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Biomedical subjects

M Meydani

Publications and source records attributed to M Meydani.

At least 91 records · Page 5Linked to original sources
PubMed1990

Acute phase response in exercise: interaction of age and vitamin E on neutrophils and muscle enzyme release.

Several host defense responses and metabolic reactions that occur during infection have been observed after exercise. We hypothesized that these reactions, known as the "acute phase response," contribute to the breakdown and clearance of damaged tissue after exercise. This hypothesis was tested with 21 male volunteers representing two ranges of age (22-29 and 55-74 yr), who ran downhill on an inclined treadmill to accentuate damaging eccentric muscular contractions. The subject groups were further divided in a double-blind placebo-controlled protocol, which examined the influence of 48 days of dietary vitamin E supplementation before the exercise. All subjects were monitored for 12 days after exercise for changes in circulating leukocytes, superoxide release from neutrophils, lipid peroxidation, and efflux of the intramuscular enzyme creatine kinase (CK) into the circulation. Among those receiving placebo, the less than 30-yr-old subjects responded to exercise with a significantly greater neutrophilia and higher plasma CK concentrations than the greater than 55-yr-old subjects. Dietary supplementation with vitamin E tended to eliminate the differences between the two age groups, primarily by increasing the responses of the greater than 55-yr-old subjects. At the time of peak concentrations in the plasma, CK correlated significantly with superoxide release from neutrophils. The association of enzyme efflux with neutrophil mobilization and function supports the concept that neutrophils are involved in the delayed increase in muscle membrane permeability after damaging exercise.

Acute-Phase Reaction↗
PubMed1989

Effect of aging on in vivo and in vitro ethanol metabolism and its toxicity in F344 rats.

To investigate the effect of aging on ethanol metabolism, 24 male and female F344 rats aged 2 and 12 mo that were fed a laboratory diet received ethanol (1.2 and 2.5 g/kg body wt) intraperitoneally. In male rats, in vivo ethanol elimination significantly decreased according to age both at high (436 +/- 38 vs. 294 +/- 27 mg/kg.h; p less than 0.01) and low (365 +/- 19 vs. 261 +/- 8 mg/kg.h; p less than 0.01) blood ethanol concentrations. Age did not influence the specific activity of hepatic or gastric alcohol dehydrogenase, whereas the activity was significantly decreased with age in the liver (p less than 0.05) and in the stomach (p less than 0.001) when related to body weight. In addition, the activity of the hepatic microsomal ethanol oxidizing system decreased significantly according to age (8.7 +/- 0.5 vs. 6.00 +/- 0.3 nmol/min.mg micr. protein; p less than 0.001). To study the response of ethanol-metabolizing enzymes to chronic ethanol ingestion, 2- and 19-mo-old male F344 rats were pair-fed nutritionally adequate liquid diets containing 36% of total calories either as ethanol or isocaloric carbohydrate for 3 wk. In this experiment specific alcohol dehydrogenase activity was not significantly affected by age, whereas the hepatic microsomal function estimated by the determination of cytochrome P450, microsomal ethanol oxidizing system, and aniline hydroxylation as well as hepatic mitochondrial low Km-acetaldehyde dehydrogenase activity was found to be markedly depressed with age (p less than 0.01). Chronic ethanol consumption increased microsomal enzyme activities in older rats to levels comparable to those observed in young animals prior to ethanol administration. Chronic ethanol feeding also resulted in an increased hepatic fat accumulation, which was significantly enhanced in older rats. In contrast to male rats, in vivo ethanol metabolism was practically identical for 2- and 12-mo-old female rats. These data demonstrate an enhanced toxicity of alcohol in older compared to younger male but not female rats associated with a delay in alcohol elimination both at high and low ethanol blood concentrations and a decrease in ethanol- and acetaldehyde-metabolizing enzyme activities.

Aging↗
PubMed1989

Postprandial changes in the plasma concentration of alpha- and gamma-tocopherol in human subjects fed a fat-rich meal supplemented with fat-soluble vitamins.

The plasma concentrations of alpha (alpha)- and gamma (gamma)-tocopherol in 10 male and 15 female subjects (n = 14) received 1 g fat/kg body wt as soybean oil, and the meal was supplemented with 100% of the RDA for fat-soluble vitamins. In expt. 2, the subjects (n = 11) received 1 g fat/kg body wt as 50% soybean oil + 50% cream, and the meal was supplemented with 200% of the RDA for fat-soluble vitamins. The ratio of gamma- :alpha-tocopherol given in the test meal of expt. 1 was 2.8:1 and in expt. 2 was 0.9:1. Blood samples were obtained 0, 3, 6, 9 and 12 h after the meal. Tocopherol concentration was measured in plasma and lipoprotein fractions. In both studies, plasma triglyceride concentration increased significantly after the meal (P less than 0.001). Mean plasma cholesterol and alpha-tocopherol concentrations were unchanged, but plasma gamma-tocopherol concentration was significantly increased at 6, 9 and 12 h after the meal (P less than 0.05). The increase in plasma gamma-tocopherol was due to increases within the triglyceride-rich lipoprotein (TRL) fraction (d less than 1.006 g/ml) at earlier timepoints, followed by a sustained increase within low density lipoprotein (LDL) and high density lipoprotein (HDL) fractions at later timepoints. In contrast, alpha-tocopherol in LDL and HDL decreased postprandially, concomitant with a rise in TRL alpha-tocopherol. Our results are consistent with the concept that there are differences in the distribution of alpha- and gamma-tocopherol in postprandial lipoproteins.

Adult↗
PubMed1989

Interleukin-1-induced anorexia in the rat. Influence of prostaglandins.

The anorexia associated with acute and chronic inflammatory or infectious conditions is poorly understood. Our objectives were to explore the anorexigenic effects of interleukin-1 (IL-1) in the rat. Recombinant human (rh) IL-1 beta, murine (rm) IL-1 alpha and to a lesser extent rhIL-1 alpha significantly reduced food intake at greater than or equal to 4.0 micrograms/kg i.p. but not at lower doses, in young (200-250 g) meal-fed rats on chow diets. The anorexic effect appears to be mediated by prostaglandins since pretreatment with ibuprofen completely blocked it, and a fish oil based diet abolished it, in comparison to corn oil or chow diets. Fish oil feeding also decreased basal and IL-1 stimulated prostaglandin E2 production by tissues in vitro (liver, brain, peritoneal macrophages) and in the whole body. Constant intravenous infusions of lower doses of IL-1 also diminished food intake, though intravenous boluses did not (reflecting rapid renal clearance). Chronic daily administration of IL-1 caused persistent inhibition of food intake for 7-17 d in chow and corn oil fed rats, but had no effect in fish oil fed rats. There was an attenuation of the effect (tachyphylaxis) after 7 d in corn oil and chow fed rats, but slowed weight gain and lower final weights were observed after 17-32 d of daily IL-1. Old (18-20 mo Fisher 344) rats showed less sensitivity to IL-1 induced anorexia. In conclusion, IL-1 is anorexigenic in the rat, but this is influenced by the structural form of IL-1, the route and chronicity of administration, the source of dietary fat, and the age of the animal. The ability of prior fat intake to influence the anorexic response to IL-1 represents a novel nutrient-nutrient interaction with potential therapeutic implications.

Animals↗
PubMed1988

Effect of dietary vitamin E and selenium on susceptibility of brain regions to lipid peroxidation.

The effect of dietary vitamin E and/or selenium (Se) supplementation (200 IU and/or 0.2 ppm, respectively) or deficiency for two months on lipid peroxidation in cerebrum, cerebellum, mid-brain, and brain stem of one-month-old male F344 rats was investigated. Dietary treatment had a minimal effect on weight gain of rats for the period tested. Plasma alpha-tocopherol (alpha-T) concentration and glutathione peroxidase (GSH-Px) activity were reflective of dietary treatments. Supplementation of diets with vitamin E and/or Se increased plasma alpha-T and/or GSH-Px activity, while diets devoid of these nutrients reduced them significantly. Increased GSH-Px activity in Se-supplemented rats was further enhanced by vitamin E supplementation. Differential concentrations of alpha-T among brain regions were affected by dietary vitamin E but not by Se. In vitro lipid peroxidation of brain homogenates was inhibited by dietary vitamin E supplementation and increased by deficiency. Addition of 0.25 mM ascorbic acid or 0.1 mM of Fe2+ to brain homogenates markedly increased in vitro lipid peroxidation. Ascorbic acid-induced lipid peroxidation was inversely correlated with dietary vitamin E and Se in cerebrum. In vitro Fe2+-addition induced the greatest stimulation of lipid peroxidation, with cerebellum and brain stem of vitamin E-deficient rats showing the highest response to Fe2+ challenge. These findings indicate that concentrations of alpha-T among the brain regions are different and can be altered by dietary vitamin E treatments, cerebellum and brain stem are more susceptible to in vitro challenge by peroxidative agents than other regions, and the degree of lipid peroxidation of brain regions is partially affected by dietary vitamin E but not by Se in the levels tested.

Animals↗
PubMed1988

Fish oil and tocopherol-induced changes in natural killer cell-mediated cytotoxicity and PGE2 synthesis in young and old mice.

Natural killer cell (NK) activity decreases and prostaglandin E2 (PGE2) level increases in aged mice. Because PGE2 is involved in control of NK activity this study was conducted to investigate whether or not decreasing PGE2 level by changing the type of dietary fat or increasing the level of vitamin E (vit. E) modulates NK activity of young and old mice. Mice were fed either a corn oil (CO) or a fish oil (FO) diet supplemented with 30 or 500 mg/kg diet of vit. E for 6 wk. To study the effect of vit. E during active immune response and oxidative stress, groups of old mice fed CO and either 30 or 500 mg/kg diet of vit. E were injected with sheep red blood cells (SRBC) prior to assessment of their NK activity. As reported by others regarding mice fed a nonpurified diet, the old mice in all dietary groups had significantly less NK activity and tended to synthesize more PGE2 than young mice. FO-fed mice synthesized less PGE2 than CO-fed mice; however, their NK activity was not higher than that of CO-fed mice. By contrast young mice fed FO had a moderately lower NK activity than those fed CO. Vit. E supplementation did not change NK activity in nonimmunized mice but was effective in preventing SRBC-induced decrease in NK activity of old mice.

Aging↗
PubMed1988

Enterohepatic circulation of newly administered alpha-tocopherol in the rat.

We have measured the magnitude of the enterohepatic circulation of newly administered [3H]-alpha-tocopherol in rats. One group of animals (day-1 rats) was used to prepare [3H]-alpha-tocopherol-containing lymph. Another set of animals (day-2 rats) was divided into control and vitamin E supplemented (+E) groups, which were used to study the enterohepatic circulation of [3H]-alpha-tocopherol from day-1 rat lymph administered into the jugular vein of day-2 rats. Mesenteric lymph duct and common bile duct cannulations were performed. The enterohepatic circulation in day-2 rats of intrajugularly administered [3H]-alpha-tocopherol in chylomicrons was found to be 1.78 +/- 0.23% for control and 0.98 +/- 0.08% for +E rats (p less than 0.01). A considerable quantity (13.3 +/- 4.3% in control vs 19.2 +/- 4.7% in +E) of [3H]-radioactivity was recovered in bile over 24 h, of which pure [3H]-alpha-tocopherol was 3.17% in control and 1.04% in +E bile. More than 95% of [3H]-radioactivity recovered in day-2 control and +E bile was more polar than alpha-tocopherol shown by high performance liquid chromatography (HPLC). In contrast, more than 95% of [3H]-radioactivity appearing in day-2 lymph was unchanged alpha-tocopherol. Thus, the magnitude of enterohepatic circulation of alpha-tocopherol is very small in rats. Quantitation of the enterohepatic circulation of vitamin E under different physiological conditions remains to be investigated.

Animals↗
PubMed1987

Effect of age and dietary fat (fish, corn and coconut oils) on tocopherol status of C57BL/6Nia mice.

The effect of age and dietary fat type on tocopherol status was investigated using young and old C57BL/6Nia mice fed semipurified diets containing 5% (by weight) fish, corn or coconut oils and supplemented with 30, 100 or 500 ppm dl-alpha-tocopheryl acetate for 6 wk. Tocopherol levels in the diets, plasma, liver, kidney and lung were measured by high performance liquid chromatography following appropriate extractions. The results indicate that mice fed fish oil maintain lower plasma and tissue tocopherol concentrations than those fed corn and coconut oils (fish less than corn oil less than coconut oil). The difference was not due to a loss of tocopherol prior to consumption, but rather appeared to occur during the absorption process. Old mice had lower plasma and liver tocopherol concentrations than young mice. Old mice fed fish oil, however, maintained plasma tocopherol levels better than young mice fed fish oil, presumably due to their larger tocopherol pool. No age effect was detected on kidney and lung tocopherol levels. It is concluded that tocopherol status is affected by age and dietary fat type, especially fish oil.

Aging↗
PubMed1986

Influence of dietary vitamin E, selenium and age on regional distribution of alpha-tocopherol in the rat brain.

Concentrations of alpha-tocopherol (alpha-T) in plasma, cerebrum, cerebellum, midbrain and brain stem and activity of selenium (Se)-dependent glutathione peroxidase (GSH-Px) in plasma were measured in 1- and 15-month-old male F344 rats fed diets containing vitamin E (E, IU/kg) and Se (ppm) in the following combinations: 30 E, 0.1 Se (control diet, minimum requirements); 200 E, 0.2 Se; 0.0 E, 0.2 Se; 200 E, 0.0 Se; 0.0 E, 0.0 Se for 8 or 20 weeks. alpha-T and GSH-Px levels in plasma were reflective of dietary treatment in young rats in which an interaction of the two nutrients was noted. A longer period of dietary vitamin E deficiency was necessary to deplete plasma alpha-T and depress GSH-Px activity significantly in the old rats. Among the brain regions of all ages, cerebrum and midbrain had the highest concentrations of alpha-T while cerebellum showed the lowest. However, cerebellum of young rats and cerebellum and brain stem of old rats had a greater alpha-T accumulation with doubly supplemented diets, whereas only cerebellum of young and old rats showed a marked increase of alpha-T with vitamin E supplementation. In old rats, vitamin E deficiency resulted in greater depletion of alpha-T in cerebellum and brain stem than cerebrum and midbrain regions. Se deficiency in brain stem of young and old rats significantly decreased alpha-T accumulation by vitamin E supplementation. Se supplementation marginally alleviates vitamin E depletion in brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1986

Vitamin E supplementation suppresses prostaglandin E1(2) synthesis and enhances the immune response of aged mice.

The potential for vitamin E to modulate prostaglandin metabolism and alter immune response in aged mice was studied. Semi-purified diets containing 30 ppm or 500 ppm dl-alpha-tocopheryl acetate (VitE) were fed for 6 weeks to young (3 months) and old (24 months) C57BL/6J mice. Delayed hypersensitivity skin test to DNFB and the proliferative response of splenocytes to T- and B-cell mitogens were assessed. Ex-vivo synthesis of Prostaglandin E2 (PGE2) was measured in spleen homogenates and serum vitamin E was measured by HPLC. Vitamin E supplementation of aged mice enhanced percent ear swelling to DNFB as well as the mitogenic response of splenocytes to Con A and LPS (P less than 0.05). Furthermore, spleen homogenates from old mice fed 30 ppm VitE had a significantly higher PGE2 level than young mice fed 30 ppm VitE and old mice fed 500 ppm VitE (3.20 +/- 0.07 micrograms/g vs. 2.60 +/- 0.08 and 2.3 +/- 0.10, respectively). Thus, the vitamin E enhanced immune response of aged mice appears to be mediated by decreased prostaglandin synthesis.

Aging↗
PubMed1986

Photon activation analysis as a new technique for body composition studies.

A study was undertaken to demonstrate the usefulness of the recently developed photon activation analysis (PAA) technique for in vivo body composition studies. PAA can be used for direct measurement of total-body oxygen, nitrogen, and carbon. Sequential measurements were made on rats fed diets of 0%, 4.2%, or 20% protein for 6 1/2 wk, and significant changes in body composition were noted. In addition, rats of different ages, strains, nutritional states, and degrees of obesity were included in a comparison of PAA results in vivo with results from chemical analysis after sacrifice of the animals. High positive correlations were found between PAA measurements of carbon and chemical analysis measurements of fat and between PAA measurements of oxygen and chemical analysis measurements of total-body water. A low positive correlation was found between PAA measurements of nitrogen and chemical analysis measurements of protein.

Activation Analysis↗
PubMed1985

Influence of dietary vitamin E and selenium on the ex-vivo synthesis of prostaglandin E2 in brain regions of young and old rats.

The potential for synthesis of prostaglandin E2 (PGE2) in cerebrum (CC), cerebellum (CM), mid-brain (MB) and brain stem (BS) was measured in 1 and 15 month old male F344 rats fed diets containing 0, 30, or 200 IU vitamin E (-E, E, +E, respectively) and 0.0, 0.1, or 0.2 ppm selenium (-Se, Se, +Se, respectively) for 8 or 20 weeks. Regardless of dietary treatments, the rank order of PGE2 synthesis was CC greater than CM greater than BS = MB in the young rats; CC greater than MB greater than BS = CM in the old rats; and CC greater than MB greater than BS greater than CM in the aged rats. PGE2 synthesis in all brain regions were significantly influenced by dietary treatments except CC. -E diets increased and +E diets decreased PGE2 production. Young rats were most susceptible to PGE2 alteration by vitamin E deficiency while old rats responded most markedly to supplementation. All brain regions showed decreases in their capacity to synthesize PGE2 with age, except MB where the opposite effect was seen. Dietary Se treatment had a minimal role in PGE2 synthesis in gross anatomical regions of brain. The degree to which PGE2 synthesis is affected is more dependent on dietary vitamin E level and tissue alpha-tocopherol content than on Se. CM and BS of aged rats appear to require more alpha-tocopherol to maintain steady state levels than other areas, thus the synthesis of PGE2 in these regions could be highly susceptible to alterations in dietary vitamin E.

Age Factors↗
PubMed1985

Dietary fat unsaturation enhances drug metabolism in cebus but not in squirrel monkeys.

Antipyrine disappearance and sleeping time following barbiturate anesthesia were assessed to evaluate the effects of dietary corn oil and coconut oil on the drug-metabolizing enzyme systems (DMES) in cebus (Cebus albifrons) and squirrel (Saimiri sciureus) monkeys. Plasma antipyrine clearance (half-life) was measured in both species before and after induction of DMES by i.v. injection of barbiturates on two consecutive days. Sleeping time was measured after administration of either pentobarbital or hexobarbital and proved to be the most demonstrable measure of diet-drug interaction. In neither cebus nor squirrel monkeys was antipyrine half-life significantly affected by dietary fat. Sleeping time for the coconut oil-fed squirrel monkeys was shorter than for those fed corn oil, whereas corn oil-fed cebus awoke sooner than the coconut oil-fed cebus. Thus, barbiturate but not antipyrine metabolism in monkeys can be influenced by dietary fat unsaturation, and the effect appears to be species dependent. Genetic differences in phospholipid metabolism are thought to underlie this difference.

Animals↗
PubMed1984

Effects of dietary methionine, methylmercury, and atrazine on ex-vivo synthesis of prostaglandin E1 and thromboxane B2.

The effects of methylmercury hydroxide' (MeHg), atrazine, and dietary methionine on the activity of blood glutathione peroxidase (GSH-Px), total blood glutathione (TGSH) level, and the ex-vivo synthesis of prostaglandin E1 (PGE1) and thromboxane B2 (TXB2) by platelets from clotted blood in rats were studied. One-month-old male Wistar rats were fed different diets (60, 100 or 140% of sulfur amino acids requirement) and treated with atrazine (0 or 500 mg/kg diet), MeHg (0, 0.5 or 1.5 mg Hg/kg/day) orally, or a combination of the two toxicants for 30-35 days. Blood was analyzed for glutathione peroxidase (GSH-Px), total mercury, TGSH, PGE1, and TXB2. The concentration of mercury in the blood was significantly affected by MeHg treatment as well as by its interaction with dietary methionine. Increasing MeHg dose in the diet decreased the activity of whole blood GSH-Px and total blood GSH while increasing ex-vivo synthesis of PGE1 and TXB2. Methionine deficiency caused a slight increase in serum PGE1 level. Overall factorial analysis for TXB2 revealed a highly significant effect of MeHg and methionine as well as their interaction on serum TXB2 level. The effect of atrazine on PGE1 and TXB2 levels was not statistically significant. The possible mechanisms of increased serum PGE1 and TXB2 levels due to MeHg toxicity are discussed.

Alprostadil↗
PubMed1983

Effects of prostaglandin modifiers and zinc deficiency on possibly related functions in rats.

Experiments were conducted to investigate the role of prostaglandins (PG) in zinc absorption and biological functions (food intake and weight gain, alkaline phosphatase activity, T-cell-mediated immune response). PG levels were modified by administering an inhibitor of their synthesis, aspirin or indomethacin in the diet. Zinc level was modified by controlling the dietary concentration. Weanling rats were fed the assigned diets for 1 month after which they were anesthetized with ether. Samples of blood, gut contents and mucosa, liver, lung and tibia were collected for zinc, PG, lymphocyte stimulation with T-cell mitogen, and alkaline phosphatase assays. There was more than 50% inhibition of PG synthesis by indomethacin and aspirin. This inhibition of PG synthesis, however, did not affect the zinc status of the rats as measured by general appearance, food intake, weight gain, organ weight, zinc concentration in different organs, serum alkaline phosphatase activity, and cell-mediated immune response to T-cell mitogens. It is concluded that under physiological conditions inhibitors of PG synthesis do not alter these zinc metabolic functions.

Alkaline Phosphatase↗