Impairment of lymphocyte function in head-injured rats: effects of standard and immune-enhancing diets for enteral nutrition

BACKGROUND: The metabolic response to head injury (HI) is characterized by a dysimmunity which may be a risk factor of a septic state. The use of immune enhancing diets (IEDs) could be a promising approach to improve immune functions. The aim of the study was to investigate the consequences of HI on lymphocyte function and to determine the effects of an enteral IED comparatively to a standard enteral nutrition. METHOD: A rat model of HI by fluid percussion was used. Twenty-five male Sprague-Dawley rats were randomized into 4 groups: rats receiving standard chow diet ad libitum (AL), rats sustaining HI and receiving standard chow diet and enteral saline (HI), rats receiving the enteral standard diet Sondalis HP (HIS), and rats receiving the IED Crucial (HIC). The two enteral diets were infused continuously during 4 days after the HI and were isocaloric, isonitrogenous and isovolumic. RESULTS: HI induced a thymus atrophy (HI vs. AL, P<0.05), and an impairment in lymphocyte CD25 receptor density responsiveness to stimulation. The IED blunted thymus atrophy and allowed to preserve the stimulation of blood and Peyer patches lymphocytes (HIC: Stimulated vs. Basal, P<0.05). CONCLUSION: IED seems more adapted for preserving lymphocyte function than standard diet in HI patients.     

Effect of Cr(VI) exposure on sperm quality: human and animal studies

The semen status of male workers occupationally exposed to hexavalent chromium(VI) was investigated. Sperm counts from exposed workers were 47.05+/-2.13 x 10(6)/ml and those from control group 88.96+/-3.40 x 10(6)/ml. Sperm motility decreased from 81.92+/-0.41% for the control group to 69.71+/-0.93% for the exposed workers. The levels of zinc, lactate dehydrogenase (LDH), and lactate dehydrogenase C4 isoenzyme (LDH-x) in seminal plasma for the exposed workers were 1.48+/-0.07 micromol/ml, 1.05+/-0.02 x 10(3) U, and 0.47+/-0.01 x 10(3) U, respectively, which were significantly lower than those of 5.72+/-0.15 micromol/ml, 1.49+/-0.02 x 10(3) U, and 0.78+/-0.15 x 10(3) U for the control group, respectively. Follicle stimulating hormone (FSH) (7.34+/-0.34 x 10(-3) IU/ml) in serum from the exposed workers was significantly higher than that (2.41+/-0.08 x 10(-3) IU/ml) from the control group. On the other hand, there were no significant differences in semen volume, semen liquefaction time, luteinizing hormone (LH) level in serum, and Cr concentration in both serum and seminal plasma between the exposed workers and the control group. Feeding Cr(VI) to rats significantly reduced the epididymal sperm counts from 87.40+/-3.85 x 10(6)/g epididymis in control group to 21.40+/-1.20 x 10(6)/g epididymis at a CrO(3) dose of 10 mg/kg body weight and to 17.48+/-1.04 x 10(6)/g epididymis at a CrO(3) dose of 20 mg/kg body weight. Exposure of rats to Cr(VI) also significantly increased the sperm abnormality from 2.75+/-0.06% in the control group to 6.68+/-0.32% in the exposed group at a CrO(3) dose of 10 mg/kg body and to 7.6+/-0.15% at a CrO(3) dose of 20 mg/kg body weight. In exposed rats, there was visible disruption in germ cell arrangement near the walls of the seminiferous tubules. The diameters of seminiferous tubules in exposed rats were smaller. These results suggest that occupational exposure to chromium(VI) leads to alteration of semen status and may affect the reproductive success of exposed workers.     

Oral administration of a glutamine-enriched diet before or after endotoxin challenge in aged rats has limited effects.

Numerous studies indicate beneficial effects of glutamine (Gln) in many models of catabolic adult rats. No data were available for aged rats. The effects of oral L-Gln-enriched diet were tested in endotoxemic 24-mo old rats. First, rats received for 7 d (from d0 to d7) an oral diet supplemented with either L-Gln [1g/(kg. d)] or casein (Cas: isonitrogenous supply) prior to lipopolysaccharide (LPS) challenge. The rats were then killed after 24 h food deprivation (from d7 to d8). Endotoxemia induced a catabolic response as shown by muscle glutamine depletion, hyperphenylalaninemia, small bowel atrophy and impaired functionality and bacterial translocation. The Gln-enriched diet did not prevent muscle Gln depletion but significantly (P 相似文献   

Effects of L-arginine-enriched total enteral nutrition on body weight gain, tumor growth, and in vivo concentrations of blood and tissue metabolites in rats inoculated with Walker tumor in the kidney

OBJECTIVE: We evaluated the effects of l-arginine-enriched total enteral nutrition (LATEN) on tumor-free and right kidney tumor-bearing rats through the determination of in vivo concentrations of metabolites to better understand intermediary metabolism in this model. METHODS: Rats were individually housed in wire cages within a controlled environment (25 degrees C and 50% relative humidity) and exposed to a 12-h light-and-dark cycle. Rats comprised the following groups: tumor-free on enteral nutrition plus l-amino acid (n = 8); tumor-free on enteral nutrition plus l-arginine (n = 8); tumor bearing on enteral nutrition plus l-amino acids (n = 8); and tumor bearing on enteral nutrition plus l-arginine (n = 8). Rats had their right kidneys inoculated with saline or tumor cells and were subjected to laparotomy or gastrostomy on day 1 and received chow diet for the next 2 days. Gastrostomy with enteral nutrition was performed on days 3 to 9. On day 9, body weight gain, tumor growth as volume, in vivo blood (microM/mL), and tissue (microM/g) metabolite concentrations were determined. The Mann-Whitney U test was used to test significance. RESULTS: LATEN in tumor-free rats decreased liver (0.25 +/- 0.03 versus 0.13 +/- 0.03 micromol/g, P < 0.05) and right kidney (0.13 +/- 0.1 versus 0.04 +/- 0.00 micromol/g, P < 0.05) ketone body concentrations. LATEN in tumor-bearing rats decreased blood pyruvate (0.17 +/- 0.01 versus 0.10 +/- 0.008 microM/mL, P < 0.005), lactate (5.2 +/- 0.3 versus 2.9 +/- 0.28 microM/mL, P < 0.01), and glucose (6.4 +/- 0.8 versus 3.7 +/- 0.5 microM/mL, P < 0.05). Glucose concentrations decreased in liver (13.9 +/- 2.0 versus 4.89 +/- 0.6 microM/g, P < 0.005) and tumor (3.5 +/- 0.8 versus 1.41 +/- 0.3 microM/g, P < 0.05). There were no changes in body weight gain (21 +/- 2.0 versus 30.3 +/- 3.6 g) or tumor growth (1.53 +/- 0.1 versus 1.26 +/- 0.01 cm(3)). CONCLUSIONS: LATEN decreased ketone body concentrations in liver and kidney in tumor-free rats, possibly due to lower ketogenesis and decreased kidney uptake. In tumor-bearing rats, LATEN decreased lacticemia and glycemia and pyruvate blood concentrations. LATEN also reduced liver and tumor glucose concentrations in tumor-bearing animals. The possibility of LATEN-induced insulin and insulin-like growth factor-1 liberation signaling these changes is discussed.     

Influence of starvation on sucrase regulation by dietary sucrose in the rat

We have studied the action of sucrose on jejunal sucrase activity. Rats (175 g) were first starved or fed a digestible carbohydrate-free diet for 60 h and then fed a high sucrose diet for varying times up to 84 h. 1) Rats starved for 60 h showed mucosal atrophy with a decrease in protein content/10 cm (18.00 +/- 1.4 versus 40.1 +/- 3 mg (controls p less than 0.001) and in villus height (357 +/- 18 versus 526 +/- 5 microns, p less than 0.001) which was fully repaired only after 60 h on the sucrose diet (528 +/- 11 microns). Rats on digestible carbohydrate-free diet showed no mucosal atrophy. 2) Starved rats had a delayed (60 h) sucrase activity response to sucrose (53 +/- 7 versus 122 +/- 4 microns/mg protein, p less than 0.001). Maximum activity was obtained after 12 h on sucrose diet in rats maintained on the carbohydrate-free diet: 38 +/- 1 versus 108 +/- 2.3 microns/mg protein, p less than 0.001. 3) Villus and crypt cell analysis after starvation and 12 h on a high sucrose diet localized the increase in sucrase activity to the villus-crypt junction. No change occurred in the upper villus. The increase was complete all along the villus by 36 h. In contrast, after the carbohydrate-free diet, sucrase activity increased maximally at all levels of the villus by 12 h on the high sucrose diet.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of low-quality dietary protein on the thymus of growing rats

The status of the thymus of growing rats fed for 45 days after weaning on a low-quality dietary protein (7.5% maize) was compared with that in an age-matched control group receiving a diet containing casein at the same concentration. At the end of the feeding period, body weight (bw) was determined and the thymus was removed; its weight and cell number and the mature T-cell population--characterized by the monoclonal antibody W3/13 using the indirect immunofluorescence technique--were determined. Thymus weight expressed as mg/bw0.75 (3.9 +/- 0.75 vs 7.7 +/- 2.0), cell number (4.4 +/- 2.2 vs 26.3 +/- 7.6), and the absolute number of W3/13+ T cells (1.59 +/- 0.75 vs 17.8 +/- 5.4) were significantly lower (p less than 0.0005) in the experimental group than in the control group. The results suggest severe atrophy of the thymus of weaning animals chronically fed a low-quality protein.     

Increased insulin sensitivity in iron-deficient rats

Iron deficient (ID) and control (C) rats were studied to determine if severe iron deficiency alters insulin-stimulated glucose disposal. Euglycemic hyperinsulinemic glucose clamps were conducted by infusing insulin (2 m mu.kg-1.min-1, constant rate) for 120 min while maintaining euglycemia. In a 12-h fasted state, ID rats were hyperglycemic (109.4 +/- 4.0 mg.dL-1 arterial plasma glucose, x +/- SEM) when compared with C rats (86.9 +/- 3.4 mg.dL-1) (P less than 0.05). Even though insulin was infused identically on a per kilogram body weight basis for both groups, the resulting hyperinsulinemia was higher in ID rats (3.1 +/- 0.27 ng.mL-1) compared with C rats (2.3 +/- 0.4 ng.mL-1) at the end of the clamp. Glucose infusion rates required to maintain euglycemia were twofold higher in ID rats (27.0 +/- 5.4 mg.kg-1.min-1) versus C rats (13.1 +/- 3.3 mg.kg-1.min-1) (P less than 0.05). Circulating lactic acid increased in both groups, and the concentrations in ID rats (3.2 +/- 0.4 mmol.L-1) were significantly higher than those in C rats (1.8 +/- 0.5 mmol.L-1) at the end of the clamp. When the efficiency of insulin to dispose glucose was evaluated by calculating the glucose disposal divided by the prevailing insulinemia, ID rats could dispose of almost twice the glucose per unit of insulin [9.0 +/- 0.6 (mg.kg-1.min-1)/(ng.mL-1)] when compared with C rats [5.6 +/- 0.9 (mg.kg-1.min-1)/(ng.mL-1)] (P less than 0.05). The data indicate that insulin sensitivity is increased in ID rats and that ID rats cannot metabolize exogenous insulin as well as C rats.     

Sucrose-induced insulin resistance in the rat: modulation by exercise and diet

Isocaloric substitution of sucrose for starch results in hyperinsulinemia and deterioration of glucose tolerance, suggesting a loss of insulin sensitivity. In this study we have quantitated the insulin resistance which develops with sucrose feeding, and evaluated the ability of dietary fiber, or an increase in skeletal muscle activity, to inhibit, or even prevent, the detrimental effect of sucrose feeding on in vivo insulin action. Thus, 6-wk-old rats were fed one of the following regimens for three weeks: a 64% cornstarch diet (C), a 32% cornstarch + 32% sucrose diet (S), the (S) diet containing added wheat bran fiber (S/F), and the (S) diet given to rats running spontaneously in exercise wheel cages (S/ET). Insulin sensitivity was evaluated by comparing steady-state plasma glucose (SSPG) concentrations at constant plasma insulin levels approximately 70 microU/ml attained during the continuous infusion of epinephrine (0.08 micrograms/kg/min), propranolol (1.7 micrograms/kg/min), glucose (8 mg/kg/min), and insulin (2.5 mU/kg/min) to each experimental group. The results show that rats fed the S diet had a significant increase (p less than 0.01) in mean (+/- SEM) SSPG concentration compared with rats fed the C diet (255 +/- 14 versus 165 +/- 3 mg/dl). SSPG concentrations, although lower (p less than 0.05) in rats fed S/F (205 +/- 8 mg/dl), were still higher (p less than 0.05) than the C levels (165 +/- 3 mg/dl). However, S/ET completely inhibited the increase in SSPG concentration seen in rats fed S and the values were actually lower (p less than 0.05) than in rats fed C (100 +/- 10 versus 165 +/- 3 mg/dl). In conclusion 1) sucrose feeding results in a loss of insulin sensitivity in normal rats; 2) addition of fiber attenuates, but does not completely prevent, the loss of insulin sensitivity associated with feeding sucrose; 3) exercise training prevents the loss of insulin sensitivity seen in sucrose-fed rats, and actually improves glucose uptake beyond that seen in the control group. These results document the profound effect of environmental factors on in vivo insulin action.     

De novo glutamine synthesis induced by corticosteroids in vivo in rats is secondary to weight loss

INTRODUCTION: Corticosteroid treatment affects muscle protein and glutamine metabolism. In the present study we aimed to clarify to what extent anorexia, weight loss and corticosteroids determine protein and glutamine metabolism in muscle. METHODS: The study was performed in Wistar rats (300-350 g, n = 40) given triamcinolone (0.25 mg/kg/day i.m.) treatment (CS group) for 14 days, sham treated free fed (FF group), sham treated pair fed (PF group) and sham treated pair weight (PW group). In vivo protein and glutamine turnover were measured using L-[2,6-3H]phenylalanine and L-[3,4-3H]glurtamine as tracer in a three compartment model across the hindquarter. RESULTS: Corticosteroid treatment decreased total body weight to a greater extent than can be explained by decreased food intake only, justifying the need for pair weight controls. Muscle weight loss was relatively greater in the corticosteroid treated rats than in the pair weight controls indicating specific corticosteroid induced changes in muscle protein metabolism. Pair weight rats increased muscle net protein breakdown rates from -5 +/- 3 nmol x 100 g body weight(-1) x min(-1) to -15 +/- 3 nmol x 100 g body weight(-1) x min(-1) (P < 0.05 vs FF). In the corticosteroid treated rats net protein breakdown rates increased to -22 +/- 4 nmol x 100 g body weight(-1) x min(-1) (P < 0.01 CS vs FF/PF) Net protein breakdown in corticosteroid treated rats was accompanied by increased glutamine efflux from the hindquarter (P < 0.05, CS vs FF/PF/PW). The latter could predominantly be explained by de novo synthesis. Furthermore, corticosteroid treatment induced a loss of plasma to free muscle glutamine gradient indicating down regulation of glutamine membrane transport rates into muscle. This effect was, however, similar in the pair weight control group and can thus be fully accounted for by the muscle weight loss. CONCLUSION: Two weeks treatment with triamcinolone increases net in vivo protein breakdown of muscle directly and indirectly due to secondary weight loss and decreased food intake. The amino acid residues are used for glutamine de novo synthesis which is exported from muscle to visceral organs by down regulation of glutamine transport systems. These changes were in majority related to muscle weight loss.     

微米及纳米SiO2粉体的急性肺毒性比较

目的 比较纳米级SiO2与微米级SiO2粉体对呼吸道染尘大鼠的急性肺毒性.方法 雄性Wistar大鼠125只,按体重分为25组.呼吸道染尘剂量μm-SiO2分别为100(A组)、300 mg/m3(B组);nm-SiO2分别为100(A'组)、300 mg/m3(B'组).1次染尘2 h后,比较6、12、24、48、72 h支气管肺泡灌洗液(bronehoalveolar lavage fluid,BALF)中细胞总数(total cellular score,TCS)及分类、总蛋白(total protein,TPr)含量、碱性磷酸酶(alkaline phosphatase,AKP)和乳酸脱氢酶(lactate dehydrogenase,LDH)活性,血清和肺组织羟脯氨酸(hydroxyproline,HyP)含量.结果 染尘后6 h A'组BALF中TCS[(55.00±8.30)×104个/ml]、B'组BALF中TCS[(52.50±9.02)×104个/ml]均高于对照组[(34.88±12.53)×104个/ml];染尘后6、24 h A'组BALF中TCS[(55.00±8.30)×104个/ml、(39.75±12.08)×104个/ml]均高于等剂量微米SiO2染尘组[(32.38±13.07)×104个/ml、(24.13±10.97)×104个/ml].48 h A'组BALF中TPr[(0.34±0.09)g/L]、B'组BALF中TPr[(0.38±0.16)g/L]含量均高于等剂量微米SiO2染尘组[(0.20±0.07)g/L、(0.21±0.05)g/L].72 h A'组BALF中LDH活力[(1.66±0.22)×103 U/L]高于等剂量微米SiO2染尘组[(1.38±0.17)×103 U/L].6、24 h B'组BALF中AKP活力[(5.14±1.47)U/100 ml、(5.86±2.41)U/100 ml]均高于等剂量微米SiO2染尘组[(3.64±0.36)U/100 ml、(3.30±2.19)U/100 m1].6、12、48、72 h A'组肺组织HyP含量[(0.532±0.053)、(0.484±0.046)、(0.591±0.096)、(0.551±0.084)μg/mg肺湿重]以及12、72 h B'组肺组织HyP含量[(0.508±0.081)、(0.565±0.053)μg/mg肺湿重]均高于等剂量微米SiO2染尘组[(0.345±0.074)、(0.368±0.095)、(0.431±0.036)、(0.399±0.080)、(0.396±0.039)、(0.465±0.062)μg/mg肺湿重].结论 本实验条件下,与微米级SiO2粉尘相比,纳米级SiO2粉尘可导致较严重的急性肺毒性.     

High-performance inulin and oligofructose prebiotics increase the intestinal absorption of iron in rats with iron deficiency anaemia during the growth phase

Considering the high frequency of anaemia due to Fe deficiency, it is important to evaluate the effects of prebiotics on the absorption of Fe. The aim of the present study was to evaluate the effects of high-performance (HP) inulin, oligofructose and synergy1 during recovery from anaemia in rats through the intestinal absorption of Fe, food intake, body growth, caecal pH and weight of the intestine. Wistar rats (n 47) were fed with rations of AIN93-G with no Fe to induce Fe deficiency anaemia. At 36?d of life, anaemic rats were divided into four groups: (1) the HP inulin group; (2) the synergy1 group; and (3) the oligofructose group, all with 100?g of the respective prebiotic per kg of ration; and (4) a control group, in which the prebiotic was replaced by maize starch. Then, 25 mg of elemental Fe/kg of ration was added to all rations to allow recovery from anaemia. The final values of Hb in the HP inulin, synergy1, oligofructose and control groups were, respectively: 98 (94-99); 83 (81-92); 100 (90-114); 77 (72-81) g/l, with a statistically significant difference (P?≤?0·001) between the oligofructose and control groups and the HP inulin and control groups. The four groups had an increase in weight and body length and had similar consumption of rations. The intestinal weight and caecal pH were significantly different between the groups that consumed prebiotics and the control group. HP inulin and oligofructose increased the intestinal absorption of Fe in rats.     

Copper deficiency does not lead to taurine deficiency in rats

Copper deficiency has been reported to cause a decrease in urinary taurine excretion in rats. We determined whether Cu deficiency would decrease taurine status and the hepatic activities of cysteine dioxygenase (CDO) and/or cysteine sulfinic acid decarboxylase (CSAD) in rats. Ten weanling male rats were assigned to either a Cu-adequate (+Cu) or Cu-deficient (-Cu) group. All rats consumed a Cu-deficient purified diet and water ad-libitum for 16 wk. The water for the (+Cu) group contained 20 mg Cu/L as CuSO(4). At wk 16, the groups differed (P < 0.05) in the following variables (means +/- SEM, -Cu vs. +Cu): body weight (BW), 375 +/- 19 vs. 418 +/- 2.9 g; food intake, 16.2 +/- 0.7 vs. 18.5 +/- 0.4 g/d; hematocrit, 0.294 +/- 0.027 vs. 0.436 +/- 0.027; hemoglobin, 95.2 +/- 9 vs 134 +/- 10 g/L; liver Cu, 8.7 +/- 2.0 vs. 65.9 +/- 2.5 nmol/g; plasma Cu, 0.38 +/- 0.09 vs. 13.4 +/- 0.61 micromol/L; plasma ceruloplasmin activity, 1.75 +/- 1.0 vs. 67.9 +/- 8.4 IU; relative heart weight, 0.56 +/- 0.04 vs. 0.35 +/- 0.02% BW; relative liver weight, 4.06 +/- 0.23 vs. 3.37 +/- 0.06% BW; and liver CSAD activity, 18.8 +/- 1.37 vs. 13.5 +/- 1.11 nmol x min(-1) x mg protein(-1). The groups did not differ at wk 16 in: plasma taurine, 249 +/- 14 vs. 298 +/- 63 micromol/L; whole blood taurine, 386 +/- 32 vs. 390 +/- 25 micromol/L; urinary taurine excretion, 82.5 +/- 15 vs. 52.0 +/- 8.3 micromol/d; liver taurine, 2.6 +/- 0.7 vs. 2.8 +/- 0.4 micromol/g; liver total glutathione, 6.9 +/- 0.48 vs. 6.3 +/- 0.40 micromol/g; liver cyst(e)ine, 96 +/- 7.1 vs. 99 +/- 5.3 nmol/g and liver CDO activity, 2.19 +/- 0.33 vs. 2.74 +/- 0.21 nmol x min(-1) x mg protein(-1). These findings support the conclusion that Cu deficiency does not affect body taurine status.     

碱性成纤维细胞生长因子对大鼠骨骼肌拉伤后纤维化的抑制作用

目的　探讨外源性碱性成纤维细胞生长因子 (bFGF)对大鼠骨骼肌拉伤后肌肉修复的影响。方法　雄性SD大鼠 18只 ,体重 2 5 0～ 30 0g ,随机分为 3组 :拉伤后bFGF干预组 (Sb)、拉伤后给予生理盐水组 (S0 )和无拉伤对照组 (Con) ,每组 6只 ,用万能材料测试仪对Sb 组以及S0 组大鼠腓肠肌造成拉伤 ,Sb 组皮下肌膜外注射bFGF(2 0 0AU d× 6d) ,S0 组注射等体积生理盐水 (5 0 μl) ,免疫组织化学染色观察各组肌肉组织中波形蛋白的表达状况 ,作为肌肉纤维化的指标 ,波形蛋白表达用其积分光密度 (integraopticaldensity ,IOD)表示。结果　肌肉损伤后波形蛋白表达增强 ,S0 组肌肉组织波形蛋白IOD值 [(2 4 .2 9± 7.91)× 10 3]高于Con组 [(5 .75± 3.87)× 10 3],Sb 组IOD值 [(15 .78± 7.72 )× 10 3]明显低于S0 组 ,差异均有显著性 (P <0 .0 1)。结论　外源性bFGF可以降低损伤肌肉组织中波形蛋白的特异性表达 ,降低肌组织纤维化程度 ,从而促进肌肉损伤后结构及功能的修复。     

Effects of soy protein supplemented with methionine on blood lipids and adiposity of rats

OBJECTIVE: The effects of soy protein isolate (SPI) versus casein on blood lipids and adiposity were investigated in rats fed methionine-equivalent diets. METHODS: Twenty-eight male Sprague-Dawley rats (230 to 250 g) were assigned in equal numbers to groups consuming SPI- or casein-based diets (20%) supplemented with L-methionine. After 28 d, blood was collected for triacylglycerol, total cholesterol, and high-density lipoprotein cholesterol assessment and epididymal fat pads were weighed. RESULTS: Food intake (519 +/- 90 versus 490 +/- 115 g), weight gain (144 +/- 35 versus 133 +/- 28 g), food efficiency ratio (0.29 +/- 0.09 versus 0.28 +/- 0.06), epididymal fat pad weights (5.409 +/- 2.076 versus 4.768 +/- 1.867 g), and serum concentrations of triacylglycerol (96.3 +/- 41.8 versus 93.4 +/- 37.4 mg/dL) and high-density lipoprotein cholesterol (32.6 +/- 7.4 versus 33.8 +/- 4.4 mg/dL) were similar between the casein and SPI groups, respectively. However, total cholesterol (73.8 +/- 17.8 versus 59.3 +/- 11.9 mg/dL) concentration was higher for the casein-fed rats than for the SPI-fed rats, respectively (P < 0.05). CONCLUSIONS: These results suggest that methionine supplementation may eliminate the decreased fat deposition previously ascribed to soy protein; however, methionine did not abolish the commonly observed hypocholesterolemic effects of soy.     

Arginine-enriched diet limits plasma and muscle glutamine depletion in head-injured rats

OBJECTIVE: Injury is associated with a depletion in glutamine (GLN) pools, which may contribute to impairment of immune and nutritional statuses. Total parenteral nutrition enriched with arginine (ARG) is able to generate GLN in surgical patients. We hypothesized that this same concept may be applicable to enteral administration and could be extended to muscle GLN reserves. This study investigated the ability of an enteral formula enriched with ARG to restore the GLN pools in an experimental model of head injury. METHODS: Twenty-five male Sprague-Dawley rats were randomized into 4 groups: ad libitum access to food, head injury plus free access to nutrition, head injury plus standard enteral nutrition (Sondalis), and an immune-enhancing diet (IED). The two enteral diets were adjusted to be isocaloric (290 kcal.kg(-1).d(-1)) and isonitrogenous (3.29 g.kg(-1).d(-1)) and were delivered for 4 d (24 h/24 h). After sacrifice, plasma and muscle amino acids were determined. RESULTS: Head injury was associated with a large depletion of muscle and plasma GLN pools that were restored by IED administration but not by the standard diet. Moreover, the IED but not the standard diet improved or normalized ornithine and glutamate pools, suggesting that the modification of GLN pools is related to ARG administration. CONCLUSION: In our model of head injury, our IED, a diet without free GLN, is efficient in restoring the plasma and muscle pools of GLN, probably due to its high ARG content.     

天麻对铅所致大鼠海马损害的拮抗作用

目的　观察并探讨天麻对铅所致学习记忆损害的拮抗作用。方法　选用 36只Wistar大鼠 ,随机分为 3组 ,每组 12只。 (1)对照组 :给予蒸馏水 ;(2 )染铅组 :醋酸铅 (0 .1g·kg-1·d-1) ;(3)天麻铅组 :醋酸铅 (0 .1g·kg-1·d-1) +天麻 (4.0g·kg-1·d-1)。每月用游泳试验测试学习记忆 1次。 3个月后处死大鼠 ,分别测定大鼠海马一氧化氮 (NO)和总抗氧化能力 (TAOC)并进行病理检查。结果　 (1)在游泳试验中 ,染铅组大鼠 5min内到达平台次数 (1、2、3月分别为 :10 .1± 1.10、7.8± 1.30、5 .4±0 .97)低于对照组 ,差异有显著性 (P <0 .0 1) ;天麻铅组大鼠到达平台的次数 (1、2、3月分别为 :11.9±0 .95、10 .9± 0 .95、9.7± 0 .96 )高于染铅组 ,差异有显著性 (P <0 .0 1)。 (2 )染铅组大鼠海马NO含量为(0 .733± 0 .0 15 ) μmol/gpro和TAOC为 (0 .94 5± 0 .0 17)U/mgpro ,低于对照组 ,差异有显著性 (P <0 .0 1) ;天麻铅组海马NO含量为 (0 .76 9± 0 .0 2 1) μmol/gpro和TAOC为 (0 .986± 0 .0 10 )U/mgpro ,高于染铅组 ,差异有显著性 (P <0 .0 1)。 (3)病理检查 :染铅组大鼠海马明显萎缩 ,细胞变性坏死、脱失明显 ,轴突溶解或消失 ;天麻铅组海马萎缩不明显 ,细胞形态基本正常 ,无明显坏死、脱失现象 ,轴     

甲萘威对雌性大鼠血清雌激素水平及抗氧化系统功能的影响

目的观察甲萘威对雌性大鼠的生殖毒性并初步探讨其机制。方法雌性SD大鼠经口染毒甲萘威,剂量为0、1.028、5.140、25.704mg·kg-1·d-1。阴道脱落细胞涂片法观察大鼠动情周期的变化;放射免疫法测定其血清雌二醇(E2)、孕酮(P4)水平;分光光度法测定其血清超氧化物歧化酶(SOD)、谷胱甘肽硫转移酶(GST)的活力以及丙二醛(MDA)、谷胱甘肽(GSH)的含量。结果各剂量甲萘威染毒组大鼠动情周期数明显低于对照组。染毒后15d大鼠动情各期出现变化,与对照组的差异有统计学意义(P<0.05,P<0.01)。25.704mg·kg-1·d-1组大鼠体重增长明显低于对照组。各剂量染毒组大鼠的多个脏器系数均明显降低。25.704mg·kg-1·d-1组大鼠血清中E2水平为(19.93±2.21)nmoll,1.028mg·kg-1·d-1组大鼠P4水平为(1.21±0.40)nmoll,与对照组[(28.76±6.12)、(0.63±0.39)nmolL]的差异均有统计学意义(P<0.05)。随染毒剂量增高,大鼠SOD活力在卵巢先降后升,在血清中略升后下降;MDA含量则呈在卵巢中渐升高、在血清中略升后降低趋势;GSH含量和GST活力在卵巢中呈先降后升趋势,但在血清中,GSH含量呈下降趋势,GST活力先上升后下降。结论甲萘威可致雌性大鼠动情周期紊乱及雌激素水平改变,对大鼠的抗氧化系统产生一定影响。     

锌对免疫器官的影响

通过建立大鼠缺锌（ＺＤ）、高锌（ＺＥ）模型，研究锌对免疫器官——骨髓、胸腺、脾脏的影响。结果表明：（１）ＺＤ、ＺＥ组体重、体重增长值、饲料效价均非常显著地低于配对（ＰＦ）组和自由喂养（ＡＬ）组，缺锌补锌（ＺＤ＋ＡＬ）组达正常水平。（２）ＺＤ组血清、毛发、股骨、肝脏锌均非常显著地低于ＰＦ、ＡＬ组，而ＺＥ组则相反，ＺＤ＋ＡＬ组达正常水平。（３）ＺＤ、ＺＥ组的胸腺重量、胸腺指数、胸腺肽量和胸腺活性均非常显著地低于ＰＦ、ＡＬ组，ＺＤ＋ＡＬ组达正常水平。（４）ＺＤ、ＺＥ组脾脏重量、脾脏指数均非常显著地低于ＰＦ、ＡＬ组，ＺＤ＋ＡＬ组达正常水平。（５）ＺＤ、ＺＥ组骨髓细胞３Ｈ一ＴｄＲ掺入率和外周血白细胞总数显著下降，其中尤以淋巴细胞减少为着。（６）骨髓细胞、脾脏淋巴细胞周期显示ＺＤ、ＺＥ组静止期细胞明显增高，而增殖期细胞下降，与ＰＦ、ＡＬ组间差别非常显著。以上结果提示，适量锌有促进免疫器官——骨髓、胸腺、脾脏发育和功能活动的作用。而缺锌和高锌则抑制免疫器官的发育和免疫细胞的功能。     

沥青烟致小鼠肺损伤及细胞周期改变的研究

目的研究沥青烟致癌和致突变作用的机制。方法用沥青烟对小鼠进行不同剂量(55、165 mg/m~3)和不同时间(30、60 d)的染毒,观察小鼠肺组织病理形态改变,并用流式细胞仪进行小鼠肺组织细胞DNA含量的检测和细胞周期的分析。结果随着沥青烟染毒时间和剂量的增加,小鼠肺组织病变表现为不同程度的不典型增生和原位癌；同时小鼠肺组织细胞各周期指数发生变化,G_1期细胞数下降,S期阻滞,进入G_2/M期的细胞减少,细胞增殖指数(PI)增加,异倍体指数(DI)升高,与对照组比较,差异均有统计学意义(P＜0．05)。染毒相同时间时,55 mg/m~3和165mg/m~3剂量组的PI均高于对照组,165 mg/m~3剂量组的DI高于55mg/m~3剂量组,差异均有统计学意义(P＜0．05或P＜0．01)。相同染毒剂量下,60 d处理组的DI[(1．16±1．51)×10~(-2)、(1．20±2．30)×10~(-2)]均高于30 d处理组[(1．14±0．88)×10~(-2)、(1．16±1．47)×10~(-2)],差异有统计学意义(P＜0．05)。结论沥青烟所致小鼠肺组织产生的癌前病变可能与细胞周期的改变有关。     

Effects of carbohydrate restriction on renal injury in the obese Zucker rat

The obese Zucker rat model of nonimmune-mediated, spontaneous focal glomerulosclerosis is ideally suited to study the influence of diet on the initiation and progression of glomerular injury. Young (6 wk) and old (33 wk) lean and obese female Zucker rats were fed a carbohydrate-restricted diet intermittently for 27 wk. Carbohydrate restriction resulted in lower body weight (460 +/- 16 versus 310 +/- 7 g, p less than 0.025), kidney weight (1.26 +/- 0.04 versus 1.07 +/- 0.05 g, p less than 0.025), and glomerular area (6930 +/- 290 versus 5780 +/- 230 micron2, p less than 0.025) in young obese Zucker rats compared to ad libitum-fed rats. Although urine-albumin excretion was substantially reduced by carbohydrate restriction in young obese Zucker rats (41.1 +/- 12.3 versus 6.9 +/- 2.9 mg/24 h, p less than 0.01), glomerular injury was not significantly altered. In old obese rats, carbohydrate restriction did not significantly reduce albuminuria or prevent the progression of glomerular injury. Thus, intermittent carbohydrate restriction failed to alter significantly either the initiation of glomerular injury in young, or the progression of nephron damage in old, obese Zucker rats.