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短期與長期葉酸缺乏對大白鼠葉酸營養狀態與肝臟細胞核,粒線體及微粒體之脂質過氧化的影響

The Short- and Long-term Effects of Folate Deficiency on Folate Status and Lipid Peroxidation in Nuclear, Mitochondrial and Microsomal Fractions Isolated from Rat Livers

摘要


The purpose of this study was to investigate the short- and long-term effects of folate deficiency on the folate status and lipid peroxidation in the nuclear, mitochondrial and microsomal fractions extracted from rat livers. Weaning Wistar male rats were fed an amino acid-defined folate-deficient basal diet (folate deficient group) or a basal diet supplemented with 8 mg folic acid/kg diet (control group) for 2 and 6 weeks. Plasma and red blood cell folate levels in the rats fed folate deficient diets for 2 or 6 weeks were significantly lower than those for the control rats (p<0.05). Hepatic folate status was decreased to 20% of the control levels by 2 weeks of feeding folate deficient diets, and further decreased to 4% of the control levels after 6 weeks of folate deficiency. The inferior hepatic folate status in folate-deficient rats was reflected by the markedly decreased folate concentrations in cytosolic and mitochondrial liver homogenate fractions. The endogenous lipid peroxidation measured by thiobarbituric acid reactive substances (TBARS) values in the liver homogenate of rats fed folate-deficient diets for 2 weeks were not different from the control group, yet significantly increased by 2.3 fold after 6 weeks of feeding folate deficient diets as compared to the control group. Lipid peroxidation induced by H2O2 or Fe2+. in liver homogenates from folate-deficient rats was higher than these in the control group. Folate deficiency for 2 weeks did not result in either endogenous or H2O2-induced lipid peroxidation damage in the nuclear, mitochondrial and microsomal fractions, except for nucelar lipid peroxidation induced by Fe2+. A 6-week folate deficiency resulted in a significant increase in endogenous microsomal TBARS values and a significant increase in H2,O2, and Fe2+ -induced lipid peroxidation damage in the nuclear, mitochondri-increase in endogenous or induced-lipid peroxidative damage either in the liver homogenates or in the intracellular organelles such as nuclear, mitochondria or microsome in rats.

並列摘要


The purpose of this study was to investigate the short- and long-term effects of folate deficiency on the folate status and lipid peroxidation in the nuclear, mitochondrial and microsomal fractions extracted from rat livers. Weaning Wistar male rats were fed an amino acid-defined folate-deficient basal diet (folate deficient group) or a basal diet supplemented with 8 mg folic acid/kg diet (control group) for 2 and 6 weeks. Plasma and red blood cell folate levels in the rats fed folate deficient diets for 2 or 6 weeks were significantly lower than those for the control rats (p<0.05). Hepatic folate status was decreased to 20% of the control levels by 2 weeks of feeding folate deficient diets, and further decreased to 4% of the control levels after 6 weeks of folate deficiency. The inferior hepatic folate status in folate-deficient rats was reflected by the markedly decreased folate concentrations in cytosolic and mitochondrial liver homogenate fractions. The endogenous lipid peroxidation measured by thiobarbituric acid reactive substances (TBARS) values in the liver homogenate of rats fed folate-deficient diets for 2 weeks were not different from the control group, yet significantly increased by 2.3 fold after 6 weeks of feeding folate deficient diets as compared to the control group. Lipid peroxidation induced by H2O2 or Fe2+. in liver homogenates from folate-deficient rats was higher than these in the control group. Folate deficiency for 2 weeks did not result in either endogenous or H2O2-induced lipid peroxidation damage in the nuclear, mitochondrial and microsomal fractions, except for nucelar lipid peroxidation induced by Fe2+. A 6-week folate deficiency resulted in a significant increase in endogenous microsomal TBARS values and a significant increase in H2,O2, and Fe2+ -induced lipid peroxidation damage in the nuclear, mitochondri-increase in endogenous or induced-lipid peroxidative damage either in the liver homogenates or in the intracellular organelles such as nuclear, mitochondria or microsome in rats.

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