Effect of dietary ascorbic acid and vitamin E on metabolic changes in rats and guinea pigs exposed to PCB

The effect of the addition of dietary ascorbic acid and/or vitamin E (all-rac-alpha-tocopheryl acetate) in rats and guinea pigs exposed to PCB (polychlorinated biphenyls) was studied. Rats were fed diets containing one of three levels of vitamin E (30, 500 or 1000 mg/kg diet) with or without PCB (200 mg/kg diet). Guinea pigs were fed diets containing PCB (40 mg/kg diet) with 200 or 1000 mg ascorbic acid/kg diet and/or 70 or 2000 mg vitamin E/kg diet. For rats fed PCB, ascorbic acid in urine was 40-fold higher and in liver, 2-fold higher than for rats fed no PCB, and thiobarbituric acid-reactive substances (TBA-RS, indicators of lipid peroxidation) in liver was 1.5-fold higher. In rats fed PCB, high dietary vitamin E significantly lowered the urinary ascorbic acid and TBA-RS. Liver ascorbic acid was lowered by high dietary vitamin E only in control rats. In guinea pigs, feeding PCB caused severe growth retardation and the liver TBA-RS was 1.8-fold higher than in guinea pigs not fed PCB. Feeding high levels of both ascorbic acid and vitamin E was more effective in reversing the growth depression and in lowering TBA-RS level (due to PCB) than feeding the vitamins separately. Ascorbic acid metabolism in rats was affected by high dietary vitamin E. The possibility of a higher requirement for ascorbic acid and vitamin E in guinea pigs exposed to PCB was indicated. Interaction of ascorbic acid and vitamin E in animals exposed to PCB was suggested.     

Differences in muscular changes in rats with vitamin E and with selenium deficiency

The recti muscles of rats with vitamin E deficiency and with selenium deficiency were examined by electron microscopy and compared. In vitamin E deficiency, the first changes occurred in blood vessels and in the extracellular components. The endothelium contained many vacuoles and less cytoplasmic organelles. The basal lamina of the endothelium appeared thicker. As it progressed, vitamin E deficiency caused abnormal pigment granules, mitochondrial degeneration, decreased numbers and irregular arrangement of muscle fibers, and irregular arrangement of z bands. On the other hand, selenium deficiency caused no abnormal changes in the recti muscles. These results suggest that selenium plays a different role from that of vitamin E which is an antioxidant.     

Long-term effects of dietary polychlorinated biphenyl and high level of vitamin E on ascorbic acid and lipid metabolism in rats

Long-term feeding of purified diets containing (per kg diet) 100 mg of polychlorinated biphenyl (PCB) and 1000 mg of vitamin E (RRR-alpha-tocopheryl acetate) to male Wistar rats was carried out. Rats fed a diet containing PCB rapidly became hypercholesterolemic and maintained high cholesterol levels throughout the 240 d of the experiment. Rats fed a high dietary level of vitamin E plus PCB had higher serum cholesterol and lower liver cholesterol than rats fed a lower level of vitamin E plus PCB. In rats fed PCB, urinary excretion of ascorbic acid was higher than in rats not fed PCB. Urinary ascorbic acid was lower in rats fed high levels of vitamin E plus PCB than in those fed the normal levels of vitamin E plus PCB. Rats fed PCB had lower liver vitamin A storage and higher vitamin A in kidney than rats not fed PCB. This implies that a redistribution of vitamin A occurred in rats fed PCB. Histological observations revealed that central halves of the hepatic lobules of rats fed PCB showed distinct changes consisting of hypertrophy of hepatocytes in the perivenous region and accumulation of vacuoles (lipid droplets) in the cells in the remaining affected portion. Administration of a high dose of vitamin E could not ameliorate this lesion while the treatment depressed effectively the lipid peroxidation. This suggests that the lipid peroxidation was not responsible for the hepatic damage induced by PCB.     

Effect of vitamin B-6 deficiency on plasma amino acid levels in chronically azotemic rats

Chronic renal failure is associated with many abnormalities in plasma amino acids. Since patients with renal failure are frequently deficient in vitamin B-6, this study examined whether vitamin B-6 deficiency may be a cause of any of the abnormal plasma amino acid concentrations observed in chronic renal failure. Sham-operated and chronically azotemic rats were pair-fed diets deficient in or replete with vitamin B-6 for 21 d. By the end of 21 d, the EGOT index rose significantly in the B-6-deficient rats but not in the B-6-replete animals. There were several differences in plasma amino acid concentrations between azotemic and control rats. Azotemia and B-6 deficiency each lowered the plasma serine concentration and raised the glycine-to-serine ratio. Plasma glycine was affected by a two-way interaction between azotemia and vitamin B-6 deficiency whereby the highest values were found in the sham-operated vitamin B-6-deficient animals. Plasma alanine and asparagine were reduced by B-6 deficiency and unchanged by azotemia. These results suggest that vitamin B-6 deficiency may contribute to several of the abnormalities in the plasma aminograms observed in chronic renal failure.     

Effect of dietary ascorbic acid intake on tissue vitamin C in mice

The effect of graded levels of dietary ascorbic acid on blood and tissue ascorbic acid levels in mice has been studied. Six levels of dietary ascorbic acid (0, 0.076, 0.5, 1, 5 and 8%) were used. Plasma ascorbic acid rose as dietary ascorbic acid intake increased from 1 to 8%. Mice fed a diet with 5 or 8% added ascorbic acid had significantly higher levels of ascorbic acid in the heart, kidney, lung, muscle and spleen than did control mice fed an ascorbic acid-free diet. Mice fed a diet with 1% added ascorbic acid had elevated ascorbic acid levels in the heart, kidney, lung and spleen. No significant change was observed in ascorbic acid level in the brain, adrenal gland or leukocytes in any of the experimental groups. Ascorbic acid level in the eyes was only slightly higher in mice fed a diet containing 8% added ascorbic acid than in control mice. The observation that the kidney had the greatest increase in ascorbic acid content suggests that the kidney may be a very important organ not only in elimination but also in catabolism of this vitamin. A diet containing 0.5 or 0.076% added ascorbic acid did not significantly increase ascorbic acid content in any of the organs studied. Mice fed a diet with 0.076% added ascorbic acid had slightly, but statistically significantly, lower levels of ascorbic acid in the liver, lung, muscle and spleen that control mice. Mice fed a diet with 0.5% added ascorbic acid had a lower ascorbic acid content in the liver and muscle than the controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

铁缺乏对大鼠维生素A代谢的影响

目的研究铁缺乏对大鼠维生素A(VA)代谢的影响。方法44只雄性SD大鼠按体重随机分为4组,每组11只,正常对照组(Ⅰ组),Fe完全缺乏VA正常组(Ⅱ组),Fe轻度缺乏VA正常组(Ⅲ组),Fe和VA轻度缺乏组(IV组)。喂饲10周后处死,测定血清视黄醇、血清视黄醇结合蛋白(RBP)、血红蛋白(Hb)、血清铁、血清铁饱和度、肝脏VA含量,肝脏视黄基酯含量,并用逆转录-聚合酶链反应(RT-PCR)法检测各组大鼠肝脏RBP mRNA的表达。结果与对照组相比,铁缺乏可以使血清视黄醇、肝脏VA含量显著降低(P<0.05),使肝脏视黄基酯与肝脏VA的摩尔比值升高,使RBP含量有降低趋势,铁缺乏时肝脏RBP mRNA表达显著降低。结论铁缺乏可能通过影响维生素A吸收、储存、转运来影响体内维生素A的营养状况。     

维生素A缺乏对大鼠铁代谢影响

目的 研究维生素A(VA)缺乏对大鼠铁营养状况和肝脏转铁蛋白受体(TfR)mRNA表达的影响.方法 雄性SD大鼠52只,按体重随机分为4组,每组13只,Fe和VA正常对照组(I组),Fe正常VA完全缺乏组(II组),Fe正常VA轻度缺乏组(Ⅲ组),Fe和VA轻度缺乏组(IV组).喂饲8周后处死,测定血清VA、血红蛋白、血清铁、血清转铁蛋白受体、血清铁蛋白、肝脏铁含量,脾脏铁含量,并用逆转录聚合酶链反应(RT-PCR)法检测各组大鼠肝脏转铁蛋白受体(TfR)mRNA的表达.结果 结果与对照组比较,VA缺乏使血清铁、血清铁蛋白含量显著降低(P<0.05),血清转铁蛋白受体水平、脾脏铁含量显著升高(P<0.05),VA缺乏时肝脏TfRmRNA表达显著增强.结论 维生素A缺乏可能通过影响铁吸收、储存、转运变改体内铁的营养状况,VA缺乏时,肝脏可能通过铁调节蛋白(IRE-ⅠRP)途径使TfR mRNA的表达水平增加.     

Effect of vitamin B12 deficiency on S-adenosylmethionine metabolism in rats

The effect of vitamin B12 (B12) deficiency on the levels of S-adenosylmethionine (SAM) in tissues and the activities of hepatic methionine synthase, methionine adenosyltransferase and glycine N-methyltransferase were investigated. The striking depression of methionine synthase activity was observed in all rats fed the B12-deficient diets with or without methionine supplementation for 150 days. The SAM level in liver was decreased by B12 deficiency. However, brain SAM level was not affected. The activities of hepatic methionine adenosyltransferase isozymes, alpha-form and beta-form, were decreased by B12 deficiency. Hepatic glycine N-methyltransferase activity in rats fed the low methionine-B12-deficient diet showed a tendency to lower, although the change the activity was not statistically significant, compared with B12-supplemented rats. It is proposed that the fall in the activity of hepatic methionine adenosyltransferase may be one of the causes of the decreased hepatic SAM level in B12-deficient rats.