Biomedical subjects

M Meydani

Publications and source records attributed to M Meydani.

At least 55 records · Page 3Linked to original sources

PubMed1997

Vitamin E inhibits low-density lipoprotein-induced adhesion of monocytes to human aortic endothelial cells in vitro.

Monocyte adhesion to human aortic endothelial cells (ECs) is one of the early events in the development of atherogenesis. ECs were used to investigate the role of vitamin E in human monocyte adhesion to ECs in vitro. ECs incubated with 40 to 193 mg/dL of low-density lipoprotein cholesterol (LDL) for 22 hours exhibited increasing dose-dependent adherence for untreated, isolated human monocytes (P < .05). ECs exposed to the highest dose of LDL (193 mg/dL) but pretreated with 19 mumol/L alpha-tocopherol for 24 hours showed a trend to lower adherence for monocytes compared with non-treated ECs (4.4 +/- 1.2% versus 7.6 +/- 1.9%; P = .09). This effect of vitamin E became more significant (P < .05) when ECs were exposed to a lower level of LDL (40 mg/dL) or were pretreated with a higher level of alpha-tocopherol (42 mumol/L) and then exposed to 80 mg/dL LDL. Presupplementation of ECs with 15, 19, and 37 mumol/L alpha-tocopherol significantly (P < .05) reduced monocyte adhesion by 6 +/- 1%, 37 +/- 6%, and 69 +/- 17%, respectively. Levels of soluble intercellular adhesion molecule-1 (sICAM-1), one of the adhesion molecules for monocytes, increased after incubation of ECs with LDL 80 mg/dL (4.7 +/- 0.7 versus 6.4 +/- 1.2 ng/mL, respectively; P < .05). Treatment of ECs with alpha-tocopherol (42 mumol/L) significantly reduced induction of sICAM-1 by LDL to 2.2 +/- 2.3 ng/mL. After exposure to LDL, prostaglandin I2 production by ECs was diminished, whereas presupplementation of ECs with alpha-tocopherol partially reversed the LDL effect. Production of interleukin-1 beta was not detectable when ECs were treated with alpha-tocopherol, LDL, or alpha-tocopherol followed by LDL. Our findings indicate that vitamin E has an inhibitory effect on LDL-induced production of adhesion molecules and adhesion of monocytes to ECs via its antioxidant function and/or its direct regulatory effect on sICAM-1 expression.

Aorta↗

PubMed1997

A closer look at vitamin E. Can this antioxidant prevent chronic diseases?

Vitamin E, the most effective natural free radical scavenger identified to date, is taking America by storm-and apparently for good reason. Reports of benefits ranging from Improved Immunity to prevention of cancer and cardiovascular disease are appearing regularly. In this article, the authors review the scientific literature to help you evaluate whether patients might benefit from supplemental vitamin E.

Cardiovascular Diseases↗

PubMed1996

Effect of vitamin E on hydrogen peroxide production by human vascular endothelial cells after hypoxia/reoxygenation.

Changes in oxidative stress status play an important role in tissue injury associated with ischemia -- reperfusion events such as those that occur during stroke and myocardial infarction. Endothelial cells (EC) from human saphenous vein and aorta were incubated for 22 h and found to take up vitamin E from media containing 0-60 mM vitamin E in a dose-dependent manner. EC supplemented with 23 or 28 mM vitamin E in the media for 22 h were maintained at normoxia (20% O2, 5% CO2, and balance N2) or exposed to hypoxic conditions (3% O2, 5% CO2, and balance N2) for 12 h, followed by reoxygenation (20% O2) for 30 min. Saphenous EC supplemented with 23 mM vitamin E produced less (p < 0.05) H2O2 than unsupplemented controls, both at normoxic condition (supplemented: 4.9 +/- 0.05 vs. control: 10.9 +/- 1.3 pmol/min/10(6) cells) and following hypoxia/reoxygenation (supplemented: 6.4 +/- 0.78 vs. control: 17.0 +/- 2.7 nmol/min/10(6) cells). In contrast, aortic EC, which were found to have higher superoxide dismutase and catalase activity than EC from saphenous vein, did not produce any detectable levels of H2O2. Following hypoxia/reoxygenation, the concentration of vitamin E in supplemented saphenous EC was 62% lower than cells maintained at normoxia (0.19 +/- 0.03 vs. 0.5 +/- 0.12 nmoles/10(6) cells, p < 0.001); in aortic EC vitamin E content was reduced by 18% following reoxygenation (0.86 +/- 0.16 vs. 0.70 +/- 0.09 nmoles/10(6) cells, p < 0.05). Therefore, enrichment of vitamin E in EC decreases H2O2 production and thus may reduce the injury associated with ischemia-reperfusion events.

Antioxidants↗

PubMed1996

Effect of vitamin E on human aortic endothelial cell responses to oxidative injury.

Reactive oxygen species produced by the cells present in the arterial wall may cause oxidative damage to cellular components altering endothelial cell (EC) function. Changes in the EC function appear to play a key role in the pathogenesis of atherosclerosis. Human aortic endothelial cells (HAEC) were employed to investigate the protective role of vitamin E upon exposure of endothelial cells to oxidative stress in vitro. HAEC assimilate d-alpha-tocopherol from the media in a dose-dependent manner. Exposure of HAEC to 16.5 mM of the free radical generator 2,2'-azobis (2-amidinopropane) hydrochloride (AAPH) for 16 h decreased cell viability (assessed by trypan blue exclusion) from 90 to 28%. HAEC preincubated with vitamin E at 15, 30, and 60 microM prior to the AAPH exposure resulted in a dose-dependent increase in resistance to oxidative stress and increased cell viability by 37, 66, and 85%, respectively. An increase in prostacyclin (PGI2) production by HAEC in response to AAPH exposure was correlated positively with cell damage and negatively with vitamin E concentration. Interleukin (IL)-1 production also increased in parallel with cell damage induced by AAPH. Vitamin E treatment significantly reduced IL-1 production after AAPH exposure. This modulatory role of vitamin E on HAEC function following exposure to an oxidative stress may reflect its antioxidant protection against lipid peroxidation.

Amidines↗

PubMed1996

Immunologic effects of marine- and plant-derived n-3 polyunsaturated fatty acids in nonhuman primates.

The effect of marine- and plant-derived n-3 polyunsaturated fatty acids (PUFAs) on T cell-mediated immune response was studied in cynomolgus monkeys. Animals were first fed a 14-wk baseline diet; 10 animals were then fed diets containing 1.3% or 3.3% of energy as eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) which the other 10 were fed diets containing 3.5% or 5.3% of energy as alpha-linolenic acid (ALA) for two consecutive 14-wk periods. Both diets significantly decreased the percentage of T cells (except 1.3% EPA + DHA), T helper cells (except 1.3% EPA + DHA and 3.5% ALA), and T suppressor cells. Proliferative response of lymphocytes to T cell mitogens significantly increased after the diet containing 3.3% EPA + DHA. Interleukin 2 production significantly increased after the diets containing 1.3% and 3.3% EPA + DHA. No significant changes in mitogenic response or interleukin 2 production were found after ALA diets. Feeding 1.3% or 3.3% EPA + DHA or 5.3% ALA significantly suppressed prostaglandin E2 production in response to T cell mitogens. Plasma tocopherol concentrations were decreased significantly only in monkeys fed ALA diets. We conclude that after adjustment for the tocopherol concentration, marine-derived n-3 PUFAs but not plant-derived n-3 PUFAs increased T cell-mediated mitogenic response and interleukin 2 production. This is most likely due to diet-induced quantitative differences in cellular fatty acid composition and, thus, in prostaglandin E2 production and tocopherol status.

Animals↗

PubMed1996

Carotenoid and tocopherol concentrations in plasma, peripheral blood mononuclear cells, and red blood cells after long-term beta-carotene supplementation in men.

To determine the effects of long-term beta-carotene supplementation on concentrations of carotenoids and tocopherols in plasma and in blood cells, fasting blood was collected from 73 randomly selected physicians from the Boston area who are participating in the Physicians Health Study (PHS). The PHS is a randomized, placebo-controlled, double-blind study. In 1982, 22,071 male physicians were assigned to one of four treatments (325 mg aspirin alone, 50 mg beta-carotene alone, both, or neither) every other day. Plasma, peripheral blood mononuclear cells (PBMCs), and red blood cells (RBCs) from physicians who have participated in the study for approximately 12 y were analyzed for carotenoids and tocopherols. Compared with the placebo group, the supplemented group had higher beta-carotene concentrations in plasma (1.73+/-0.16 compared with 0.54+/-0.06 micromol/L0, RBCs (91.5+/-9.7 compared with 31.2+/-4.2 pmol/g hemoglobin), and PBMCs (61.6+/-10.3 compared with 15.5+/-2.5 pmol/10(7) cells). There were no differences in other carotenoids or tocopherols in plasma, RBCs, and PBMCs between these two groups. The beta-carotene concentrations. Plasma cryptoxanthin correlated with both RBC and PBMC cryptoxanthin concentrations but plasma lycopene correlated only with PBMC lycopene concentrations. These data suggest that plasma may not be the best indicator of carotenoid status. Furthermore, long-term beta-carotene supplementation in men results in higher beta-carotene concentrations in plasma, RBCs and PBMCs without lowering concentrations of other carotenoids or tocopherols.

Aged↗

PubMed1996

Fatty acid-related functions.

The first recommendations for specific nutrient quantities that must be obtained to support health were made by the US Department of Agriculture before 1939. Hazel Stiebeling was the leader of this effort and the scientific background was published in the Yearbook of Agriculture. The recommendations clearly stated that food must be available to provide the nutrients to support health. The science of nutrition in the United States is engaged in the most thorough review and reexamination of the recommended dietary allowances in at least a generation of nutrition scientists. There is a new awareness of nutrition complexity and the likelihood of identification of new essential nutrients. This meeting was devoted to the search for functional endpoints to reach quantitative estimates of dietary substances needed to support a function. Included in that concept is determining a range of individual needs and identifying factors that alter these needs. We give the rationale for endpoints of fatty acid metabolism related to platelets and the risk of thrombosis, give the rationale for the recommendation for a new nutrient, and show the necessity for including nutrient interaction in the determination of needs for two nutrients.

Blood Platelets↗

PubMed1996

Natural killer cell activity in elderly men is enhanced by beta-carotene supplementation.

Natural killer (NK) cell activity has been postulated to be an immunologic link between beta-carotene and cancer prevention. In a cross-sectional, placebo-controlled, double-blind study we examined the effect of 10-12 y of beta-carotene supplementation (50 mg on alternate days) on NK cell activity in 59 (38 middle-aged men, 51-64 y; 21 elderly men, 65-86 y) Boston area participants in the Physicians' Health Study. No significant difference was seen in NK cell activity due to beta-carotene supplementation in the middle-aged group. The elderly men had significantly lower NK cell activity than the middle-aged men; however, there was no age-associated difference in NK cell activity in men supplemented with beta-carotene. beta-carotene-supplemented elderly men had significantly greater NK cell activity than elderly men receiving placebo. The reason for this is unknown; however, it was not due to an increase in the percentage of NK cells, nor to an increase in interleukin 2 (IL-2) receptor expression, nor to IL-2 production. beta-carotene may be acting directly on one or more of the lytic stages of NK cell cytotoxicity, or on NK cell activity-enhancing cytokines other than IL-2, such as IL-12. Our results show that long-term beta-carotene supplementation enhances NK cell activity in elderly men, which may be beneficial for viral and tumoral surveillance.

Aged↗

PubMed1995

Damage to cultured lens epithelial cells of squirrels and rabbits by UV-A (99.9%) plus UV-B (0.1%) radiation and alpha tocopherol protection.

The purpose of this research is to observe the near-UV radiation induced damage to cultured rabbit and squirrel lens epithelial cells as related to destruction and alterations of specific biochemical targets in the cells and to determine protective effects on the cells and targets that are provided by alpha-tocopherol. Confluent monolayers of cultured rabbit and squirrel lens epithelial cells were exposed to black light (BL) lamps, which emit predominantly UV-A radiation. These cells received a mixture 3 J/cm2 of UV-A and 4 mJ/cm2 of UV-B per h. This mixture is termed near UVA (i.e.: predominantly UV-A). Cells were exposed in Tyrode's or in MEM without or with alpha-tocopherol added at 2.5-10 micrograms/ml. Analyses of cell viability and survival, the physical state of cytoskeletal actin, and the activities of Na-K-ATPase and catalase were made. Exposure to near UVA damaged these cells as measured by vital staining and colony forming ability. Pretreatment with alpha-tocopherol decreased the magnitude of near UVA cytotoxicity. Near UVA exposure in MEM always produced more damage to the cells and biochemical targets than in Tyrode's. Cytoskeletal actin was degraded and the activities of Na-K-ATPase and catalase were markedly inhibited by UV-exposure. All of these targets were at least partially protected by alpha-tocopherol in the medium. Without alpha-tocopherol added to the media, the viability and survival of the cells did not recover even after 25 h of incubation. Cell viability was better protected from near UVA by alpha-tocopherol than was the ability to grow into colonies. This indicates that alpha-tocopherol protects actin, catalase, and Na-K-ATPase from near UVA damage.

Actins↗

PubMed1995

Vitamin E.

Explore the source record for details and available documents.

Animals↗

PubMed1995

Dietary saturated fatty acids: a novel treatment for alcoholic liver disease.

BACKGROUND & AIMS: Lipid peroxidation may be important in the pathogenesis of alcoholic liver injury. The purpose of this study was to determine whether a saturated fatty acid-based therapy (palm oil) could decrease lipid peroxidation and alcoholic liver injury during ethanol withdrawal. METHODS: Three groups of male Wistar rats (5 rats/group) were studied. Rats in group 1 were fed a fish oil-ethanol diet for 6 weeks; rats in groups 2 and 3 were fed a fish oil-ethanol diet for 6 weeks before treatment with fish oil-dextrose (group 2) or palm oil-dextrose (group 3) for 2 weeks. Liver samples were analyzed for histopathology, lipid peroxidation, fatty acid composition, cytochrome P450 2E1 activity, and tocopherol levels. RESULTS: By 6 weeks, all rats had developed fatty liver, inflammation, and necrosis. Group 2 showed minimal histological improvement, whereas group 3 showed near normalization of the histology. The improvement in group 3 was associated with decreased lipid peroxidation and P450 2E1 activity. Higher levels of omega-3 fatty acids were detected in group 2 than group 3. Tocopherol levels were similar among the groups. CONCLUSIONS: A diet enriched in saturated but not unsaturated fatty acids reversed alcoholic liver injury. This effect may be explained by down-regulation of lipid peroxidation.

Animals↗

PubMed1995

Aging and dietary modulation of elastase and interleukin-1 beta secretion.

Aging is associated with diminished immune function that may stem from alterations in arachidonic acid metabolism and lipid peroxidation. This study sought to determine if dietary modification of fatty acids influenced neutrophil and monocyte secretion after an in vivo inflammatory stress in older human subjects. Volunteers participated in protocols that forced their quadriceps muscles to lengthen during tension development (eccentric stress). These protocols can cause inflammatory foci in the muscle as well as alterations in circulating leukocyte function. In this study, in vivo neutrophil degranulation was assessed by plasma elastase concentrations, and mononuclear cell function was assessed by interleukin-1 beta (IL-1 beta) secretion in vitro. In response to eccentric stress, older subjects (> 60 yr old) taking a placebo had no apparent elastase response, whereas those taking fish oil supplements responded with a 142% increase in plasma elastase (P = 0.011), similar to responses of younger reference subjects (< 33 yr old) taking no supplement. Overall, elastase responses correlated with individual plasma arachidonic acid-to-eicosapentaenoic acid ratios (r = -0.881, P = 0.004). Thus apparent age-related differences in elastase release were reconciled by individual differences in fatty acid nutriture. No significant temporal changes in urinary lipid peroxide excretion or IL-1 beta secretion were observed; however, age-associated differences were found.

Adult↗

PubMed1995

High-dose vitamin E supplementation has no effect on ethanol-induced pathological liver injury.

The effect of alpha-tocopherol (alpha-T) supplementation on ethanol-induced liver damage was studied. The intragastric feeding rat model was used in this study. Both normal and alpha-T supplemented animals (3125 IU/kg body weight) were fed liquid diet and ethanol for 1 mo. In pair-fed animals, ethanol was isocalorically replaced by dextrose. The blood ethanol level in the ethanol-fed groups was between 150 to 350 mg/dl. Lipid peroxidation was assessed by measuring liver thiobarbituric acid reactive substances (TBARS) and conjugated dienes. Liver damage was assessed by light microscopy. Overall, chronic ethanol treatment resulted in increase in TBARS and conjugated dienes in both normal (60% and 35%, P < .01, respectively) and alpha-T-supplemented groups (50% and 47%, P < .01, respectively). In animals receiving either dextrose or ethanol and regular diet, there was a significant inverse correlation between liver alpha-T and TBARS (r = 0.88, P < 0.01) and conjugated dienes (r = -0.75, P < .05). In contrast, in the vitamin E-supplemented rats, a significant positive correlation was observed between liver alpha-T, TBARS (r = 0.78, P < .01) and conjugated dienes (r = 0.87, P < .01). Of major significance is that alpha-T supplementation had no effect on ethanol-induced pathological changes in the liver. In conclusion, these results show that in the intragastric feeding model, alpha-T supplementation had no protective effect on ethanol-induced liver damage.

Animals↗

PubMed1994

Effect of chronic ethanol feeding on plasma and liver alpha- and gamma-tocopherol levels in normal and vitamin E-deficient rats. Relationship to lipid peroxidation.

The effects of chronic ethanol intake on the levels of alpha-tocopherol and gamma-tocopherol in serum and liver of both vitamin E-deficient and normal rats were studied. An intragastric feeding rat model was used. Both normal and vitamin E-deficient animals were fed a liquid diet and ethanol for 1 month. In pair-fed animals, dextrose was isocalorically replaced by ethanol. The blood ethanol level in the ethanol-fed animals was between 150 and 250 mg/dL. Liver peroxidation was determined by measuring thiobarbituric acid reactive substances (TBARS). Plasma alanine aminotransferase (ALT) was increased by 3-fold in vitamin E-deficient ethanol-fed rats compared with normal ethanol-fed rats. Plasma alpha- and gamma-tocopherol were decreased in the normal ethanol-fed rats by 22.3 and 65%, respectively (P < 0.01). Liver alpha- and gamma-tocopherol were also decreased by 51.7 and 76%, respectively (P < 0.01). Vitamin E-deficient animals had significantly lower mean plasma alpha-tocopherol (5670 vs 530 ng/mL, P < 0.01), and ethanol feeding did not decrease the levels any further. However, ethanol feeding decreased liver alpha- and gamma-tocopherol by 58.5 and 56.5% (P < 0.01), respectively, beyond the already low levels observed in this group. There was an inverse correlation between liver TBARS and liver alpha-tocopherol (r = -0.59, P < 0.05) and gamma-tocopherol (r = -0.65, P < 0.02). Also of significance is that ethanol feeding decreased the plasma and liver gamma-tocopherol more than the alpha-tocopherol in both normal and vitamin E-deficient animals. In conclusion, ethanol feeding markedly decreased both alpha- and gamma-tocopherol in livers of normal and vitamin E-deficient rats, but it only decreased plasma levels of tocopherols in normal rats. The higher ALT in vitamin E-deficient animals and the inverse correlation between TBARS and alpha- and gamma-tocopherol suggest that enhanced lipid peroxidation is associated with greater severity of liver injury induced by ethanol in vitamin E-deficient rats.

Alanine Transaminase↗

PubMed1994

Assessment of the safety of high-dose, short-term supplementation with vitamin E in healthy older adults.

The effect of daily supplementation of 800 mg dl alpha-tocopheryl acetate for 30 d on general health, nutrient status, hepatic and renal function, intermediary metabolism, hematological status, plasma nutrients and antioxidant status, thyroid hormones, and urinary creatinine concentrations was studied in 32 healthy elderly (> 60 y) people who participated in a double-blind, placebo-controlled, residential trial. The subjects reported no side effects due to the supplements. Supplementation had no effect on body weight, plasma total protein, albumin, glucose, total cholesterol and triglycerides, conjugated and unconjugated bilirubin, alkaline phosphatase, indicators of hepatic and renal function, hematologic status, thyroid hormones, or serum and urinary creatinine concentrations and creatinine clearance. Supplementation did cause a significant increase in serum vitamin E, and a small (5%) but significant (P < 0.05) increase in plasma zinc in the vitamin E-supplemented group. Thus, short-term supplementation with 800 mg vitamin E/d has no adverse effect on healthy older adults.

Aged↗

PubMed1994

Age differences in eicosanoid production of mouse splenocytes: effects on mitogen-induced T-cell proliferation.

In order to determine the contribution of suppressive factors secreted from macrophages to the age-associated decline in T-cell mediated mitogenic responses, experiments were conducted to characterize eicosanoid and H2O2 production, total cellular fatty acid, and vitamin E composition of splenocytes isolated from young (4 mo) and old (24 mo) C57BL/6NIA mice. An age-related increase was observed in Ca++ ionophore A23187-stimulated ex-vivo production of prostaglandin (PG) E2, leukotriene (LT) B4, and LTC4 (p < .01), and in concanavalin A (ConA)-stimulated PGE2 production (p < .01). No age-related difference was observed in ex-vivo production of 12- and 15-hydroxyeicosatetranoic acid (HETE). The age-related increase in PGE2 production was also observed in lipopolysaccharide-stimulated peritoneal macrophages of C57BL/6NIA mice and ConA and phytohemagglutinin (PHA)-stimulated splenocytes isolated from DBA mice. Inhibition of cyclooxygenase with indomethacin resulted in increased ConA-stimulated proliferation of splenocytes from old mice (p < .01), while 5-lipoxygenase inhibition did not have an effect on mitogen induced proliferation. Furthermore, PGE2 addition to purified splenic T-cells decreased their proliferation. No age-related differences were observed in total cellular fatty acid composition, vitamin E level, or ex-vivo production of H2O2 from splenocytes stimulated with 10 or 100 ng phorbol myristate acetate (PMA). These data indicate that aging is associated with increased production of PG and LT from activated splenocytes. Inhibition of PGE2 but not LT production enhances mitogenic responses of old mice, suggesting a contributory role for PGE2 in the age-associated decline of T-cell responsiveness to polyclonal mitogens.

Aging↗

PubMed1994

Beta-carotene supplementation increases antioxidant capacity of plasma in older women.

The antioxidant effect of dietary beta-carotene supplementation on the peroxidation potential of plasma was investigated in a randomized double-blind, placebo-controlled study. Twelve healthy women (62-80 y) supplemented their usual daily diet with 90 mg of beta-carotene (n = 6) or placebo (n = 6) capsules for 3 wk. Plasma concentrations of beta-carotene, alpha- and gamma-tocopherol, ascorbate, urate, bilirubin and in vitro production of phosphatidylcholine hydroperoxides (PC-OOH) and utilization of plasma antioxidants in the presence of 50 mmol/L 2,2'-azobis (2-aminopropane) hydrochloride (AAPH), a free radical generator, at 37 degrees C were measured before and after dietary treatment. Plasma beta-carotene increased from 0.76 +/- 0.16 to 6.45 +/- 1.16 micromol/L (P < 0.05) in supplemented but not placebo-treated subjects. The plasma concentrations of other antioxidants did not change significantly in either group. beta-Carotene supplementation did not affect basal levels of plasma PC-OOH as measured by HPLC post-column chemiluminescence but did affect AAPH-induced production of PC-OOH. Before supplementation, the induction period of plasma PC-OOH production was 2.4 +/- 0.4 h, with levels reaching 5.39 +/- 1.50 micromol/L after 6 h of incubation. After supplementation, the induction period increased significantly to 4.2 +/- 0.4 h (P < 0.01), with a lower PC-OOH production of 2.16 +/- 0.90 micromol/L after 6 h (P < 0.05). In this system, plasma ascorbate concentrations were depleted first, followed by loss of bilirubin and alpha-tocopherol and then by the sequential loss of gamma-tocopherol, urate and beta-carotene. These results indicate that beta-carotene supplementation increases the plasma antioxidant capacity of older women.

Aged↗

PubMed1994

In vitro glutathione supplementation enhances interleukin-2 production and mitogenic response of peripheral blood mononuclear cells from young and old subjects.

The effect of in vitro glutathione (GSH) supplementation on mitogenic response, interleukin-1, interleukin-2 and prostaglandin E2 production, and cellular GSH level in peripheral blood mononuclear cells (PBMC) from healthy young and old human subjects was studied. In vitro addition of GSH increased cellular GSH level (P < 0.001). Glutathione supplementation at concentrations between 2 to 10 mmol/L enhanced lymphocyte proliferation but at low concentrations (0.5 and 1 mmol/L) decreased mitogenic response. Glutathione-induced enhancement of lymphocyte proliferation due to phytohemagglutinin or concanavalin A was greater in the PBMC from old subjects than in those from young subjects. At optimal concentration (5 mmol), GSH increased interleukin-2 production (P < 0.05) and decreased prostaglandin E2 and leukotriene B4 production (P < 0.01) in both age groups. Furthermore, decreased PBMC mitogenic response by in vitro addition of prostaglandin E2 was reversed by GSH supplementation. Glutathione did not have an effect on interleukin-1 production by PBMC from young subjects; however, GSH supplementation tended (P = 0.08) to increase interleukin-1 production by PBMC from old subjects. We conclude that GSH supplementation enhances T cell-mediated mitogenic response in young and old subjects. This effect is due at least in part to decreased eicosanoid production.

Adult↗