Effect of dietary ascorbic acid, cholesterol and PCB on cholesterol concentrations in serum and liver in a rat mutant unable to synthesize ascorbic acid

The effect of ascorbic acid deficiency and excessive ascorbic acid intake on serum and liver levels of cholesterol and lipids was investigated in ODS-od/od (OD) rats fed a normal diet, a cholesterol-containing diet or a polychlorinated biphenyl (PCB)-containing diet. The OD rat is a rat mutant unable to synthesize ascorbic acid. In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and normal levels of cholesterol in serum and liver is about 300 mg of ascorbic acid/kg diet. In control (ODS-+/+) rats that can synthesize ascorbic acid, dietary addition of 0.5% cholesterol and 0.25% cholic acid caused elevation of cholesterol concentrations in serum and liver, elevation of total lipids in liver and reduction of the ratio of high density lipoprotein (HDL) cholesterol to total cholesterol in serum. Dietary addition of PCB (200 mg/kg diet) caused elevation of serum concentration of cholesterol and of the ratio of HDL-cholesterol to total cholesterol in serum. In OD rats fed a normal diet, ascorbic acid deficiency slightly elevated serum concentration of cholesterol, elevated liver concentration of cholesterol and reduced the ratio of HDL-cholesterol to total cholesterol in serum; and ascorbic acid excess did not affect serum and liver concentrations of cholesterol and the ratio of HDL-cholesterol to total cholesterol in serum. In OD rats fed a cholesterol-containing diet, ascorbic acid deficiency elevated serum and liver concentrations of cholesterol, and did not affect the ratio of HDL-cholesterol to total cholesterol in serum; and ascorbic acid excess did not affect serum and liver concentrations of cholesterol and the ratio of HDL-cholesterol to total cholesterol in serum.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ascorbic acid deficiency elevates serum level of LDL-cholesterol in a rat mutant unable to synthesize ascorbic acid

The effect of ascorbic acid deficiency on serum levels of high density lipoprotein- (HDL-), low density lipoprotein- (LDL-), very low density lipoprotein- (VLDL-) and chylomicron-cholesterol was examined in ODS-od/od rat (ODS rat), that is a rat mutant unable to synthesize ascorbic acid. Male ODS rats were fed an ascrobic acid-free diet for 20 days. In another two groups, the diet supplemented with 300 mg ascorbic acid/kg diet was fed either ad libitum (ad libitum control) or in pair-feeding (pair-fed control). Pair-fed rats received the same amount of diet as rats fed the ascorbic acid-free diet. Serum level of total cholesterol in the ad libitum control rats, ascorbic acid-deficient rats, and the pair-fed control rats were 100.1 +/- 8.4 mg/dl, 92.8 +/- 6.2 mg/dl and 72.2 +/- 4.8 mg/dl, respectively. The level of LDL-cholesterol in ascorbic acid-deficient rats was significantly higher than that in the ad libitum control or that in the pair-fed control. The level of HDL-cholesterol in ascorbic acid-deficient rats was lower than that in the ad libitum control, but was not changed as compared with that in the pair-fed control. Ascorbic acid deficiency did not affect serum level of VLDL-cholesterol or chylomicron-cholesterol as compared with those in the controls. These results demonstrate that ascorbic acid deficiency causes the elevation of serum level of LDL-cholesterol both in ad libitum feeding condition and pair feeding condition.     

Dietary ascorbic acid depresses plasma and low density lipoprotein lipid peroxidation in genetically scorbutic rats.

The effects of dietary ascorbic acid on plasma lipoprotein and liver lipid peroxide concentrations were examined using ODS od/od rats with a genetic defect in the ability to synthesize ascorbic acid. ODS od/od rats were fed purified diets supplemented with 0 to 300 mg ascorbic acid/kg diet for 21 d. An ascorbic acid-free diet induced body weight loss, depleted ascorbic acid in the plasma and increased thiobarbituric acid-reactive substances in the plasma and liver as compared with rats fed ascorbic acid supplemented diets and with normal ODS +/+ rats fed the ascorbic acid-free diet. Increasing ascorbic acid concentration in the diet inhibited the development of these ascorbic acid deficiency symptoms in a dose-dependent manner. The dietary requirement of ascorbic acid to maintain normal body weight gain and plasma lipid peroxide concentrations was approximately 150 mg ascorbic acid/kg diet. On the other hand, even 300 mg ascorbic acid/kg diet was insufficient to maintain a hepatic concentration of ascorbic acid comparable to that in the liver of ODS +/+ rats. The lipid peroxide concentration in plasma LDL and liver was significantly elevated in ODS od/od rats fed the ascorbic acid-free diet. Supplementing the diet with 300 mg ascorbic acid/kg kept those concentrations within the normal ranges seen in the ODS +/+ rats.     

Cholesterol metabolism in inherently scorbutic rats (ODS rats)

We observed the cholesterol metabolism of a colony of Wistar rats with a hereditary defect in vitamin C synthesizing ability (the ODS (osteogenic disorder-Shionogi) rats) in six kinds of experiments. Female ODS rats aged 36 days had a low HDL (high-density lipoprotein)-cholesterol level in serum as compared with age-matched control rats in spite of the absence of scorbutic symptoms. Female ODS rats aged 63 days which revealed severe scorbutic symptoms had a very low HDL-cholesterol level (mean value; 17 mg/dl). And male ODS rats, whose lives had been prolonged by supplementing with L-ascorbic acid, also had lower serum HDL-cholesterol and had increased total cholesterol in serum and liver when the acid supplement dose was relatively insufficient. On the other hand, we examined HDL2- and HDL3-cholesterol levels in serum to determine the mechanism of low HDL-cholesterol. As a result, we observed a low HDL2-cholesterol level in ODS rats but normal HDL3-cholesterol level. But the authors observed no decrease of LCAT (lecithin: cholesterol acyltransferase) activity in serum of ODS rats. These results could be due to disturbance of lipid metabolism in a vitamin C-deficient condition, that is to say, there might be abnormalities of the cholesterol excretion pathway of bile acid from liver, and maturity of the HDL-cholesterol particle due to other factors except that of LCAT activity.     

Effect of dietary ascorbic acid, cholesterol and PCB on cholesterol and bile acid metabolism in a rat mutant unable to synthesize ascorbic acid

The effect of acute or chronic ascorbic acid deficiency on the activity of hepatic cholesterol 7 alpha-hydroxylase and fecal excretion of bile acids was investigated in ODS-od/od (OD) rats (a rat mutant unable to synthesize ascorbic acid) fed a purified basal diet or purified diets containing either cholesterol (2%) or polychlorinated biphenyl (PCB) (200 mg/kg). In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and normal levels of cholesterol in serum and liver is about 300 mg of ascorbic acid/kg diet. In OD rats fed the basal diet, acute or chronic ascorbic acid deficiency did not affect the activity of hepatic cholesterol 7 alpha-hydroxylase and fecal excretion of bile acids. However, in OD rats fed diets containing either cholesterol or PCB, acute ascorbic acid deficiency caused a higher level of serum cholesterol, a lower activity of hepatic cholesterol 7 alpha-hydroxylase and a lower excretion of fecal bile acids than in OD rats fed a basal diet containing an adequate level of ascrobic acid. It is concluded that acute ascorbic acid deficiency causes a hypercholesterolemia due to the depression of bile acid synthesis in OD rats fed a purified diet with cholesterol or PCB.     

Effect of dietary fiber on hypercholesterolemia induced by dietary PCB or cholesterol in rats

Effects of 0.03% polychlorinated biphenyls (PCB) in the diet and various dietary fibers [konjac mannan (KM), pectin, sodium carboxymethyl cellulose (CMC) and cellulose] at a 5% level in the diet on serum and liver lipid metabolism and urinary ascorbic acid were studied. A comparison between dietary PCB and 1% cholesterol in the diet was also made. Serum albumin, protein, total and high density lipoprotein (HDL)-cholesterol, triglyceride, urinary and liver ascorbic acid, liver cholesterol and total lipids were increased in rats fed PCB. Pectin or KM depressed the elevation in serum protein, total and HDL-cholesterol, triglyceride and liver lipids due to PCB intake. Cellulose or CMC had no significant effect on these indices. Urinary ascorbic acid was not decreased by these dietary changes. Serum total cholesterol and low density lipoprotein (LDL) plus very low density lipoprotein (VLDL)-cholesterol, and liver total lipids, and cholesterol were significantly higher, and serum HDL-cholesterol and triglyceride were significantly lower in the cholesterol-fed group as compared to PCB-fed rats. Addition of KM to a cholesterol diet significantly depressed serum total cholesterol and LDL plus VLDL-cholesterol, liver cholesterol and total lipids. It seems likely that cholesterol metabolism is quite different during dietary PCB and cholesterol feeding.     

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 deficiency of vitamins C and/or E on lipoprotein metabolism in osteogenic disorder Shionogi rat,a strain unable to synthesize ascorbic acid

The effects of vitamin C and/or E deficiency on lipoprotein metabolism were investigated in the inherently scorbutic Osteogenic Disorder Shionogi (ODS) rat. In the vitamin C-deficient (C-def) group, marked increases in plasma VLDL and LDL cholesterol were observed (by comparison with the vitamins C- and E-sufficient control group). In rats kept deficient in both vitamin C and vitamin E (C,E-def), LDL cholesterol was significantly higher than in the C-def group even though the levels of VLDL and HDL cholesterol were similar between the two groups. TBARS values for the LDL fraction in the C-def group were of the same magnitude as in the E-def group, and these values were significantly higher than those obtained for the control group. In the C,E-def group, the values were even higher than in the E-def and C-def groups. The nondenatured PAGE of the LDL fraction indicated the appearance of HDLc in the C-def and C,E-def groups. The SDS-PAGE of the LDL fraction showed increased apo B-48 in the C-def and C,E-def groups and increased apo E in the C,E-def group. Decreased plasma LCAT activity in the E-def, C-def, and C,E-def groups indicated an alteration in HDL metabolism as a result of oxidation. These results suggest that lipid peroxidation and some distinct features of lipoprotein metabolism resulting from vitamin C deficiency become more significant when vitamin E is also deficient along with vitamin C deficiency.     

高水平维生素E对大鼠血脂、肝脂及肝脂质过氧化的作用

采用成年Wistar大鼠为实验动物,雌雄各半。1组为基础饲料对照组,2组为高脂饲料对照组,3、4、5组分别以维生素E30、60、120mg/d灌胃,同时喂饲高脂饲料。实验8周后停止灌胃并改饲基础饲料5周至实验结束。 研究表明:1.高水平维生素E(60和120mg/d)对高脂饲料诱导的大鼠肝实质细胞中性脂肪蓄积及肝脏(体内)脂质过氧化的增加均有明显抑制作用。2.高水平维生素E(30、60和120mg/d)无明显降低大鼠血清胆固醇、甘油三酯及增加血清高密度脂蛋白胆固醇的作用。大鼠血清维生素E与胆固醇水平呈正相关关系,与高密度脂蛋白胆固醇无明显相关。提示维生素E可能并无抑制高脂血症的作用。3.喂饲高脂饲料时雌鼠血清胆固醇的反应比雄鼠敏感,维生素E灌胃时雌鼠血清维生素E的反应比雄鼠敏感,提示存在性别差异。     

荞杞方便粥对高脂血症大鼠的调节血脂作用

在高脂饲料中加入３０％的荞杞方便粥饲喂Ｗｉｓｔａｒ雄性大鼠３周的结果提示：荞杞方便粥具有减轻脂质代谢紊乱大鼠血清总胆固醇（ＴＣ）和低密度脂蛋白胆固醇（ＬＤＬＣ）含量、ＬＤＬＣ／ＨＤＬＣ比值及致动脉粥样硬化指数（ＡＩ）升高的作用,对血清甘油三酯（ＴＧ）和高密度脂蛋白胆固醇（ＨＤＬＣ）无明显影响,对大鼠摄食及生长无不良影响。     

Manganese, iron and lipid interactions in rats

The interactive effects of manganese, iron and lipid on mineral status, manganese-dependent superoxide dismutase (MnSOD) activity and lipoprotein composition were investigated by feeding weanling rats two levels of manganese (0.4 or 56 micrograms Mn/g diet), two levels of iron (29 or 109 micrograms Fe/g diet) and either 12% high-linoleic acid safflower oil or 12% high-oleic acid safflower oil for 8 wk. Rats fed the manganese-deficient diets had decreased heart MnSOD activity; depressed tibia and kidney manganese concentrations; lowered plasma and high density lipoprotein (HDL) cholesterol, HDL protein and HDL apo E concentrations; and elevated HDL protein/cholesterol ratios. Ingestion of supplemental iron slightly decreased heart MnSOD activity and tibia and kidney manganese concentrations but had no effect on hematocrits or on plasma and HDL cholesterol levels. Rats fed the linoleic acid-rich rather than the oleic acid-rich oil had increased heart MnSOD activity but had unchanged plasma and HDL cholesterol levels. The decrease in plasma and HDL cholesterol levels with manganese deficiency appeared not to be a result of increased lipid peroxidation but may have resulted from decreased cholesterol synthesis and/or secretion.     

Ascorbic acid deficiency stimulates hepatic expression of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1, in scurvy-prone ODS rats

ODS rat has a hereditary defect in ascorbic acid biosynthesis and is a useful animal model for elucidating the physiological role of ascorbic acid. We previously demonstrated by using ODS rats that ascorbic acid deficiency changes the hepatic gene expression of acute phase proteins, as seen in acute inflammation. In this study, we investigated the effects of ascorbic acid deficiency on the production of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1 (CINC-1), in ODS rats. Male ODS rats (6 wk of age) were fed a basal diet containing ascorbic acid (300 mg/kg diet) or a diet without ascorbic acid for 14 d. Obvious symptoms of scurvy were not observed in the ascorbic acid-deficient rats. Ascorbic acid deficiency significantly elevated the serum concentration of CINC-1 on d 14. The liver and spleen CINC-1 concentrations in the ascorbic acid-deficient rats were significantly elevated to 600% and 180% of the respective values in the control rats. However, the lung concentration of CINC-1 was not affected by ascorbic acid deficiency. Ascorbic acid deficiency significantly elevated the hepatic mRNA level of CINC-1 (to 480% of the value in the control rats), but not the lung mRNA level. These results demonstrate that ascorbic acid deficiency elevates the serum, liver and spleen concentrations of CINC-1 as seen in acute inflammation, and suggest that ascorbic acid deficiency stimulate the hepatic CINC-1 gene expression.     

Vitamin C deficiency exerts paradoxical cardiovascular effects in osteogenic disorder Shionogi (ODS) rats

Vitamin C is considered to be a very efficient water-soluble antioxidant, for which several new cardiovascular properties were recently described. The aim of this study was to determine in vivo the effects of a severe depletion of vitamin C on cardiac and vascular variables and reperfusion arrhythmias. For this purpose, we used a mutant strain of Wistar rats, osteogenic disorder Shionogi (ODS). After 15 d of consuming a vitamin C-deficient diet, ODS rats had a 90% decrease in plasma and tissue levels of ascorbate compared with ODS vitamin C-supplemented rats and normal Wistar rats. However, plasma antioxidant capacity, proteins, alpha-tocopherol, urate, catecholamines, lipids, and nitrate were not influenced by the vitamin C deficiency in ODS rats. Moreover, there was no difference between ODS vitamin C-deficient and -supplemented rats in heart rate and arterial pressure. After 5 min of an in vivo regional myocardial ischemia, various severe arrhythmias were observed, but their intensities were not modified by vitamin C in vitamin C-deficient ODS rats. The vascular reactivity, measured in vitro on thoracic arteries, was not altered by ascorbate deficiency in ODS rats. These unexpected results suggest that unidentified compensatory mechanisms play a role in maintaining normal cardiac function and vascular reactivity in vitamin C-deficient rats.     

Different effects of zinc and copper deficiency on composition of plasma high density lipoproteins in rats

Male Sprague-Dawley rats (six per group) were fed an egg white-based diet containing 0 or 5 micrograms/g Cu with 1, 10, 100 or 1000 micrograms/g Zn. After 6 wk of feeding, the rats were killed, and the tissues were processed for trace element, lipid and lipoprotein analysis. Copper deficiency was associated with a higher concentration of plasma free cholesterol, high density lipoprotein (HDL) cholesterol and HDL apolipoproteins. Plasma total cholesterol was not significantly affected. No significant differences were noted in HDL lipid composition. However, HDL apo E and apo A-I concentrations were higher with copper deficiency. Lecithin:cholesterol acyltransferase (LCAT) was not affected in a consistent manner by copper status. Varying the amount of zinc in the diet did not produce significant changes in plasma total cholesterol, plasma free cholesterol, HDL cholesterol, or HDL apolipoprotein concentrations. However, HDL from zinc-deficient rats were enriched in free cholesterol and depleted in triglycerides. Furthermore, the concentration of HDL apo C increased as the level of dietary zinc increased.     

Effects of diets rich in fermentable carbohydrates on plasma lipoprotein levels and on lipoprotein catabolism in rats

This study was conducted to examine the effects of a combination of several dietary fibers (5% guar gum, 5% apple pectin, 15% wheat bran, 22% soybean fiber) and crude potato starch (23%) on plasma lipids and lipoproteins and on liver lipid concentration in rats fed a diet containing either 15% lard or 5% oil with or without dietary cholesterol/cholic acid. Male Wistar rats ate the test diets for 3 wk. The incorporation of fiber and crude potato starch into the diet resulted in a significant enlargement of the cecum; it also increased the concentration of volatile fatty acids and the pool of acetate, propionate and butyrate. Feeding this fermentable carbohydrate decreased plasma cholesterol and triglyceride levels in rats given a low fat diet and prevented the expected rise in plasma cholesterol and triglycerides in rats fed cholesterol/cholic acid or lard. Further studies of high density lipoprotein (HDL) composition, 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMG-CoA reductase) activity and 125I-labeled human low density lipoprotein (LDL) turnover were done in the group fed the low fat diet without added cholesterol/cholic acid. The study of the HDL fraction in rats fed a diet rich in fermentable carbohydrates demonstrated a decrease in the HDL1 subpopulation and in the proportion of apolipoprotein E. Plasma clearance of intravenously injected 125I-labeled LDL was faster in rats fed this diet than in rats fed the fiber-free diet. In the liver, cholesterol and triglyceride levels were depressed whereas the activity of HMG-CoA reductase was increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evidence that polyunsaturated lecithin induces a reduction in plasma cholesterol level and favorable changes in lipoprotein composition in hypercholesterolemic rats

For 30 d adult rats were fed a hypercholesterolemic (H) diet (25% saturated fat, 1% cholesterol and 0.5% cholic acid) containing different amounts of saponins (1% or 0.2%) and/or purified polyunsaturated lecithin (2.5% or 0.7%). Lecithin induced a striking reduction in the plasma levels of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) cholesterol as well as an increase in the level of high density lipoprotein (HDL) cholesterol. Saponins had only a very slight effect in lowering the level of VLDL cholesterol. Apoprotein A-I was unexpectedly present in VLDL, IDL and LDL after feeding rats the H diet and disappeared only after lecithin feeding. The activity of plasma lecithin-cholesterol acyltransferase was higher when the two lecithin diets were fed than when the other diets were fed. Fecal excretion of neutral sterols was unmodified by the various diets whereas acid steroid excretion increased after lecithin feeding. Saponins, when added with lecithin to the diet, reduced the beneficial effect of lecithin. The results indicate that polyunsaturated lecithin induced a reduction in plasma cholesterol, possibly through an increased formation of HDL particles.     

Alteration of serum lipoprotein metabolism by polychlorinated biphenyls and methionine in rats fed a soybean protein diet

The effects of dietary supplementation of methionine to a 20% soybean protein isolate diet on serum lipoprotein profiles and secretion rate of VLDL in rats receiving polychlorinated biphenyls (PCB) were investigated. Serum cholesterol levels were higher in rats fed PCB or a methionine supplement than in controls. The effects of PCB and methionine were synergistic. The feeding of PCB resulted in more cholesterol in all fractions of serum lipoproteins tested, especially HDL (HDL1 and HDL2). Dietary supplementation of methionine primarily increased HDL cholesterol. The elevation of serum lipoprotein cholesterol due to PCB and/or methionine was significant in HDL1, which showed alpha-mobility. These results showed that methionine and PCB significantly influenced HDL metabolism. The secretion rate of VLDL was higher in rats fed PCB than in controls, but the addition of methionine to diets did not affect the secretion rate of VLDL cholesterol. This implies that PCB increased serum cholesterol partly through the stimulation of VLDL cholesterol secretion.     

鲨烯、苔条、紫菜、花菜对大鼠血清胆固醇的作用

通过喂养试验,观察了11种食物和1种食物提取物(鲨烯),对大鼠血清胆固醇浓度的作用。结果发现,鲨烯、苔条、紫菜、花菜均有降低血清T-C的作用,其中鲨烯和苔条还能促进HDL-C的增高。与对照组相比,鲨烯组大鼠血清T-C,LDL-C和VLDL-C分别下降50.5％、60.8％和53.7％,而HDL-C则增高56.5％。苔条组大鼠血清T-C,LDL-C和VLDL-C分別下降34.9％,42.7％、和31.4％,而HDL-C增高58.3％。紫菜组和花菜组大鼠血清T-C则分别下降29.4％和36.7％。     

Effect of ethanol on lipoprotein synthesis and fecal sterol excretion

The effect of variable doses of ethanol on plasma lipoprotein composition, lipoprotein synthesis and fecal sterol excretion was examined in male, atherosclerosis susceptible squirrel monkeys. Primates were divided into three groups: 1) Controls fed isocaloric liquid diet; 2) Low Ethanol monkeys given liquid diet with vodka substituted isocalorically for carbohydrate at 12% of calories; and 3) High Ethanol animals fed diet plus vodka at 24% of calories. Circulating high density lipoprotein (HDL) free cholesterol and phospholipid, very low density-low density lipoprotein (VLDL-LDL) total cholesterol, and total plasma cholesterol and triglyceride were significantly elevated in High Ethanol primates compared to the other treatments. However, the percent distribution of cholesterol among the lipoprotein fractions was identical for the three groups. There were no significant differences in serum glutamate oxalo-acetate transaminase. High Ethanol primates also had significantly greater HDL free cholesterol specific activity following intravenous injection of ³H mevalonolactone compared to the other groups while radioactive VLDL-LDL free cholesterol was elevated in both High and Low Ethanol animals. Although, total fecal bile acid mass was significantly greater in both alcohol treatment groups compared to Controls, fecal neutral sterol specific activity was only higher in monkeys fed the high ethanol diet. This study provides evidence that ethanol at 24% of calories: 1) raises HDL cholesterol levels by enhancing lipoprotein synthesis; 2) increases the fecal output of newly synthesized cholesterol without causing liver dysfunction; and 3) maintains a constant relative distribution of cholesterol among lipoprotein classes.     

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.