Evaluation of dietary essentiality of vitamins for Penaeus monodon (Fabricius)

The effect of exclusion of individual water-soluble (thiamine, riboflavin, pyridoxine, cyanocobalamin, pantothenic acid, folic acid, niacin, biotin, choline, inositol, ascorbic acid) and fat-soluble vitamins (vit. A, D, K and E) in semi-purified diets on growth and survival of juvenile shrimp, P. monodon was studied in the laboratory for 8 weeks. Diets lacking riboflavin and vitamin K did not affect growth and survival of shrimp. However, deletion of inositol and choline resulted in poor growth. Maximum growth was observed in the control diet (C1) which was supplemented with all vitamins. Diet deficient in ascorbic acid, biotin, folic acid, niacin, thiamine and alpha-tocopherol resulted in poor appetite and poorer feed conversion efficiency. All treatments except the control (C1) resulted in histological changes in the digestive gland cells. Detachment or destruction of the epithelial cells was observed in all treatments lacking individual vitamins but more severely in the treatment without a vitamin supplement followed by inositol, choline and ascorbic acid deficient diets.     

Effect of different doses of ascorbic acid on thyroid activity in rats at different levels of dietary protein intake.

Rats, which can synthesize vitamin C, react similarly to graded doses of ascorbic acid as guinea pigs. Low doses of ascorbic acid stimulate and high doses inhibit the thyroid activity of rats which are supplied with normal and high percentages of protein. The stimulatory effect of low doses of ascorbic acid on hyperactive thyroid of high protein fed animals is additive. Ascorbic acid has no significant effect on the thyroid of low protein fed animals (deficient diet supplied for 21 days). In the initial stages of protein deficiency (deficient diet supplied for 11 days) the effectiveness of vitamin C on thyroid of rats was still significant. Deiodinase enzyme activity of peripheral tissues is markedly reduced in animals supplied with 2% of protein for 21 days, but this effect is less intense in animals supplied with 2% of protein for 11 days.     

Effect of dietary vitamin C on the growth performance and innate immunity of juvenile cobia (Rachycentron canadum)

This study was conducted to evaluate the effects of dietary vitamin C on growth performance, hematologic parameters and innate immune responses in juvenile cobia, Rachycentron canadum. Seven practical diets were formulated to contain 0.0 (as the basal diet), 13.6, 27.2, 54.4, 96.6, 193.4 and 386.5 mg ascorbic acid equivalent kg(-1) diet. Each diet was fed to triplicate groups of juvenile cobia with initial body weight of 5.5 g in 500-L cylindrical fiberglass tank. The results of 8 weeks feeding trial showed that typical vitamin C-deficient signs such as spinal deformation and body nigrescence were observed in the fish fed the basal diet. Fish fed the basal diet had significantly lower weight gain, specific growth rate (SGR), protein efficiency ratio (PER) and feed efficiency (FE) than those fed the diets supplemented with vitamin C, but no significant differences were observed among diets supplemented with vitamin C. However, survival rate was significantly affected by the dietary vitamin C levels, fish fed the basal diet had lower survival rate than those fed the diets supplemented with vitamin C. The ascorbic acid concentration in liver was correlated positively with the dietary vitamin C levels, however, the thiobarbituric acid reactive substances (TBARS) concentrations in liver was not significantly affected by the dietary vitamin C levels, although, fish fed the basal diet had the highest TBARS values among all treatments. The activities of serum lysozyme, superoxide dismutase (SOD), alkaline phophatase (AKP) and total immunoglobulin (Ig) were significantly influenced by the dietary vitamin C levels, fish fed the basal diet had lower lysozyme, SOD, AKP and total Ig than those fed diets supplemented with vitamin C. The serum glucose and triglyceride concentrations were significantly affected by the dietary vitamin C levels. Fish fed the basal diet had lower red blood cell and hemoglobin values than those fed the vitamin C supplemented diets. The challenge experiment with Vibrio harveyi showed that lower cumulative survival was in fish fed the unsupplemented diet, the cumulative survival were significantly increased with increase of the dietary ascorbic acid levels from 13.6 to 96.6 mg kg(-1), while the cumulative survival reached plateau when dietary ascorbic acid levels increased from 96.6 to 386.5 mg kg(-1). These results indicated that dietary vitamin C did significantly influence on growth performance and immune response of juvenile cobia.     

Vitamin C partially reversed some biochemical changes produced by vitamin E deficiency

Feeding a basal diet free of vitamins E and C to weanling male rats for 8 months resulted in biochemical changes characteristic of vitamin E deficiency. These included increased liver thiobarbituric acid values; decreased blood GSH levels, plasma vitamin E levels, and glutathione peroxidase activities; and increased activities of plasma pyruvate kinase, glutamic-oxaloacetic transaminase, creatine kinase, lactic dehydrogenase, and malic dehydrogenase. Tube-feeding vitamin C for 21 days resulted in partial reversal effects on the above parameters except activities of glutathione peroxidase, lactic dehydrogenase, and malic dehydrogenase. The results suggest that vitamin C may spare in part the metabolism of vitamin E through its antioxidant property.     

Lack of effect of experimental ascorbic acid deficiency on bile acid metabolism, sterol balance, and biliary lipid composition in man

Extensive studies in animal models indicate that subclinical ascorbic acid deficiency impairs the conversion of cholesterol to bile acid, elevates plasma cholesterol levels, and predisposes to development of cholesterol cholelithiasis. The present study was designed to see if this is also true in man. Five normal volunteers were hospitalized in a metabolic ward and placed on a controlled diet containing 3-4 mg of ascorbic acid each day. Ascorbic acid supplementation was given as follows: control period I (days 1-33), 75 mg/day; deficient period (days 34-96), 0 mg/day; and repletion period (days 97-101), 1000 mg/day. In addition, three of the subjects were studied during a second control period (days 102-139) during which they were given 75 mg/day of ascorbic acid. Ascorbate levels at the end of both control periods were 0.87-1.34 mg/dl in plasma and 19.4-29.5 micrograms/10(8) cells in leukocytes. At the end of the deficient period these levels were 0.09-0.15 mg/dl in plasma and 6.2-10.0 micrograms/10(8) cells in leukocytes, levels approaching those seen in scurvy. There was no effect of ascorbic acid deficiency on plasma cholesterol and triglycerides; plasma cholesterol in high, very low, and low density lipoprotein fractions; biliary lipid composition and saturation index of gallbladder bile; synthesis, fractional turnover, or pool size of either cholic or chenodeoxycholic acids; output of fecal acid or neutral sterols; and fecal sterol balance. Total bile acid pool size calculated by the one-sample technique was reduced 11% in the deficient period compared to control period I (P less than 0.005), and increased to 98.7% of the baseline levels in control period II. However, total bile acid pool calculated by the Lindstedt method did not change during deficiency. These data demonstrate that short-term subclinical ascorbic acid deficiency near the scorbutic range has no significant effect on bile acid and cholesterol metabolism in man.     

Zooplankton preference of two species of freshwater ornamental fish larvae

The study aimed at evaluating the ascorbic acid (AA) concentrations in the liver and blood of the Mediterranean sea bream (Sparus aurata L.) after being fed Rovimix Stay C‐25 (RS C‐25) at three different levels (0, 200 and 800 mg kg^?1 of AA) over 45 days. RS C‐25 is a mixture of equal parts of AA monophosphate, diphosphate and polyphosphate, containing a 25% AA equivalent. Increasing RS C‐25 levels in the diet yielded an increasing ascorbic acid content in the plasma and liver, showing a good sea bream utilization of this source of vitamin C. Dietary vitamin C did not affect the growth rate or feed efficiency during the 45‐day experiment. After 75 days, fish fed a vitamin C‐free diet displayed a severe depletion of AA in the liver.     

维生素C对凡纳滨对虾生长及抗病力的影响

以不同水平维生素C 2 磷酸酯 (添加量分别为 0、75、15 0、30 0和 6 0 0mg/kg)的饲料喂养凡纳滨对虾 10周 ,研究维生素C 2 磷酸酯对凡纳滨对虾生长及抗病力的影响。结果显示 :在养殖前 4周 ,饲料中添加维生素C 2 磷酸酯显著促进凡纳滨对虾的生长 ,然而对对虾的成活以及饲料利用不产生影响 (P >0 0 5 ) ;而到实验后期添加维生素C 2 磷酸酯不能促进凡纳滨对虾的生长 ,却显著提高凡纳滨对虾的成活率 (P <0 0 5 )。维生素C 2 磷酸酯对对虾体水分、脂肪、蛋白质和维生素C在肝胰脏中的积累量的影响显著 (P <0 0 5 ) ,对对虾体灰分影响不显著 (P >0 0 5 )。维生素C 2 磷酸酯对对虾血清中超氧化物歧化酶活力无显著影响 ,饲料中未添加维生素C或过量添加 (超过 30 0mg/kg饲料 )均导致血清中酚氧化酶活力、血细胞总数和溶菌酶活力的显著下降。以生长、成活和酚氧化酶活力为指标 ,饲料中维生素C 2 磷酸酯的适宜添加量为 15 0mg/kg。     

Changes in the cholesterol content of high-density plasma lipoproteins in guinea pigs in the presence of a raised exogenous cholesterol intake and different degrees of vitamin C saturation

The cholesterol content of the high-density plasma lipoproteins (d over 1.1 g.cm-3) of guinea-pigs with experimental vitamin C deficiency, followed by realimentation with suboptimal (1 mg/animal per day) or optimal (10 mg/animal per day) doses of L-ascorbic acid for 6-9 weeks in the continued presence of an elevated alimentary cholesterol intake (0.5 g/kg diet), did not exceed 5% of the total plasma cholesterol concentration and did not alter significantly with changes in the degree of vitamin C saturation of the organism. The maximum total body tissue cholesterol concentrations were found in C-deficient guinea-pigs (plasma, adrenals) and in the group with partial vitamin C deficiency (liver, brain); the lowest values were found in the group whose organism was fully saturated with vitamin C. Under conditions of a raised cholesterol intake, ascorbic acid stimulated its elimination from the organism, but did not affect the proportion of plasma cholesterol bound in high-density lipoproteins.     

Amelioration of diet-induced nonalcoholic steatohepatitis in rats by Mn-salen complexes via reduction of oxidative stress

Background

Nonalcoholic steatohepatitis (NASH), a progressive stage of nonalcoholic fatty liver disease (NAFLD), is characterized by steatosis (accumulation of triacylglycerols within hepatocytes) along with inflammation and ballooning degeneration. It has been suggested that oxidative stress may play an important role in the progress of NAFLD to NASH. The aim of present study was to determine whether antioxidant supplementations using EUK-8, EUK-134 and vitamin C could improve the biochemical and histological abnormalities associated with diet-induced NASH in rats.

Methods

NASH was induced in male N-Mary rats by feeding a methionine - choline deficient (MCD) diet. The rats were fed either normal chow or MCD diet for 10 weeks. After NASH development, the MCD-fed rats were randomly divided into four groups of six: the NASH group that received MCD diet, the EUK-8 group which was fed MCD diet plus EUK-8, the EUK-134 group which was fed MCD diet plus EUK-134 and the vitamin C group which received MCD diet plus vitamin C. EUK-8, EUK-134 and vitamin C (30 mg/kg body weight/day) were administered by gavage for eight weeks.

Results

Treatment of MCD-fed rats with salens reduced the sera aminotransferases, cholesterol, low density lipoprotein contents, the extent of lipid peroxidation and protein carbonylation whereas the HDL-C cholesterol levels were significantly increased. In addition, EUK-8 and EUK-134 improved steatosis, ballooning degeneration and inflammation in liver of MCD-fed rats.

Conclusion

Antioxidant (EUK-8, EUK-134 and vitamin C) supplementation reduces NASH-induced biochemical and histological abnormalities, pointing out that antioxidant strategy could be beneficial in treatment of NASH.     

Effect of oral methionine and vitamin E on blood lipid peroxidation in vitamin B6 deficient rats

Lipid peroxidation in blood of vitamin B6 deficient rats was significantly increased when compared to pair-fed controls. The observed increased lipid peroxidation in vitamin B6 deficiency was correlated with high levels of lipids, metal ions and low levels of antioxidants, alpha-tocopherol, ascorbic acid and reduced GSH. Supplementation of methionine or vitamin E along with the vitamin B6 deficient diet restored the levels of antioxidants to near normal and also protected against oxidative stress. However plasma TBARS level as well as total lipids were still elevated in M-B6 diet fed rats and normalized in E-B6-d rats.     

Evidence for the influence of vitamin C on age- and heat exposure-dependent deterioration of biochemical function in rat's liver and kidney

Molecular mechanisms responsible for age-dependent deterioration of biochemical functions have not been completely revealed as yet. We studied the role of ascorbic acid food supplementation in young and aged acute heat-exposed rats. The duration of heat exposure (40±0.5 °C) for heat-exposed Wistar rats, at the age of 35 days and 22–24 months, was approximately 2 h. In the aged heat-unexposed animals cholesterol and triglycerides were considerably high, whereas tissues ascorbic acid, glutathione and methylglyoxal were significantly low. Administration of vitamin C reverted these age-associated differences to the status comparable to young rats. The role of vitamin C supplementation was almost the same in young heat-exposed animals. In this direction in young rats suppression of LTC₄ synthesis is evident during acute heat exposure as a result of vitamin C treatment. The importance of vitamin C treatment for young heat-exposed rats is in the protection of apoptosis, if it is determined across the LTC₄ changes. In contrary, in old heat-exposed rats, vitamin C does not suppress the apoptotic processes. The results suggest that oxidative and apoptotic processes in the liver and the kidney as a result of the acute heat exposure is presumably subject of ascorbic acid deficiency.     

Effects of phosphorus and vitamin C deficiency,vitamin A toxicity,and lipid peroxidation on skeletal abnormalities in Atlantic halibut (Hippoglossus hippoglossus)

Dietary nutrients play an important role in skeletal tissue metabolism of fish. Deficiency and toxicity of certain nutrients have been linked to bone deformities in larval and juvenile fish. The pathogenesis of skeletal disorders in larval and juvenile fish from the same genetic stock, cultured under similar environment conditions is often difficult to distinguish when marginal deficiencies of multiple nutrients are involved. A study was conducted to characterize the skeletal deformities linked to the deficiency of phosphorus and ascorbic acid, vitamin A toxicity and lipid peroxidation in juvenile halibut. Five experimental diets containing a low level of phosphorus (0.5% dry matter basis), no vitamin C supplement, high level of vitamin A (80 000 IU kg^?1) and oxidized marine fish oil (peroxide value, 7.53 meq kg^?1) and a control diet based on cod fillet and vitamin free casein were fed to juvenile Atlantic halibut for 14 weeks in an attempt to characterize the skeletal deformities. Phosphorus, ascorbic acid, retinol, and α‐tocopherol concentrations of liver and kidney were measured at 0 and 14 weeks. Reduced vertebral ash and phosphorus content were observed in fish fed the low phosphorus diet. Skeletal abnormalities included abnormal hemal and neural spines in the hemal region and scoliosis in the cephalic and hemal regions of the vertebral column. Hepatic and kidney ascorbic acid concentrations were significantly lower in the group fed no ascorbic acid supplement. Skeletal abnormalities were scoliosis and lordosis primarily in the hemal region of the vertebral column. High levels of vitamin A in the diet caused increased hepatic retinol content and scoliosis spanning the cephalic/prehemal and anterior hemal regions of the vertebral column. Fish fed the oxidized oil diet showed increased thiobarbituric acid (TBA) value in the liver and muscle tissue with no significant decrease in hepatic vitamin E concentration. The most frequent skeletal deformity observed was scoliosis, spanning the cephalic/prehemal regions as well as the anterior hemal region of the vertebral column. The pattern and type of abnormalities observed in fish fed these experimental diets were similar to those observed in a commercial halibut hatchery.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Effect of high‐dose vitamin C supplementation on growth,tissue ascorbic acid concentrations and physiological response to transportation stress in juvenile silver pomfret,Pampus argenteus

This study investigated the effect of high‐dose vitamin C supplementation on growth, tissue ascorbic acid concentrations and physiological response to transportation stress in juvenile silver pomfret, Pampus argenteus (initial average weight 6.2 ± 0.2 g). Three practical diets were formulated to contain 100 (control), 450 and 800 mg ascorbic acid/kg diet, respectively, supplied as l‐ascorbyl‐2‐polyphosphate. Each diet was fed to triplicate groups of fish in circular tanks (3 m ø, 1.5 m depth) (60 fish/tank) for 9 weeks. Growth did not change significantly with dietary vitamin C levels, although an improvement tendency with an increase in vitamin C supplementation was observed. Ascorbic acid concentrations in the liver and muscle of fish fed diets containing graded levels of vitamin C were positively correlated with dietary levels of this vitamin. Tissue ascorbic acid concentrations significantly increased with increasing vitamin C supplementation. After 9 weeks, the fish were subjected to transportation stress for 4 h to determine the influence of high vitamin C supplementation on the physiological response to this stressor. Serum cortisol, glucose and lactate levels significantly increased in stressed fish. Serum cortisol and glucose concentrations after stress were significantly higher in fish fed the control diet (7.91 μg L^?1 and 0.80 mm , respectively) than in the other groups. However, there were no significant differences in serum cortisol and glucose levels after stress between the 450 and 800 mg kg^?1 diets. No significant change could be found in serum lactate levels after stress among the different treatments. In conclusion, the dietary administration of high doses of vitamin C could reduce stress in silver pomfret and increase the survival of fish under stress conditions.     

Ibotenic acid-induced lesions of the medial septum increase hippocampal membrane associated protein kinase c activity and reduce acetylcholine synthesis: prevention by a phosphatidylcholine/vitamin B12 diet

Ibotenic acid infusion into the medial septum (MS) results in biochemical alterations in the hippocampus. The biochemical events involved in this neuronal lesion are poorly understood. We investigated the effect of a purified diet supplemented with egg phosphatidylcholine (PC) and vitamin B(12) on ibotenic acid-medicated biochemical changes in the rat hippocampus and crude synaptosomal membranes. Male Wistar rats with this MS lesion were fed a purified diet (control diet) or a purified diet supplemented with 5.7 g PC and 125 microg vitamin B(12) per 100 g (experimental diet) for 18 days. Sham-operated rats were fed the control diet. Compared with the sham-operated rats, MS-lesioned rats fed the control diet showed increased activity of membrane-bound protein kinase C (PKC), decreased activity of choline acetyltransferase, and decreased concentrations of acetylcholine in the hippocampus. The ratio of cholesterol to phospholipid in the crude synaptic membrane was lower in the lesioned rats than in the sham-operated rats, but this was not accompanied by any alteration in membrane lipid fluidity. MS-lesioned rats fed the experimental diet showed lowered PKC activity and elevated acetylcholine concentrations than did rats fed the control diet, but there were no significant effects on choline acetyltransferase activity and the lipid ratio. The ibotenic acid-mediated elevation of PKC activity was observed as early as 2 days postinjury in the control diet-fed rats but not in the experimental diet-fed rats. We propose that ibotenic acid mediates pathophysiologic actions through the activation of PKC and that PC combined with vitamin B(12) ameliorates the second messenger-mediated injury.     

Vitamin C - vitamin E interaction in juvenile lake sturgeon (Acipenser fulvescens R.), a fish able to synthesize ascorbic acid

The hypothesis that vitamin C interacts with vitamin E in vivo was investigated in juvenile lake sturgeon. Ten-month old lake sturgeon were fed diets supplemented with either 0 or 1250 mg ascorbic acid/kg diet concomitantly with either 0 or 200 mg α tocopherol/kg diet for 7 weeks at 17°C. Dietary vitamin C supplement resulted in significant increases of ascorbate concentrations in the posterior kidney and liver of sturgeon. Dietary vitamin E omission affected liver concentrations of α-tocopherol (10.0 ± 4.5 μg/g) in comparison to sturgeon fed a diet supplemented with vitamin E and vitamin C (99.5 ± 22.9 μg/g). Dietary vitamin C supplement decreased liver α-tocopherol concentration in vitamin E-deprived sturgeon. Also, vitamin E supplement lowered posterior kidney and liver ascorbic acid concentrations in vitamin C-deprived sturgeon. Gulonolactone oxidase and dehydroascorbic acid reductase activities were stimulated in groups fed vitamin C. Thiobarbituric acid-reactive substances concentrations (an indicator of lipid peroxidation) were higher in sturgeon fed either of vitamins as compared to sturgeon deprived of both vitamins. The results suggested that large doses of vitamins C and E may be prooxidant in vivo.     

Essential role of intracellular glutathione in controlling ascorbic acid transporter expression and function in rat hepatocytes and hepatoma cells

Although there is in vivo evidence suggesting a role for glutathione in the metabolism and tissue distribution of vitamin C, no connection with the vitamin C transport systems has been reported. We show here that disruption of glutathione metabolism with buthionine-(S,R)-sulfoximine (BSO) produced a sustained blockade of ascorbic acid transport in rat hepatocytes and rat hepatoma cells. Rat hepatocytes expressed the Na(+)-coupled ascorbic acid transporter-1 (SVCT1), while hepatoma cells expressed the transporters SVCT1 and SVCT2. BSO-treated rat hepatoma cells showed a two order of magnitude decrease in SVCT1 and SVCT2 mRNA levels, undetectable SVCT1 and SVCT2 protein expression, and lacked the capacity to transport ascorbic acid, effects that were fully reversible on glutathione repletion. Interestingly, although SVCT1 mRNA levels remained unchanged in rat hepatocytes made glutathione deficient by in vivo BSO treatment, SVCT1 protein was absent from the plasma membrane and the cells lacked the capacity to transport ascorbic acid. The specificity of the BSO treatment was indicated by the finding that transport of oxidized vitamin C (dehydroascorbic acid) and glucose transporter expression were unaffected by BSO treatment. Moreover, glutathione depletion failed to affect ascorbic acid transport, and SVCT1 and SVCT2 expression in human hepatoma cells. Therefore, our data indicate an essential role for glutathione in controlling vitamin C metabolism in rat hepatocytes and rat hepatoma cells, two cell types capable of synthesizing ascorbic acid, by regulating the expression and subcellular localization of the transporters involved in the acquisition of ascorbic acid from extracellular sources, an effect not observed in human cells incapable of synthesizing ascorbic acid.     

Relative resistance of the hamster to aortic atherosclerosis in spite of prolonged vitamin E deficiency and dietary hypercholesterolemia. Putative effect of increased HDL?

Male golden hamsters were rendered hypercholesterolemic by feeding diets enriched with cholesterol and fat. In the first series of experiments, 5% butter and 1% cholesterol were added to a chow diet and plasma cholesterol levels were maintained at 350–390 mg/dl over the entire experimental period. Groups of hamsters and their age controls consuming the chow diet, were killed after 7, 15 and 20 months when the aorta was examined for atherosclerosis by determination of cholesterol mass. In the controls, aortic total cholesterol (TC) increased with age by 28% and esterified cholesterol increased to 11% of TC. In the hypercholesterolemic animals aortic TC was only 28% higher than in the controls and cholesteryl ester was also 11.5% of TC. In the second series, one group of hamsters were fed a semi-purified diet deficient in vitamin E, containing 1% cholesterol and 10% lard; a second group received the same diet, but supplemented with vitamin E. Controls consumed local chow. After 7 months on the vitamin E deficient diet plasma α-tocopherol was 0.05 mg/l, in those supplemented with vitamin E it was 20 mg/l, while in the controls it was 3.3 mg/l. Plasma thiobarbituric acid reactive substances (TBARS) were higher in the vitamin E deficient group and there was a greater propensity of lipoproteins (d < 1.063 g/ml to peroxidation in vitro than in the vitamin E supplemented group. Plasma cholesterol was 366 mg/dl in the vitamin E deficient, 336 mg/dl in the vitamin E supplemented group, and 64 mg/dl in controls. Aortic cholesterol was 79.1 in vitamin E supplemented and 84.4 μg/ 10 mg dry weight in vitamin E deficient hamsters. In both series of experiments, HDL amounted to 36–41% of plasma TC in the hypercholesterolemic animals and 59–62% in the controls. In conclusion: the hamster appears to be quite resistant to atherosclerosis in face of sustained hypercholesterolemia, even in the presence of increased peroxidative stress caused by vitamin E deficiency. This relative resistance could be related to commensurate increase in plasma HDL which was observed in both series of experiments. Since vitamin E deficiency did not enhance aortic cholesteryl ester deposition, the protective effect of HDL seems to be related to its role in reverse cholesterol transport, rather than in prevention of peroxidation.     

Plasma Ascorbic Acid,A Priori Diet Quality Score,and Incident Hypertension: A Prospective Cohort Study

Vitamin C may reduce risk of hypertension, either in itself or by marking a healthy diet pattern. We assessed whether plasma ascorbic acid and the a priori diet quality score relate to incident hypertension and whether they explain each other’s predictive abilities. Data were from 2884 black and white adults (43% black, mean age 35 years) initially hypertension-free in the Coronary Artery Risk Development in Young Adults Study (study year 10, 1995–1996). Plasma ascorbic acid was assessed at year 10 and the diet quality score at year 7. Eight-hundred-and-forty cases of hypertension were documented between years 10 and 25. After multiple adjustments, each 12-point (1 SD) higher diet quality score at year 7 related to mean 3.7 μmol/L (95% CI 2.9 to 4.6) higher plasma ascorbic acid at year 10. In separate multiple-adjusted Cox regression models, the hazard ratio of hypertension per 19.6-μmol/L (1 SD) higher ascorbic acid was 0.85 (95% CI 0.79–0.92) and per 12-points higher diet score 0.86 (95% CI 0.79–0.94). These hazard ratios changed little with mutual adjustment of ascorbic acid and diet quality score for each other, or when adjusted for anthropometric variables, diabetes, and systolic blood pressure at year 10. Intake of dietary vitamin C and several food groups high in vitamin C content were inversely related to hypertension, whereas supplemental vitamin C was not. In conclusion, plasma ascorbic acid and the a priori diet quality score independently predict hypertension. This suggests that hypertension risk is reduced by improving overall diet quality and/or vitamin C status. The inverse association seen for dietary but not for supplemental vitamin C suggests that vitamin C status is preferably improved by eating foods rich in vitamin C, in addition to not smoking and other dietary habits that prevent ascorbic acid from depletion.