Chronic marginal vitamin A status affects the distribution and function of T cells and natural T cells in aging Lewis rats.

Although both vitamin A (VA) deficiency and aging are independently associated with alterations in immune function, the effects of marginal VA status or VA supplementation on the immune system during aging were not studied. A long-term dietary study was conducted in a rat model of aging to quantify changes in T-cell populations in blood and spleen, including T-cells bearing a marker of natural killer (NKT) cells. The study included nine treatment groups [three levels of dietary VA: marginal (0.35 RE/kg diet), control (4.0 RE/kg diet), and supplemented (50 RE/kg diet); and three age groups: young (2-3 mo), middle-aged (8-10 mo), and old 20-22 mo); diets were fed continuously from weaning to the end of the study period. CD3(+)/CD4(+) T-cells decreased in percentage and number in blood with age, CD8(+) cells increased (%), and the CD4/CD8 ratio decreased. Conversely, aging was associated with increased NKT cells (phenotype CD3(intermediate)/NKR-P1(+)). Based on regression analysis of flow cytometry data, the phenotype of most NKT cells was CD3(intermediate)/NKR-P1(+)/CD28(-). NKT cells, which are most likely of extrathymic origin, accounted for most of the decrease in the CD4/CD8 ratio. Marginal VA status, particularly in older rats, was associated with increases in the percentage of CD8(+) T cells, percentage and number of NKT cells, and peripheral blood cell anti-CD3epsilon-stimulated proliferative response, and decreases in the CD4/CD8 T-cell ratio and splenic cell interleukin-2 production. These differences and the reciprocal changes observed for NKT cells vs. T- and classical NK cells in aging VA-marginal rats suggest that low VA status during aging may increase the risk of infectious or neoplastic diseases that require a normal balance of T-cell or NK-cell responses.     

Vitamin A deficiency decreases natural killer cell activity and interferon production in rats.

We examined the effect of vitamin A deficiency on natural killer (NK) cell activity and interferon (IFN) production. Rats were weaned at 16 or 21 d of age onto semisynthetic diets containing either 0 or 4 micrograms retinol/g diet. At the time of study, retinol-depleted rats had serum vitamin A concentrations less than 7% of those of pair-fed controls. In two studies, rats exhibited no external signs of retinol deficiency, but with further depletion some symptoms were observed. Splenic NK cell activity against chromium-51-labeled YAC-1 cells was significantly decreased in vitamin A-depleted rats (22-80% of values for control rats, depending on the degree of retinol deficiency), regardless of the ratio of effector to target cells used. When vitamin A-depleted rats were repleted orally with retinol, NK cell activity was consistently normalized. To understand the possible mechanisms involved in decreasing NK cell activity, we investigated IFN production by concanavalin A-stimulated spleen cells from vitamin A-depleted, from repleted and from control animals. IFN titers were significantly decreased (22-33% of values for control rats) in supernatants of spleen cell cultures of the vitamin A-depleted rats. Repletion with vitamin A resulted in IFN activities ranging from 80 to 130% of controls. Adding alpha/beta IFN in vitro to the spleen cells of vitamin A-depleted animals increased their NK cell activity. The number of spleen cells reacting with a monoclonal antibody specific for rat NK cells was slightly lower in retinol-depleted rats, but not enough to account for the differences in NK cell and IFN activities. These data suggest that vitamin A deficiency affect the nonspecific arm of the immune system, possibly by altering the functional capacity of cells to produce lymphokines needed for the generation of an appropriate cytolytic response.     

Iron deficiency alters DMBA-induced tumor burden and natural killer cell cytotoxicity in rats.

Natural killer (NK) cell activity is impaired in iron-deficient rats. Natural killer cells destroy tumor cells; therefore, iron-deficient rats may be less able to combat cancer growth. Natural killer cell cytotoxicity, both basal and interferon gamma (IFN gamma)-stimulated, was studied in moderately and severely iron-deficient rats challenged with the carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Female weanling rats were fed ad libitum semipurified diets containing 8, 13 or 42 mg Fe/kg. A pair-fed group was fed the 42 mg Fe/kg diet at the level consumed by the 8 mg Fe/kg group. Following 6 wk of dietary treatment, DMBA-treated rats received a single intragastric dose of DMBA. Dietary treatment was continued. Rats were killed at 1, 4, 8, 14 and 20 wk post-DMBA treatment. Natural killer cell cytotoxicity (both basal and IFN gamma-stimulated) was analyzed. Feeding the 13 mg Fe/kg diet resulted in lower NK cell activity (P = 0.006) and greater tumor burden (P = 0.045) and tumor incidence. Interferon gamma treatment relieved the lower NK cell cytotoxicity observed in moderate iron deficiency. Feeding the 8 mg Fe/kg diet impaired NK cell activity (P = 0.006), but tumor burden and incidence were less than in moderate iron deficiency. In this model, iron deficiency, particularly moderate iron deficiency, contributed to cancer development and compromised NK cell cytotoxicity.     

Human natural killer cell function and their interactions with dendritic cells

Natural killer (NK) cells have long been considered as "primitive" and "non-specific" effector cells. However, the past 10 years have witnessed dramatic progress in our understanding of how NK cells function and their role in innate defenses. Thanks to specialized inhibitory receptors specific for MHC-class I molecules, they can sense the decrease or loss of these molecules, a typical condition of potentially dangerous cells such as tumor or virally-infected cells. NK cell triggering and lysis of these cells is mediated by several activating receptors and co-receptors that have recently been identified and cloned. While normal cells are usually resistant to the NK-mediated attack, a remarkable exception is represented by dendritic cells (DC). In their immature form (iDC), they are susceptible to NK-mediated lysis because of the expression of low levels of surface MHC-class I molecules. Since the process of DC maturation (mDC) is characterized by the surface expression of high levels of MHC-class I molecules, mDC become resistant to NK cells. Exposure to live bacteria induces rapid DC maturation and, thus, resistance to NK cells. The cross-talk between DC and NK cells is more complex and involves also a DC-dependent NK cell activation and proliferation. Thus, two important players of the innate immunity may be involved in a coordinated regulation of critical events occurring at the interface between innate and adaptive immunity.     

A marginal vitamin A status alters the distribution of vitamin A among parenchymal and stellate cells in rat liver

The aim of this study was to determine whether the distribution of vitamin A between parenchymal and stellate cells in rats with low vitamin A liver reserves is different from that observed in rats with adequate reserves. Retinol and retinyl esters were quantitated in parenchymal and stellate cells of the liver of three groups (n = 3) of adult Sprague-Dawley rats with mean total liver vitamin A reserves of 1.2, 14.5 and 28.9 micrograms retinol/g fresh liver for groups 1, 2 and 3, respectively. The amount of vitamin A per 10(6) cells was similar in parenchymal and stellate cells of group 1, whereas in groups 2 and 3, a much higher amount was found in stellate cells (11-fold and 27-fold higher, respectively). In group 1, 83% of the liver vitamin A was present in parenchymal cells. As liver stores rose, however, a progressively greater amount was stored in stellate cells. In group 3, 82% of the liver vitamin A was found in stellate cells. In groups 2 and 3, 87-91% of the vitamin A was found as retinyl ester, whereas in group 1, 52% was found as retinol. The retinyl ester composition was similar in parenchymal and stellate cells, major esters being palmitate (84%) and stearate (10%), with smaller amounts of oleate (2.5%) and other esters. Thus, in rats with low liver vitamin A reserves, most of the liver vitamin A is found in parenchymal cells.     

Effects of acute starvation on vitamin A status in rats.

Maintenance of vitamin A stores in the body is dependent on a number of basic metabolic processes. These processes, such as protein and carbohydrate metabolism, are disrupted in acute starvation, and, as a result, alterations in vitamin A status may result. We investigated this possibility in 8-week-old Sprague-Dawley male rats. The rats were starved for 24, 48, and 72 hr but had free access to water. At 24 hours of starvation, the plasma retinol concentration was depressed, but not significantly so. After 48 and 72 hours of starvation, however, the plasma retinol concentration decreased to less than half of the control values (61 +/? 4 vs 124 +/? 12 nmol/dl at 72 hours, mean +/? SEM, (p less than 0.005). The hepatic retinoid (retinyl esters + retinol) concentration (nmol/g liver) was increased at 24 and 48 hours of starvation compared to controls (p less than 0.05), and by 72 hours the concentration was 56% greater in starved rats than in fed controls (p less than 0.001). The total hepatic retinoid content (mumol/total liver) was decreased moderately at all periods of starvation compared to controls (p less than 0.05). In both starved and fed animals, the total hepatic content per 100 g body weight, a measure of total vitamin A reserves, was statistically the same. These results demonstrate that acute starvation in rats alters the vitamin A equilibrium between the plasma and hepatic stores without affecting the overall vitamin A reserves.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dietary vitamin E and beta-carotene sources influence vitamin A and E storage in young rats fed marginal and adequate vitamin E

The effects of two vitamin E levels (30 and 75 IU/kg diet) and the interrelation of two vitamin E sources [dl-alpha-tocopheryl acetate (dl-alpha-TA) and d-alpha-tocopheryl acid succinate (d-alpha-TAS)] and three vitamin A sources [retinyl palmitate (RP), all-trans synthetic beta-carotene (SBC), and natural beta-carotene (NBC)] were studied. Dietary vitamin A sources provided 4,000 IU/kg. Twelve groups of Fischer 344 rats (10/group) were fed designated diets for eight weeks. For RP, SBC, and NBC, the increase in each vitamin E source from a marginal to an adequate dietary level caused a significant increase in liver and heart alpha-tocopherol. Among rats fed diets with an adequate level of vitamin E, d-alpha-TAS was not as effective as dl-alpha-TA in increasing liver alpha-tocopherol levels. Plasma retinol was lower in rats fed d-alpha-TAS than in those fed dl-alpha-TA. Among rats fed diets with an adequate level of dl-alpha-TA, those fed SBC had significantly higher liver and heart alpha-tocopherol concentrations than did all other groups (p < 0.05). Liver retinol equivalents for rats fed NBC were approximately 66% lower than those in rats fed SBC or RP (p < 0.05). The roles of the two vitamin E sources in alpha-tocopherol metabolism are not equivalent. These data indicate that vitamin A source influences the magnitude of the tissue vitamin A and E changes in response to the two vitamin E sources.     

Effect of micronutrient status on natural killer cell immune function in healthy free-living subjects aged >/=90 y

BACKGROUND: Natural killer (NK) cells play a role in natural immunity against tumor and infected cells. Advanced aging is associated with functional impairment of NK cells and increased susceptibility to nutritional deficiencies. OBJECTIVE: Our objective was to test whether micronutrient status affects NK cell activity in an older population. DESIGN: The relations between NK cell variables (percentage of leukocytes and cytotoxicity) and blood concentrations of selected micronutrients were studied in 62 healthy, free-living northern Italian subjects (25 men, 37 women) aged 90-106 y. Anthropometric measurements were also made. RESULTS: All subjects were well nourished according to age-specific anthropometric norms but many of them had micronutrient deficiencies. The prevalence of micronutrient deficiency was highest for selenium (in approximately 50% of both sexes), zinc (in 52% of men and 41% of women), and vitamin B-6 (in 40% of men and 59% of women), followed by vitamin A (in 16% of men and 27% of women) and vitamin E, vitamin B-12, and folate (each in <10% of both sexes). Ubiquinone-10 status was inadequate in 40% of women and 24% of men (P = 0.02). The percentage of NK cells was associated with serum zinc (men: r = 0.573, P = 0. 007; women: r = 0.373, P = 0.031) and selenium (women: r = 0.409, P = 0.018) concentrations. In women only, NK cell cytotoxicity at different effector-target cell ratios was positively associated with plasma vitamin E and ubiquinone-10 concentrations (P < 0.05). No significant associations with NK cell variables were found for the other measured nutrients. CONCLUSIONS: The results of this study strengthen the hypothesis that individual micronutrients may affect the number and function of NK cells in old age. The study also confirms the high prevalence of micronutrient deficiencies in healthy and apparently well-nourished persons aged >/=90 y.     

Regulation of hepatic vitamin A storage in a rat model of controlled vitamin A status during aging

It is currently unknown whether the capacity of the liver to esterify and store vitamin A (VA) changes as a function of long-term VA intake or age. The objective of this study was to investigate whether age and/or VA status are factors for the hepatic expression of cellular retinol-binding protein (CRBP), the esterification of retinol by lecithin:retinol acyltransferase (LRAT) and the accumulation of VA and lipids in liver. Two factors, VA intake and age, were studied in a 3x3 design. Diets denoted as VA-marginal, control and supplemented contained 0.35, 4 and 25 mg retinol equivalents/kg diet, respectively; male Lewis rats were fed these diets from weaning until the ages of 2-3 mo (young), 8-10 mo (middle-aged) and 18-20 mo (old) (n = 6/group. Liver CRBP mRNA differed (two-way ANOVA) with dietary VA (P<0.0001) and age (P<0.05). Hepatic LRAT activity increased with dietary VA (P<0.0001). Age was not a factor (P = 0.47) although there was an interaction of age and dietary VA (P<0.0001). Hepatic LRAT activity was correlated (r = 0.633, P<0.0001) with plasma retinol at physiologic concentrations. In VA-supplemented rats of all ages, the plasma molar ratio of total retinol:retinol-binding protein (RBP) exceeded 1, and liver VA and total lipid concentrations were elevated. However, tests of liver function had previously been shown to be within normal values. Thus, the capacity of the liver for retinol esterification by LRAT was not diminished by age or the accumulation of VA and other lipids. We conclude the following: 1) hepatic LRAT activity is regulated across a broad, physiologic range of dietary VA; 2) LRAT activity is regulated throughout life; and 3) the capacity for hepatic VA storage is high throughout life.     

A cross-sectional study on the relationship of job stress with natural killer cell activity and natural killer cell subsets among healthy nurses

The present study investigated the effects of job stress on cellular immune function, such as NK cell activity and NK cell subsets. The participants were 61 female nurses aged 23-59, who worked in a public psychiatric hospital in Ishikawa, Japan. Each subject completed the Nursing Job Stressor Scale (NJSS) and their NK cell activity and lymphocyte surface antigens (CD16+56+) were evaluated as immune system parameters. The NJSS has seven subscales: conflict with other nursing staff, nursing role conflict, conflict with physicians or autonomy, conflict with death or dying, quantitative work load, qualitative work load and conflict with patients. Factors influencing NK cell activity, and the proportion and cell counts of CD16+56+ lymphocytes were evaluated. Increase in quantitative work load significantly decreased NK cell activity. Conversely, no linear relationship was observed between qualitative work load and immunological variables, with the highest percentage of CD16+56+ lymphocytes observed among participants in the medium work load group. The other five NJSS subscales did not relate to immune parameters. In conclusion, the results suggest that perceived job strains, particularly quantitative work load, decreased NK cell function.     

Socioeconomic status and cell aging in children

Theory suggests that chronic stress associated with disadvantaged social status may lead to acceleration in the rate of decline in physiological functioning. The purpose of this study is to examine the association between parental socioeconomic status (SES) and leukocyte telomere length (LTL), a marker of cell aging, in children. We examined SES and LTL in 70 white and black US children aged 7-13 who participated in the community-based AMERICO (Admixture Mapping for Ethnic and Racial Insulin Complex Outcomes) study. LTL was assessed using the polymerase chain reaction (PCR) method. Parental education was positively associated with child LTL, net of controls for sex, age, race/ethnicity, and family income. Compared to children with at least one college-educated parent, children whose parents never attended college had telomeres shorter by 1,178 base pairs, which is roughly equivalent to 6 years of additional aging. Socioeconomic disparities in cell aging are evident in early life, long before the onset of age-related diseases.     

Evaluation of vitamin B-6 status and function of rats fed excess pyridoxine

We compared the vitamin B-6 status of 12-wk-old rats (n = 12) fed excess (1400 mg/kg diet) or the recommended level (7 mg/kg diet, control) of pyridoxine (PN) hydrochloride to test if excess vitamin B-6 would cause tissue depletion of pyridoxal phosphate (PLP), the active coenzyme form of vitamin B-6. Plasma PLP, tryptophan-load test results, food intake, and tissue and body weights were not different at wk 6. Red blood cell endogenous alanine aminotransferase activity and PLP concentration were elevated (P less than 0.01) in rats fed 1400 mg PN.HCl/kg diet. In contrast, PLP concentration in muscle was significantly lower (P = 0.01) in rats fed excess vitamin B-6 (9.7 +/- 0.8 nmol/g, mean +/- SEM) than in controls (14.9 +/- 1.4). PLP concentration in other tissues, including plasma, was not affected. In rats fed excess vitamin B-6, pyridoxal was increased in all tissues examined (P less than 0.05), and total vitamin B-6 was increased in plasma, red blood cells and kidneys (P less than 0.05). Total glycogen phosphorylase (a + b) activity in the gastrocnemius was not affected, but phosphorylase a activity was increased in rats fed excess vitamin B-6 (P = 0.025). Concentrations of dopamine and metabolites in the caudate nucleus of the basal ganglia were not affected. A transient, but significant, elevation in acoustic startle response, a central nervous system reflex, was observed in rats fed excess vitamin B-6. The depletion in muscle PLP could not hae been predicted by either plasma or red blood cell PLP concentration, although the latter did reflect vitamin B-6 intake.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of acute starvation on vitamin A status in rats

Maintenance of vitamin A stores in the body is dependent on a number of basic metabolic processes. These processes, such as protein and carbohydrate metabolism, are disrupted in acute starvation, and, as a result, alterations in vitamin A status may result. We investigated this possibility in 8-week-old Sprague-Dawley male rats. The rats were starved for 24, 48, and 72 hr but had free access to water. At 24 hours of starvation, the plasma retinol concentration was depressed, but not significantly so. After 48 and 72 hours of starvation, however, the plasma retinol concentration decreased to less than half of the control values (61 +/- 4 vs 124 +/- 12 nmol/dl at 72 hours, mean +/- SEM, (p less than 0.005). The hepatic retinoid (retinyl esters + retinol) concentration (nmol/g liver) was increased at 24 and 48 hours of starvation compared to controls (p less than 0.05), and by 72 hours the concentration was 56% greater in starved rats than in fed controls (p less than 0.001). The total hepatic retinoid content (mumol/total liver) was decreased moderately at all periods of starvation compared to controls (p less than 0.05). In both starved and fed animals, the total hepatic content per 100 g body weight, a measure of total vitamin A reserves, was statistically the same. These results demonstrate that acute starvation in rats alters the vitamin A equilibrium between the plasma and hepatic stores without affecting the overall vitamin A reserves.(ABSTRACT TRUNCATED AT 250 WORDS)     

Insensitivity of the tryptophan-load test to marginal vitamin B-6 intake in rats.

The tryptophan-load test for vitamin B-6 nutritional status was administered to adult female Long-Evans rats fed graded levels of pyridoxine hydrochloride (PN.HCl) in two experiments, and its sensitivity to marginal vitamin B-6 intake was evaluated. In Experiment 1, rats were 4-h meal-fed an AIN-76A (20% casein) diet devoid of PN.HCl for 3 wk, then repleted (n = 12) for 6 wk with 4-h pair-fed meals of either 0.25, 0.5, 1.0 or 7.0 (control) mg PN.HCl/kg diet. In Experiment 2, rats (n = 16) were pair-fed for 10 wk either 0.0, 0.5, 1.0 or 7.0 (control) mg PN.HCl/kg diet, with 24-h access to food. Vitamin B-6 nutritional status was assessed at the end of each experiment. Except in rats fed 0 mg PN.HCl/kg diet, mean body weights were not significantly different among diet groups of either experiment. Plasma pyridoxal phosphate (PLP), pyridoxal and total vitamin B-6 concentrations, determined by HPLC, were very sensitive to gradations in dietary PN.HCl concentrations (P less than 0.05). Red blood cell endogenous and PLP-stimulated alanine and aspartate aminotransferase activity did not statistically differentiate all levels of dietary vitamin B-6, although the calculated activity coefficient for each enzyme (stimulated/endogenous activity) did. Urinary xanthurenic acid excretion following a tryptophan load [24.5 mumol (5 mg) L-tryptophan/100 g body weight, injected intraperitoneally] was significantly (P less than 0.05) elevated compared with controls only in the group fed 0 mg PN/HCl/kg diet. At the tryptophan dose used here, the tryptophan-load test was not useful in detecting marginal vitamin B-6 intake in rats.     

Iron status and stores decline with age in Lewis rats

In the context of a larger study examining the interaction of vitamin A (VA) status and age on immune function, we examined age-related changes in hematologic and iron status variables in male Lewis rats. Animals were fed a nutritionally adequate purified diet containing either 0.35 (marginal), 4.0 (control) or 50 (supplemented) mg retinol equivalents (as retinyl palmitate) per kg of diet from the time of weaning until killing at 8-10 (middle-aged) or 20-22 (old) mo of age. Neither VA nor VA and age interaction effects were significant for most iron variables examined. After controlling for body weight, old rats had significantly lower hemoglobin, hematocrit and plasma iron than middle-aged rats. This decrease in hematologic and transport iron variables was not accompanied by a shift of iron into other storage compartments. Old rats also had significantly lower total iron content and iron concentration in liver, spleen and bone marrow. Hemosiderin iron in marrow smears correlated significantly (r = 0.43-0.76, P: < 0.05) with chemical estimates of iron in storage, transport and functional pools. Old rats also tended to have less stained iron in femur marrow smears. Thus, body iron in functional, transport and storage compartments, namely the liver, spleen and bone marrow, were significantly lower in old than in middle-aged rats. Although iron stores and status are usually considered to increase with advancing age, our data show a consistent pattern of lower hematologic and storage iron variables in old than in middle-aged Lewis rats. Future research is indicated to understand the biology and functional consequences of the observed age-associated decline in body iron.     

Canthaxanthin and excess vitamin A alter alpha-tocopherol, carotenoid and iron status in adult rats.

beta-Carotene and excess vitamin A have been shown to reduce plasma alpha-tocopherol when fed to young rats. The present study assessed the effects of beta-carotene, excess vitamin A and canthaxanthin (4,4'-diketo-beta-carotene) on carotenoid, alpha-tocopherol and iron status in adult retired breeder rats. Male 8- to 10-mo-old rats (10/group) were fed varying levels of vitamin A as retinyl palmitate, beta-carotene and canthaxanthin ad libitum for 8 wk. The AIN-76A diet was modified to contain 16% (wt/wt) fat and 50% carbohydrate (control) plus beta-carotene or canthaxanthin at 0, 0.048 (BC1 or CX1) and 0.2% (BC2 or CX2) of the diet. These compounds were fed with and without excess retinyl palmitate (RP, 220 mg/kg). Higher relative liver weights were observed in CX- and RP-fed groups. Plasma retinyl esters were detected in all RP-fed groups. Plasma retinyl palmitate was 1.6- and 1.5-fold higher in RP-BC and RP-CX groups, respectively, than in the RP groups. Plasma and liver beta-carotene and canthaxanthin were 11-54% and 26-74% lower, respectively, with excess retinyl palmitate feeding. Feeding canthaxanthin and retinyl palmitate but not beta-carotene, resulted in lower levels of plasma alpha-tocopherol. Liver non-heme iron levels were also lower in CX-fed rats irrespective of retinyl palmitate feeding. These results extend to adult rats previous findings that excess retinyl palmitate alters vitamin E and carotenoid status prior to the manifestation of clinical signs of hypervitaminosis A. Additionally, canthaxanthin feeding lowers alpha-tocopherol and iron status in adult rats.     

Cardiac structure and function in vitamin B-12-deprived rats.

The effect of prolonged vitamin B-12 deprivation in rats on the histological structure of heart and on cardiac linoleic acid oxidation has been investigated. Offspring from pregnant females fed vitamin B-12-deficient diets were fed the deprivation diet for up to 16 months, and the development of B-12 deficiency was monitored by determination of urinary methylmalonic acid levels. These levels averaged 4.2 mg/day by 9 months of B-12-deprivation diet, and 142 mg/day after 16 months. The hearts of these animals were characterized by extensive fibrosis, and electron microscopy revealed cardiac mitochondria that were grossly enlarged and distorted. The metabolic defect of B-12 deprivation in heart muscle was determined in isolated hearts during recirculating perfusion of labeled propionic acid. Both the uptake and oxidation of propionic acid were markedly reduced in hearts from B-12-deprived rats (16 months) compared with controls, and the site of the metabolic block, i.e., accumulation of labeled methylmalonate, was established. Vitamin B-12 deprivation did not affect the extraction of recirculating labeled linoleic acid by perfused hearts, in contrast to the effect on propionic extraction. Furthermore, the oxidation of the extracted fatty acid was markedly increased over controls. Analysis of the circulating media after 45-minute perfusions showed no accumulation of labeled methylmalonate but did contain significantly less succinate than perfusion media from control hearts. The results are discussed with respect to cardiac structure and to the oxidative pathway(s) for polyunsaturated fatty acids.     

不同营养方式对肝硬化大鼠肝切除术后肝脏自然杀伤细胞的影响

目的 探讨不同营养方式对肝硬化大鼠肝切除术后肝脏自然杀伤(NK)细胞数量和活性的影响。方法 采用硫代乙酰胺诱导大鼠肝硬化模型。将20只肝硬化大鼠按随机号码表法随机分为肠内营养组和肠外营养组,每组10只,分别于肝切除术后1d开始进行为期5d的肠内营养和肠外营养。应用流式细胞术测定大鼠肝脏NK细胞百分率;4 h51Cr释放法测定肝脏NK细胞的杀伤活性。结果 肠内营养组的肝脏NK细胞百分率（22.2％±1.7％比17.4％±1.8％,P=0.000）和NK细胞杀伤活性均明显高于肠外营养组（41.6％±2.3％比37.1％±2.2％,P=0.000）。结论 肠内营养可以增加肝硬化大鼠肝切除术后肝脏NK细胞的百分率和杀伤活性。