skeletal structures of toxic compounds were methyl 9-(2′-n-propylcyclohexyl) nonanoate and/or methyl 8-(2′-n-butylcyclohexyl) octanoate and contained two double bonds. Moreover, the authors noticed the presence of four positional isomers of the double bonds. <BR>To know toxic effects of cyclic fatty acids, feeding experiments were carried out. Rats were given a diet containing 2.24.9% cyclic fatty acids for three weeks and the inhibition of body weight gain, hypertrophy and/or hyperplasy of liver, and a little decrease of digestibility were observed. Analyses of liver lipids revealed the symptom of fatty liver accompanied by the increase of neutral lipids and phospholipids. Histopathological changes were also observed in nuclei, cytoplasms and intercellular substances of liver cells by histological examination. <BR>To investigate the absorption of cyclic fatty acids which caused pathological changes, component fatty acids of plasma and liver lipids were determined by gas chromatography-mass spectrometry (GC-MS). The presence of these cyclic fatty acids was observed in both plasma and liver. This result indicated the possibility of the absorption of these cyclic fatty acids through small intestine. Furthermore, cyclic fatty acids were also found in neutral lipids, phospholipids and cholesteryl esters fractions of liver lipids. <BR>To know the relationship between the skeletal structure of cyclic fatty acids and toxicity, cyclic fatty acids were reduced and administered orally to mice. The hydrogenated cyclic fatty acids showed less toxicity than the original acids. <BR>From these results, we concluded that cyclic fatty acids are absorbed through small intestine and cause fatty liver and the other histopathological changes. Thus one of the reasons for the toxic effect of cyclic fatty acids is attributable to the metabolic injury in liver.
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重合油の構造と栄養価に関する研究 (第11報) : 熱重合油の毒性発生機構 (1)

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