Urinary ascorbic acid levels following the withdrawal of large doses of ascorbic acid in guinea pigs

Male guinea pigs received sodium ascorbate solution [equivalent to 1 g ascorbic acid/(kg body weight.d)] by intraperitoneal injection for 4 wk. During the ascorbic acid treatment period, plasma and urinary ascorbic acid levels rose markedly. Three weeks after the ascorbic acid treatment was withdrawn, mean urinary ascorbic acid levels were significantly lower than their corresponding basal levels. At both 2 and 5 wk after withdrawal of ascorbic acid treatment, mean plasma ascorbic acid levels were below normal. The results indicate that these animals had experienced a transient withdrawal effect after administration of large doses of ascorbic acid that lasted about 1 wk. This, in turn, indicates that the rate of ascorbic acid turnover was probably increased during treatment, and this effect persisted even after the ascorbic acid was withdrawn. Examination of data from each individual experimental animal revealed that the pattern of urinary ascorbic acid excretion after the withdrawal of large doses of ascorbic acid varied from animal to animal. Among the twelve experimental guinea pigs, seven had abnormally low urinary ascorbic acid levels 2-4 wk after the withdrawal of the large doses of ascorbic acid.     

Histamine and ascorbic acid: a survey of women in labor at term and significantly before term

In ascorbic acid-requiring species (human, guinea pig), elevations of circulating histamine occur as the result of marginal ascorbic acid status. Marginal ascorbic acid status during pregnancy is associated with preeclampsia, abruption, and prematurity. Furthermore, circulating histamine is known to be elevated in these complications perhaps as a result of placental dysfunction which diminishes normal placental histaminase. We hypothesized that women with preeclampsia and premature labor would have elevated histamine and the lowest concentrations of ascorbic acid. Plasma total whole blood histamine and ascorbic acid were surveyed in women in term (T) and preterm (PT) labor. Blood histamine was elevated in PT compared to T labor but so was plasma ascorbate, indicating that marginal ascorbate status does not cause the elevated circulating histamine observed in PT. However, marginal ascorbate status concomitant with reduced placental histaminase may contribute to further increases in circulating histamine and to any pathology which might result from elevated histamine. Regression analysis of histamine on ascorbate for T and PT labor revealed a significant inverse relationship between ascorbate and histamine only in PT labor (p less than 0.027). An unexpected finding was that a history of maternal cigarette smoking, to a degree which resulted in marginal ascorbic acid status, confounded the relationship between ascorbate and circulating histamine in T labor.     

Effect of a single oral dose of ascorbic acid on body temperature and trace mineral fluxes in healthy men and women.

Several metabolic changes characteristic of the acute-phase response were examined in healthy men and women following a single 1 g dose of ascorbic acid. Utilizing a placebo-controlled, double-blind protocol, oral body temperatures were recorded in rested, fasted subjects (0900 hr) prior to the consumption of 1 g L-ascorbic acid or placebo (n = 10/group). Temperatures were recorded hourly for the next 8 hours, and again the next morning in the rested, fasted state (0900 hr). Blood samples, collected at 0, 4, and 24 hours post-dose, were analyzed for plasma ascorbate, iron, and zinc. Mean oral body temperature was significantly elevated 2 hours post-dose in the experimental subjects compared to controls (+0.7 degrees F, p = 0.03). In the vitamin-dosed subjects, mean plasma ascorbate rose 32% over the control value after 4 hours (1.11 +/? 0.08 and 0.84 +/? 0.06 mg/100 ml, ns). Serum iron levels were similar in the two groups at 0 and 4 hours post-dose, but at 24 hours post-dose mean serum iron of the vitamin-dosed subjects fell to 73% of that recorded for the control subjects (77 +/? 8 and 105 +/? 10 micrograms/100 ml, p = 0.04). Plasma zinc levels were similar for both groups at 0, 4, and 24 hours post-dose. These data indicate that ascorbate administration, at a level commonly supplemented in the US diet, elicits several host metabolic responses similar to those observed following exposure to infectious or inflammatory agents. These metabolic changes are most likely due to the reducing potential of the vitamin and may factor in the reported prophylactic success of vitamin C supplementation.     

Effect of a single oral dose of ascorbic acid on body temperature and trace mineral fluxes in healthy men and women

Several metabolic changes characteristic of the acute-phase response were examined in healthy men and women following a single 1 g dose of ascorbic acid. Utilizing a placebo-controlled, double-blind protocol, oral body temperatures were recorded in rested, fasted subjects (0900 hr) prior to the consumption of 1 g L-ascorbic acid or placebo (n = 10/group). Temperatures were recorded hourly for the next 8 hours, and again the next morning in the rested, fasted state (0900 hr). Blood samples, collected at 0, 4, and 24 hours post-dose, were analyzed for plasma ascorbate, iron, and zinc. Mean oral body temperature was significantly elevated 2 hours post-dose in the experimental subjects compared to controls (+0.7 degrees F, p = 0.03). In the vitamin-dosed subjects, mean plasma ascorbate rose 32% over the control value after 4 hours (1.11 +/- 0.08 and 0.84 +/- 0.06 mg/100 ml, ns). Serum iron levels were similar in the two groups at 0 and 4 hours post-dose, but at 24 hours post-dose mean serum iron of the vitamin-dosed subjects fell to 73% of that recorded for the control subjects (77 +/- 8 and 105 +/- 10 micrograms/100 ml, p = 0.04). Plasma zinc levels were similar for both groups at 0, 4, and 24 hours post-dose. These data indicate that ascorbate administration, at a level commonly supplemented in the US diet, elicits several host metabolic responses similar to those observed following exposure to infectious or inflammatory agents. These metabolic changes are most likely due to the reducing potential of the vitamin and may factor in the reported prophylactic success of vitamin C supplementation.     

Effect of ascorbic acid nutriture on blood histamine and neutrophil chemotaxis in guinea pigs

Histamine suppresses certain immune responses, including neutrophil chemotaxis. The present study examined whether the histamine-lowering effect of ascorbate was accompanied by enhanced chemotaxis in guinea pigs. Animals were fed low ascorbate, adequate or high ascorbate diets (0.5, 2.0 or 50 mg ascorbate.100 g body wt-1.d-1) for 4 wk. Mean liver ascorbate paralleled dietary intake, and these values differed significantly. Blood histamine was significantly depressed in the high ascorbate group compared to the adequate and low ascorbate groups, and liver ascorbate was inversely correlated to blood histamine levels (r = -0.64, P less than 0.001). The random migration of neutrophils was not significantly affected by vitamin dosage. Leukocyte chemotaxis was significantly impaired in low ascorbate animals compared to that of animals with adequate ascorbate nutriture. Leukocyte chemotaxis in high ascorbate animals did not differ significantly from that in the adequate or low ascorbate groups. Furthermore, chemotaxis was significantly lower when cells extracted from animals with adequate ascorbate nutriture were incubated in low ascorbate or high ascorbate serum rather than in autologous serum. These data suggest that the histamine-lowering effect of supplemental ascorbate does not appear to enhance leukocyte chemotaxis and that serum from guinea pigs fed low or high levels of ascorbate appears to contain factors that depress chemotaxis.     

Levels of minerals in serum and urine of guinea pigs following intraperitoneal administration of ascorbate

The effect of ascorbic acid administration on the levels of urinary and serum mineral nutrients, Ca, Cu, Fe, K, Mg, Mn, Na and Zn in guinea pigs has been studied. Male guinea pigs received sodium ascorbate solution (equivalent to 1 g ascorbic acid/kg body weight/day) by intraperitoneal injection for 4 weeks. During the ascorbic acid treatment period, serum and urinary ascorbic acid rose markedly. The large quantities of ascorbic acid intake did not influence serum levels of all eight minerals studied when experimental values were compared with controls using the two-tailed Student's t-test. However, when the one-tailed t-test was used, serum copper and zinc levels of the experimental guinea pigs were significantly lower than their respective control values. Excepting sodium, derived from injected sodium ascorbate, no differences in daily urinary excretion of the other seven minerals were observed.     

Cerebrospinal fluid ascorbic acid levels during the neonatal period.

Corresponding plasma and cerebrospinal fluid ascorbic acid levels were determined in 13 term and 17 preterm newborn infants during the neonatal period. On the first day of life preterm C.S.F ascorbate value of 5.2 +/- 0.8 mg/dl (mean +/- S.E.) was higher than the 3.8 +/- 0.3 mg/dl value in term infants (P less than 0.1). Later determinations during the neonatal period did not demonstrate a difference between term and preterm C.S.F ascorbate values and levelled at 2.9 +/- 0.2 mg/dl. There was a significant negative correlation between the C.S.F/plasma ascorbate ratio and the plasma ascorbate levels and the shape of the regression line was suggestive of a saturable active ascorbate transport from the plasma into the cerebrospinal fluid. Ascorbic acid in the C.S.F of additional six neonates with a neurological disorder was lower than expected on the basis of their plasma levels, the C.S.F/plasma ascorbate ratios being 8.3 +/- 0.9 in the apparently normal infants and 3.7 +/- 0.6 in the neurological patients, (P less than 0.025). The possible mechanism of ascorbate loss from the central nervous system is discussed and it is speculated that ascorbic acid administration following a neurological insult may prove beneficial.     

Long-term effects of inadequate and excessive dietary ascorbate on bile acid metabolism in the guinea pig

The effects of long-term chronic ascorbic acid deficiency and excessive ascorbic acid consumption on bile acid metabolism and biliary lipid composition were studied in guinea pigs. Male, weanling guinea pigs were fed a cereal-based scorbutigenic diet for 19 or 21 weeks. Ascorbic acid was administered either orally at 0.15 (group A) or 2.0 (group B) mg/100 g body weight, or it was mixed in the diet at levels of 500 (group C), 16-22 (group D), or 20,000 mg/kg (group E). Chronic ascorbic acid deficiency (groups A and D) caused depression of hepatic cytochrome P-450 levels and elevation of plasma cholesterol. Excessive ascorbate consumption did not alter these parameters relative to control levels. In contrast to results obtained in guinea pigs fed low or high amounts of ascorbate for 7-9 weeks, prolonged consumption of inadequate or excessive ascorbate resulted in little or no change in bile acid metabolism and biliary lipid composition except that bile acid pool size was increased 12% as a result of excessive ascorbate ingestion. Results of the present study suggest that there may be important differences in the guinea pig's metabolic response to ascorbic acid deficiency and ascorbic acid excess, depending on the length of the experimental period.     

Influence of erythorbic acid on ascorbic acid retention and elimination in the mouse

Large quantities of ascorbic acid or erythorbic acid were administered to Swiss mice over a period of seven months. Urinary ascorbic acid and erythorbic acid were determined two weeks before termination of the experiment. At the end of the experiment, ascorbic acid and erythorbic acid contents in plasma, liver and brain tissues were measured. In the ascorbic acid-treated mice, there was a marked elevation in plasma and urine ascorbate levels, and there was a 38% increase of ascorbate level in the liver but there was no substantial increase in ascorbate levels in the four brain regions studied, namely the cerebrum, cerebellum, medulla and brain stem, upon large intake of ascorbic acid. In the erythorbic acid-treated mice, erythorbic acid is well absorbed by the gastrointestinal tract, enters the blood stream, and is rapidly excreted in the urine. The results show that erythorbic acid is able to replace 45% of ascorbic acid in the liver and 28-39% of ascorbic acid in the brain tissues. Although erythorbic acid appears in the blood at significantly high level, it does not lower blood ascorbate levels.     

Testosterone enanthate a possible reversible male contraceptive

The effect of chronic treatment with testosterone enanthate (TE) on sperm production and plasma testosterone levels was evaluated in 16 healthy male volunteers. During the induction of azoospermia each subject received 200 mg TE twice a week for 2 weeks once a week for 2 weeks, and once every other week for a month. Subsequently an attempt was made to maintain azoospermia by administration of 200 mg TE every 3 weeks. The induction phase resulted in suppression of sperm production to azoospermia or oligospermia of less than 100,000/ml. However, the schedule of injections during the maintenance phase did not maintain the azoospermic state. Consequently, the frequency of injections for maintenance was increased to 200 mg TE every 2 weeks. This maintained sperm counts below 3 million/ml in all subjects. Thereafter the maintenance schedule was changed to 200 mg TE every 10–12 days; on this regimen, azoospermia or oligospermia of less than 100,000/ml was maintained in all subjects. Blood testosterone levels rose approximately 100% over the baseline level during the induction phase but returned to pretreatment range during maintenance phase.This study demonstrates that testosterone enanthate can induce azoospermia and maintain the azoospermic state without elevation of circulating testosterone levels outside the pretreatment range. These findings suggest the feasibility of using a testosterone preparation as an effective male contraceptive. A larger number of subjects must be evaluated to determine the exact dose requirements and the possibility of side effects subsequent to chronic administration of this steroid.     

Effects of chronic ethanol exposure on sleep in rats.

Sleep disturbance is a common complaint in alcoholics. When polysomnographic studies are performed in alcoholics, reductions in slow wave sleep are a common finding; however, few studies have evaluated the effects of chronic alcohol exposure on sleep in animal models. In the present study, the sleep EEG was evaluated in 40 Wistar rats who were exposed to chronic alcohol or control conditions in vapor chambers. Rats were exposed to ethanol vapors or control chambers for 6 weeks and then withdrawn. Sleep EEG was recorded before exposure (baseline), immediately following exposure, and 5 weeks after withdrawal from the ethanol/control chambers. In the ethanol-exposed animals, blood ethanol levels averaged 192 mg/dL over 6 weeks of exposure. Chronic ethanol exposure and withdrawal was not found to affect either slow wave sleep latency or slow wave sleep duration; however, overall spectral power as well as power in the delta, theta, and beta frequencies were significantly reduced following chronic exposure (2-4 Hz, [F(1, 17) = 18.11, p = 0.001], 4-6 Hz, [F(1, 17) = 15.98, p = 0.001], 6-8 Hz [F(1, 17) = 15.52, p = 0.001], 8-16 Hz band [F(1, 17) = 18.73, p < 0.0001], 16-32 Hz [F(1, 17) = 10.13, p = 0.005], and 1-50 Hz [F(1, 17) = 17.03, p = 0.001]. After 5 weeks of withdrawal, significant decreases still persisted in the delta and theta frequencies (2-4 Hz [F(1, 16) = 6.21, 0.024], 4-6 Hz [F(1, 16) = 6.26, 0.024], and 6-8 Hz [F(1, 16) = 4.84, p = 0.043]). These findings suggest that spectral analysis of the EEG is a highly sensitive measure of the effects of ethanol on sleep. These findings additionally demonstrate that chronic ethanol exposure can produce persistent diminution in the systems that generate cortical slow waves in the rat and thus may provide a model for understanding the mechanisms underlying sleep disturbances associated with alcoholism.     

Effects of elevated d-alpha(RRR)-tocopherol dosage in man

A study was conducted to investigate the effects of a megadosage of free RRR-alpha-tocopherol in healthy college student volunteers. Of 19 volunteers, 14 were given daily doses of 600 mg (900 IU) of RRR-alpha-tocopherol for 12 weeks, and the remaining 5 were given identical placebo capsules. The investigation was performed by the single-blind method. Alpha-tocopherol levels were measured in plasma, red blood cells (RBCs), platelets, leucocytes (WBCs), and buccal mucosal cells. Alpha-tocopherol in plasma, RBCs, and WBCs rose, reached a maximum level 4 weeks after commencement of administration, and then remained at a plateau, while platelet and buccal cell levels reached a maximum level after 12 weeks of administration. The maximum levels in all the subjects were 2.5 to 3 times the baseline values. During the study, there were no changes in laboratory values for thyroid, liver, or kidney functions, and coagulation activity (including the vitamin K-dependent Hepaplastin test and PIVKA-II) or immunoglobulin levels. Healthy status continued without any abnormal symptoms, and without any subjective complaints on the questionnaire. In the control group also, no changes occurred during the investigation. Gamma-tocopherol changes were measured in plasma and RBCs. As plasma and RBC tocopherol levels rose after administration, the isomer levels were suppressed in both plasma and RBCs.     

Time-course of the change in blood pressure level in magnesium-deficient Wistar rats

The aim of the present study was to determine whether a severely Mg-deficient diet can modify blood pressure in rats and whether these alterations in blood pressure are associated with a change in in vivo cardiovascular reactivity, alteration in plasma lipids and modification of the production of hormones involved in blood pressure regulation. Weanling male Wistar rats were pair-fed for 40 weeks with control (960 mg Mg/kg) and Mg-deficient (80 mg Mg/kg) diets. At 2 weeks, blood pressure was lower in Mg-deficient rats, while heart rate was greater than in controls. Mg-deficiency-induced hypotension was transitory and the administration of antihistamine agents inhibited the appearance of this hypotensive phase, suggesting that histamine may play a role in lowering blood pressure. Until 15 weeks, blood pressures were similar for control and Mg-deficient rats. Thereafter, blood pressure rose gradually until the end of the experiment in Mg-deficient rats. Heart rate remained higher in hypertensive Mg-deficient rats. After 21 weeks, in vivo cardiovascular reactivity to noradrenaline was lower and reactivity to angiotensin II was unchanged in hypertensive Mg-deficient rats. At 2 and 21 weeks, hypomagnesaemia was accompanied by higher plasma levels of Ca, triacylglycerols and cholesterol. Plasma renin activity was higher at week 2, whereas levels of plasma angiotensin converting enzyme were lower at 2 and 21 weeks in Mg-deficient rats. The plasma aldosterone level was higher at 2 and 21 weeks while the vasopressin level did not change. Plasma corticosterone levels were lower at 2 weeks and higher at 21 weeks. It is concluded that Mg deficiency induced a transitory hypotension followed by a sustained hypertension in rats. The release of vasodilator inflammatory agents may contribute to the early hypotension. The hypertensive phase may be explained by the increased sympathetic nervous activity induced by Mg deficiency even though the contribution of several hormonal systems implicated in blood pressure regulation remains to be elucidated.     

Prolonged vitamin C supplementation and recovery from demanding exercise

The aim of the present study was to investigate whether 2 weeks of vitamin C supplementation affects recovery from an unaccustomed bout of exercise. Sixteen male subjects were allocated to either a placebo (P; n = 8) or vitamin C group (VC; n = 8). The VC group consumed 200 mg of ascorbic acid twice a day, whereas the P group consumed identical capsules containing 200 mg of lactose. Subjects performed a prolonged (90-min) intermittent shuttle-running test 14 days after supplementation began. Post-exercise serum creatine kinase activities and myoglobin concentrations were unaffected by supplementation. However, vitamin C supplementation had modest beneficial effects on muscle soreness, muscle function, and plasma concentrations of malondialdehyde. Furthermore, although plasma interleukin-6 increased immediately after exercise in both groups, values in the VC group were lower than in the P group 2 hours after exercise (p < .05). These results suggest that prolonged vitamin C supplementation has some modest beneficial effects on recovery from unaccustomed exercise.     

Cholesterol-lowering effects of plant sterol esters and non-esterified stanols in margarine, butter and low-fat foods.

OBJECTIVES: To determine the efficacy on plasma cholesterol-lowering of plant sterol esters or non-esterified stanols eaten within low-fat foods as well as margarine. DESIGN: Randomised, controlled, single-blind study with sterol esters and non-esterified plant stanols provided in breakfast cereal, bread and spreads. Study 1 comprised 12 weeks during which sterol esters (2.4 g) and stanol (2.4 g)-containing foods were eaten during 4 week test periods of cross-over design following a 4 week control food period. In Study 2, in a random order cross-over design, a 50% dairy fat spread with or without 2.4 g sterol esters daily was tested. SUBJECTS: Hypercholesterolaemic subjects; 22 in study 1 and 15 in study 2. MAIN OUTCOME MEASURES: Plasma lipids, plasma sterols, plasma carotenoids and tocopherols. RESULTS: Study 1-median LDL cholesterol was reduced by the sterol esters (-13.6%; P<0.001 by ANOVA on ranks; P<0.05 by pairwise comparison) and by stanols (-8.3%; P=0.003, ANOVA and <0.05 pairwise comparison). With sterol esters plasma plant sterol levels rose (35% for sitosterol, 51% for campesterol; P<0.001); plasma lathosterol rose 20% (P=0.03), indicating compensatory increased cholesterol synthesis. With stanols, plasma sitosterol fell 22% (P=0.004), indicating less cholesterol absorption. None of the four carotenoids measured in plasma changed significantly. In study 2, median LDL cholesterol rose 6.5% with dairy spread and fell 12.2% with the sitosterol ester fortified spread (P=0.03 ANOVA and <5% pairwise comparison). CONCLUSION: 1. Plant sterol esters and non-esterified stanols, two-thirds of which were incorporated into low-fat foods, contributed effectively to LDL cholesterol lowering, extending the range of potential foods. 2. The LDL cholesterol-raising effect of butter fat could be countered by including sterol esters. 3. Plasma carotenoids and tocopherols were not reduced in this study. SPONSORSHIP: Meadow Lea Foods, Australia.     

Vitamin C status and physical working capacity in adolescents

The effect of ascorbic acid supplementation on physical working capacity was studied in young adolescent boys in which the concomitant biochemical riboflavin and pyridoxin deficiencies were corrected by medicamentous prophylaxis. After daily administration for two months of 70 mg ascorbic acid, the mean plasma vitamin C in the experimental group (n = 49) rose from 0.33 to 1.49 mg/dl (p less than 0.001) and the prevalence of deficient plasma vitamin C values (less than 0.20 mg/dl) decreased from 52.3 percent to zero. The improvement in vitamin C biochemical status was also accompanied by a statistically significant increase in VO2 max. (p less than 0.01). There were no significant changes neither in the mean plasma vitamin C values nor in the mean VO2 max. in the control group subjects (n = 42). The increase in VO2 max. in the experimental group was primarily the result of an increase of VO2 max. in subjects with initially lower values. When data from both experimental and control groups were pooled together, a positive and significant association was found between VO2 max. and the increase of plasma vitamin C values below 1.0 mg/dl. No further increase in VO2 max. was observed when vitamin C plasma values reached 1.0 mg/dl or more. The two regression lines crossed at X = 0.86 mg/dl. This cut off point of plasma vitamin C level corresponds to a dietary intake of about 80 mg of ascorbic acid per day. The results of this study are in agreement with the suggested optimal ascorbic acid daily intake obtained by kinetic studies with (1-14C) ascorbic acid.     

Vitamin C pharmacokinetics of plain and slow release formulations in smokers

BACKGROUND & AIMS: Combination of the antioxidants ascorbic acid in slow release formulation and alpha-tocopherol can retard the progression of atherosclerosis. In order to determine if differences in formulation could explain some of the different results in the intervention trials we determined selected pharmacokinetics for two different formulations of ascorbic acid together with alpha-tocopherol. METHODS: Single-blinded, randomised, placebo-controlled intervention study with 48 healthy men, aged 20-65 years, smoking > or = 5 cigarettes/day. Subjects received 250 mg plain release ascorbic acid and 91 mg plain release d-alpha-tocopheryl acetate, 250 mg slow release ascorbic acid and 91 mg plain release d-alpha-tocopheryl acetate or placebo twice daily for 4 weeks. A series of blood samples were collected after administration of the first dose and repeated after 4 weeks of supplementation. RESULTS: The fluctuation of ascorbic acid plasma concentrations decreased significantly (P = 0.003) after 4 weeks supplementation in the slow versus the plain release group. CONCLUSIONS: This study shows that there were pharmacokinetic differences between plain and slow release formulations of ascorbic acid. However, these effects are small and unlikely to be of significant clinical importance.     

Bioavailability of vitamin C from mashed potatoes and potato chips after oral administration in healthy Japanese men

Potato (Solanum tuberosum) tubers contain vitamin C (VC) and commercial potato chips have more VC content per wet weight by dehydration during frying. However, intestinal absorption of VC from orally ingested potatoes and its transfer to the blood remains questionable. The present study was designed to determine whether the dietary consumption of potatoes affects VC concentration in plasma and urinary excretion of VC in human subjects. After overnight fasting, five healthy Japanese men between 22 and 27 years of age consumed 87 g mashed potatoes and 282 g potato chips. Each portion contained 50 mg of VC, 50 mg VC in mineral water and mineral water. Before and after a single episode of ingestion, blood and urine samples were collected every 30 min or 1 h for 8 h. When measured by subtraction of the initial baseline value before administration of potatoes from the values measured throughout the 8 h test period, plasma VC concentrations increased almost linearly up to 3 h. Subsequently, the values of potato-fed subjects were higher than those of water, but did not differ significantly from those of VC in water (P = 0·14 and P = 0·5). Less VC tended to be excreted in urine during the 8 h test than VC in water alone (17·0 (sem 7·5) and 25·9 (sem 8·8) v. 47·9 (sem 17·9) μmol/mmol creatinine). Upon human consumption, mashed potatoes and potato chips provide VC content that is effectively absorbed in the intestine and transferred to the blood. Clearly, potatoes are a readily available source of dietary VC.     

Protonated nanostructured aluminosilicate (NSAS) reduces plasma cholesterol concentrations and atherosclerotic lesions in Apolipoprotein E deficient mice fed a high cholesterol and high fat diet

The aim of this work was to assess the effect of chronic administration of protonated nanostructured aluminosilicate (NSAS) on the plasma cholesterol levels and development of atherosclerotic lesions in Apolipoprotein (ApoE) deficient mice fed a high cholesterol and high fat diet. Apolipoprotein E (ApoE) deficient mice were divided into the following treatment groups: protonated NSAS 1.4% (w/w), untreated control and 2% (w/w) stigmastanol mixed with high-cholesterol/high-fat diet. Animals were treated for 12 weeks, blood samples were withdrawn every 4 weeks for determination of plasma cholesterol and triglyceride levels. At the end of the study the aortic roots were harvested for assessment of atherosclerotic lesions. NSAS at 1.4% (w/w) and stigmastanol at 2% (w/w) treatment groups showed significant decreases in plasma cholesterol concentrations at all time points relative to the control animals. The lesion sum area in 1.4% (w/w) NSAS and 2% (w/w) stigmastanol groups were significantly less from the control animals. In conclusion, in this study, the effectiveness of chronic administration of protonated NSAS material in the reduction of plasma cholesterol levels and decrease in development of atherosclerotic lesions was demonstrated in Apo-E deficient mice model.     

Acute and chronic ethanol alter somatosensory-evoked potentials in conscious rats.

This study examined the effects of acute and chronic ethanol on cortical somatosensory-evoked potentials (SEPs) of laboratory rats. Evoked potentials were recorded following stimulation of the left hindpaw before and after injection of either saline or ethanol. Animals were then chronically exposed to ethanol in vapor inhalation chambers for five weeks. Recordings of SEPs before and after acute ethanol injection were then obtained 24 h and again seven days after withdrawal from ethanol exposure. The results indicate that acute ethanol produced a dose-dependent reduction in SEP amplitude, but did not alter peak latencies. Chronic ethanol exposure and withdrawal resulted in a significant increase in preinjection baseline response amplitudes when measured at 24 h after withdrawal, but not at seven days, and this treatment did not alter response latency or the effects of acute ethanol administration.