Effect of Iron Supplementation on Oxidative Stress and Intestinal Inflammation in Rats with Acute Colitis

In this study, we investigated the effect of intraperitoneal iron dextran (100mg/100 g body weight) on oxidative stress and intestinal inflammation in rats with acute colitis induced by 5% dextran sulfate sodium. In both colitis and healthy animals, disease activity index, crypt and inflammatory scores, colon length, plasma and colonic lipid peroxides, and plasma vitamins E, C, and retinol were assessed. The results showed that iron-supplemented groups had moderate iron deposition in the colonic submucosa and lamina propria. In the colitis group supplemented with iron, colon length was significantly shorter; disease activity index, crypt, and inflammatory scores and colonic lipid peroxides were significantly higher; and plasma -tocopherol was significantly lower compared to the colitis group without iron supplementation. There was no intestinal inflammation and no significant increase in colonic lipid peroxides in healthy rats supplemented with iron. In conclusion, iron injection resulted in an increased oxidative stress and intestinal inflammation in rats with colitis but not in healthy rats.     

Systemic Iron Supplementation Replenishes Iron Stores Without Enhancing Colon Carcinogenesis in Murine Models of Ulcerative Colitis: Comparison with Iron-Enriched Diet

Ulcerative colitis (UC) patients frequently require iron supplementation to remedy anemia. The impact of systemic iron supplementation (intraperitoneal injection) on UC-associated carcinogenesis was assessed in mice subjected to cyclic dextran sulfate sodium (DSS) treatment and compared with dietary iron enrichment. Systemic iron supplementation, but not a twofold iron diet, remedied iron deficiency as indicated by the histochemical detection of splenic iron stores. A twofold iron diet, but not systemic iron, increased iron accumulation in colonic luminal contents, at the colonic mucosal surface, and in superficial epithelial cells. Colitis-associated colorectal tumor incidence after 15 DSS cycles was not affected by systemic iron (2/28; 7.1%) compared to nonsupplemented controls (4/28; 14.1%) but was significantly increased by the twofold iron diet (24/33; 72.7%) (P < 0.001). Mechanistic study revealed that systemic iron had no effect on DSS-induced inflammation, or colonic iNOS and COX-2 protein levels, compared to controls. Systemic iron supplementation for 16 weeks replenished splenic iron in a spontaneous colitis model (interleukin-2-deficient mice) and significantly reduced colonic inflammation compared to interleukin-2 (–/–) controls without increasing hyperplastic lesions. These results suggest that iron supplemented systemically could be used to remedy anemia in UC patients without exacerbating inflammation or enhancing colon cancer risk. These findings need to be verified in clinical studies.This work was supported by Research Project Grant RPG-00-034-01-CNE from the American Cancer Society and NIH Grant RO1CA104741-01A1 (G.-Y.Y.).     

Stress Increases Susceptibility to Oxidative/Nitrosative Mucosal Damage in an Experimental Model of Colitis in Rats

Inflammatory bowel diseases (IBDs) are multifactorial processes. Clinical and animal studies indicate that emotional stress may contribute to the onset and progress of these diseases. On the other hand, enhanced free radical production in mucosal cells has been also implicated in the pathogenesis of IBD. Using an experimental model of colitis induced by intrarectal instillation of 2,4,6-trinitrobenzene sulfonic acid (TNBS) plus ethanol (vehicle), we sought to determine whether prior exposure to immobilization stress modifies the susceptibility to oxidative damage in colonic mucosa. Several groups of Wistar rats were used: control (C) and stressed (by immobilization of 6 hr every day during 10 days; S) groups and rats receiving a colitis-inducing dose of TNBS on day 5 (30 mg; TNBS30) and a noninflammatory dose of TNBS on day 5 (5 mg; TNBS5) with or without stress (prior exposure, days 0-5, and after, days 5-10). At the 10th day, colonic tissue was dissected and processed for biochemical studies. TNBS30 led to body weight loss, macroscopic colonic ulceration, and inflammation (determined by histological parameters and myeloperoxidase [MPO] activity) and to an increase in inducible nitric oxide synthase (NOS-2) activity and expression. TNBS5-instilled animals' body weight and biochemical inflammatory parameters were not significantly different from those in control animals. Interestingly, while stress did not modify body weight, macroscopic aspect of the mucosa, or NOS activity in animals receiving TNBS30, immobilization increased body weight loss, MPO levels, and malondialdehyde (MDA; an indicator of lipid peroxidation) levels after TNBS5. On the other hand, stress increased NOS-2 activity and immunohistochemical expression after instillation of TNBS5. Moreover, constitutive, Ca2+ -dependent NOS activity decreased in stressed animals instilled with TNBS5 compared with nonstressed animals receiving TNBS5 (-28.5 +/- 6.6%; P < 0.05). These findings indicate that previous exposure to stressful stimuli is a factor in susceptibility to oxidative damage in experimental colitis and support a possible protective effect of treatment of stress before and during the development of inflammation in the colon.     

Correlations Between Iron Status Markers During Normal Pregnancy in Women with and without Iron Supplementation

The aim was to evaluate relationships between iron status markers (haemoglobin, erythrocyte indices, serum iron, serum transferrin, serum transferrin saturation, serum ferritin) in normal pregnancy. Iron status markers were measured at 4-week-intervals during pregnancy and postpartum in 120 healthy women; 62 had daily treatment with tablets containing 66 mg ferrous iron, 58 were treated with placebo. Placebo-treated: Ferritin displayed positive correlations with transferrin saturation during 2nd and 3rd trimester. There were positive correlations between ferritin, erythrocyte MCV and MCH during 2nd and 3rd trimester and postpartum. Prior to delivery and postpartum, ferritin demonstrated positive correlations with haemoglobin. Transferrin saturation showed positive correlations with MCV, MCH and MCHC during 2nd and 3rd trimester and postpartum. Transferrin saturation displayed positive correlations with haemoglobin prior to delivery and postpartum. Iron-treated: In general, there were no correlations between iron status markers. Positive correlations appeared postpartum between ferritin, transferrin saturation and MCHC but not with haemoglobin. Transferrin saturation showed a positive correlation with MCH postpartum, but not with haemoglobin. Conclusion: The patterns of relationships in placebo-treated women were consistent with iron deficient erythropoiesis.     

Iron Absorption during Iron Supplementation in Blood Donors

The total amount of iron absorbed from a total supplementation of 2000 mg of iron was studied after a blood donation. 10 regular blood donors and 10 subjects without previous blood loss were included in the study. No subject had received any iron treatment before the investigation. Both groups were given one sustained release tablet containing 100 mg of iron as Fe SO₄ once daily for 20 days. The iron in these tablets was labelled with ⁵⁹Fe. The total amount of iron absorbed from the tablets was measured by a whole body counting technique. Laboratory tests including haematological data, desferrioxamine tests and sternal marrow punctures were made before and after the iron treatment. The non-donors lost a mean amount of 215 mg iron by phlebotomy and the total iron absorption from the tablets was only 94 mg (4.7%). In the regular blood donors the corresponding iron loss was 276 mg and the absorption was 280 mg (14%). The iron supplementation given in this study covered the iron losses in the regular blood donors but not in the non-donors. This iron prophylaxis will prevent a depletion but not a reduction of the iron stores in blood donors with high donation frequency.     

Insecure Attachment in a Subgroup with Ulcerative Colitis Defined by ANCA Status

This study is the first test of the novel hypothesis that perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) marks an etiological division between stress-susceptible and stress-neutral ulcerative colitis. Subjects were 47 UC patients with known p-ANCA status (19 p-ANCA-positive, 28 p-ANCA-absent). Controls were 77 university students. Subjects and controls completed the Reciprocal Attachment Questionnaire. Subjects were categorized as avoidant/nonavoidant and anxious/nonanxious based on scores for compulsive self-reliance and compulsive care seeking, respectively. A higher prevalence of avoidant attachment was present in p-ANCA-absent (58.6%) than p-ANCA-positive subjects (22.2%, chi-square = 5.95, P < 0.02). There was no difference in the prevalence of anxious attachment between p-ANCA-absent and p-ANCA-positive subjects. There was no difference in clinical and psychiatric variables between groups. This finding provides support for a psychobiological contribution to UC in a subgroup identified by the absence of p-ANCA.     

Prophylactic Administration of Topical Glutamine Enhances the Capability of the Rat Colon to Resist Inflammatory Damage

Glutamine is an important nutrient for the GI tract and has been shown to exert a protective effect on the bowel. Nonetheless, in the context of IBD, data demonstrating a therapeutic role for glutamine has been inconclusive. IBD is associated with oxidative stress caused by reactive oxygen species. We aimed to investigate the effect of topical glutamine administration in rats before or after induction of colitis by trinitrobenzenosulfonic acid. In study I glutamine enemas were given beginning 2 days before or on the same day of induction of colitis. Inflammation severity was assessed by macroscopic and microscopic score and tissue myeloperoxidase activity. In study II glutamine enemas were given for 3 days without induction of colitis: mitotic index and colonic crypt length were measured, as well as water-soluble low molecular weight antioxidants and energy-rich phosphate levels (by HPLC). Results showed that glutamine significantly decreased indexes of inflammation when administered before induction of colitis. Glutamine caused an increase in the mitotic index and the levels of water-soluble low molecular weight antioxidants and energy-rich phosphates. We conclude that glutamine exerts a beneficial effect only when administered before induction of colitis, by increasing the resistance of the colonic tissue to inflammatory injury. This effect is probably mediated by increasing the antioxidant capacity and energy level of the tissue.     

Decreased Total and Corrected Antioxidant Capacity in Patients with Inflammatory Bowel Disease

Oxidative stress and depletion of antioxidants may play a key role in the pathogenesis of inflammatory bowel disease (IBD)-related intestinal damage. A new automated assay for the determination of blood total antioxidant capacity (TAC), based on the crocin bleaching method, has been used for the measurement of TAC and corrected TAC (cTAC) in patients with ulcerative colitis (UC) and Crohn's disease (CD) in comparison to healthy controls (HC). Ninety-four patients with UC, 97 patients with CD, and 72 HC were included in this study. Serum TAC was measured in all patients and controls on an Olympus AU-600 chemistry analyzer using a TAC kit. cTAC was calculated from TAC after subtraction of the interactions due to endogenous uric acid, bilirubin and albumin. Mean serum TAC as well as cTAC levels were significantly lower in both UC and CD patients compared with HC (P < 0.0001). Patients with active UC had no different TAC and cTAC compared to those with inactive disease. Patients with active CD had significantly lower mean TAC compared to those with inactive disease but cTAC was not different between the two phases of disease activity. Patients with proctitis had significantly higher TAC and cTAC compared to patients with left-sided colitis and total colitis. In CD patients no association between disease localization and these markers was found. TAC and cTAC are significantly reduced in IBD patients compared with controls irrespective of disease activity. The decreased antioxidant defenses may be a primary phenomenon severely compromising the mucosa and therefore increase susceptibility to oxidative tissue damage.     

Do Vitamin E and Selenium Have Beneficial Effects on Trinitrobenzenesulfonic Acid-Induced Experimental Colitis

The balance between oxidant and antioxidant systems may be important in the pathogenesis and/or maintenance of tissue injury in ulcerative colitis. This study was designed to evaluate the effects of vitamin E and selenium supplementations on tissue injury and oxidative stress in trinitrobenzenesulfonic acid-induced ulcerative colitis in rats. Trinitrobenzenesulfonic acid administration severely changed the normal architecture of the colon and significantly increased the levels of malondialdehyde, protein carbonyl, and xantine oxidase (P < 0.001) in the colon homogenates of these rats. Supplementation of selenium to the trinitrobenzenesulfonic acid-treated rats neither improved the histopathological findings nor decreased the levels of malondialdehyde and protein carbonyl. Vitamin E supplementation reduced the levels of malondialdehyde and protein carbonyl but did not improve the colonic lesions. Supplementation of vitamin E + selenium significantly reduced both the severity of colonic lesions and the levels of malondialdehyde and protein carbonyl. In conclusion, we suggest that antioxidants and specific micronutrients may have beneficial effects in the treatment of ulcerative colitis.     

Therapeutic Role for Bismuth Compounds in TNBS-Induced Colitis in the Rat

The 2,4,6-trinitrobenzene sulfonic acid (TNBS) -induced model of chronic inflammation of the rat colon was used to determine the efficacy of bismuth subsalicylate (BSS), bismuth subcitrate (CBS), and 5-aminosalicylic acid (5-ASA) administered in enema form. A novel bismuth compound 1, 2-bis[2-(1,3-dithiobismolane)thio]ethane [Bi₂(EDT)₃] was also tested. On day 1 colitis was induced with 50 mg TNBS/50% ethanol in female Sprague-Dawley rats, while controls received a saline enema. On day 3, twice-daily treatment with enemas of either saline, BSS, CBS, Bi₂(EDT)₃, or 5-ASA were initiated in the colitis and control rats. All rats were killed on day 14, and the colons excised, weighed, rated macroscopically, and then fixed for hematoxylin and eosin staining. Blinded microscopic scoring was used to determine injury and healing in all groups. Colon mass and macroscopic scores were increased (P < 0.05) in the group of rats treated with TNBS (N = 16) compared to saline controls (N = 12). Colon mass and macroscopic scores in controls treated with BSS (N = 4), CBS (N = 4), Bi₂(EDT)₃ (N = 4), and 5-ASA (N = 4) alone did not differ from saline control animals. Macroscopic scoring showed a decrease (P < 0.05) in the degree of damage in the group of rats treated with TNBS plus BSS (N = 15), TNBS plus Bi₂(EDT)₃ (N = 10) and TNBS plus CBS (N = 4) compared to the group of rats treated with TNBS plus saline (N = 16). A decrease (P < 0.05) in injury and an increase (P < 0.05, Kruskal-Wallis) in healing was observed in the groups of rats treated with TNBS plus BSS, TNBS plus CBS, and TNBS plus 5-ASA compared to the group of rats treated with TNBS plus saline. It appeared that Bi₂(EDT)₃ was not protective against injury at the microscopic level but that the novel Bi₂(EDT)₃ has an effective healing capacity at the macroscopic level. We conclude that BSS and CBS decrease injury and/or promote healing as effectively as 5-ASA in this model.     

Iron Metabolism and Oxidative Status in Patients with Hb H Disease

To evaluate the iron metabolism and oxidative status in patients with Hb H disease, we investigated 43 patients with Hb H disease, including eight deletional Hb H disease patients and 35 nondeletional Hb H disease patients and 20 healthy controls. The levels of hematological parameters, serum ferritin, hepcidin, superoxide dismutase (SOD), malondialdehyde (MDA) and total antioxidant capacity (TAC), were examined. We found higher serum ferritin levels and lower hepcidin, MDA and TAC levels in Hb H disease patients than in controls. The hepcidin level in Hb H disease patients was positively correlated with MDA and TAC levels but not with serum ferritin and SOD levels. The patients with nondeletional Hb H disease showed higher serum ferritin and Hb H concentrations than those patients with deletional Hb H disease. However, no statistically significant differences in SOD, MDA and TAC levels were found in patients with deletional and nondeletional Hb H disease. Oxidative stress and antioxidant defense were related to hepcidin levels. Our study indicated that hepcidin might be an important parameter for monitoring the iron metabolism and oxidative status of Hb H disease patients.     

复方青黛颗粒对大鼠溃疡性结肠炎模型的影响

目的 :观察复方青黛颗粒对大鼠溃疡性结肠炎模型的影响 ,为临床用药的有效性提供实验依据。方法 :采用异种异体结肠粘膜组织致敏法。将 SD大鼠随机分为空白对照组 ,模型对照组 ,复方青黛颗粒高、中、低剂量组 ,泻痢消胶囊组。连续给药 4周。空白对照组和模型对照组灌胃给予等量生理盐水 ;末次给药后 2 4 h,大鼠眼眶采血 ,测定乳酸脱氢酶和淀粉酶含量 ;处死大鼠 ,计数全结肠溃疡点和充血点 ;称结肠湿重 ,计算肠重指数。结果 :复方青黛颗粒 3个剂量组大鼠的溃疡数和充血指数显著减少或降低 ,与模型对照组比较差异有非常显著性意义 (P <0 .0 1) ,各剂量组大鼠的结肠重量和肠重指数 ,都有显著增加 ,中、高两剂量组与模型对照组比较差异有显著性意义(P <0 .0 5 ,<0 .0 1) ;血清乳酸脱氢酶含量较模型对照组有降低趋势 (P >0 .0 5 ) ,复方青黛颗粒组均有使模型动物降低的血清淀粉酶含量明显恢复的作用 ,与模型对照组比较差异有显著性意义 (P <0 .0 5或 <0 .0 1)。结论 :复方青黛颗粒对溃疡性结肠炎模型大鼠有显著的治疗作用     

Therapeutic Potential of Two Probiotics in Inflammatory Bowel Disease as observed in the Trinitrobenzene Sulfonic Acid Model of Colitis

Purpose  The pathogenesis of inflammatory bowel disease is thought to be a multifactorial process. One of the leading hypotheses is that an imbalance in normal gut flora induces an excessive immune response and contributes to inflammation in the gastrointestinal tract. Administration of probiotic bacteria reduces symptoms in patients suffering from inflammatory bowel diseases, probably via both manipulation of the microflora and stimulation of the intestinal immune system. In the current study the therapeutic potential of two different probiotics–Lactobacillus GG and a mixture of Streptococcus thermophilus, Lactobacillus acidophilus, and Bifidobacterium longum (YO-MIX™ Y 109 FRO 1000)—in a rat model of colitis were evaluated. Methods  Male Wistar rats were administered probiotics for three days simultaneously with colitis induction. Colonic damage was evaluated histologically and biochemically and colonic tissues, as well as fecal samples, were used for bacterial studies using 16S rRNA gene primers. Results  Probiotics administration reduced the relative amounts of the pathogenic bacteria Aeromonas and Escherichia coli in the colonic tissue. However, whereas both probiotics affected colon morphology, only Lactobacillus GG administration reduced myeloperoxidase activity. Conclusions  We report the therapeutic rather than preventive potential of two different probiotics in an animal model of colitis. Reprints are not available.     

Expression of Alkaline Sphingomyelinase in Yeast Cells and Anti-inflammatory Effects of the Expressed Enzyme in a Rat Colitis Model

Alkaline sphingomyelinase (Alk-SMase) is a key enzyme in the intestinal tract for digestion of dietary sphingomyelin (SM), which generates lipid messengers with cell-cycle regulating effects. The enzyme is significantly decreased in ulcerative colitis and colon cancer. Based on this information, we wanted to investigate whether the enzyme had preventive effects against murine colitis. We report herein a method to express a biologically active Alk-SMase from Pichia pastoris yeast cells. By using the expressed enzyme to treat a rat colitis model induced by dextran sulfate sodium, we found that intrarectal instillation of Alk-SMase once daily for 1 week significantly reduced the inflammation score and protected the colonic epithelium from inflammatory destruction. We found a tendency for decreased tumor necrosis factor (TNF)-α expression in the Alk-SMase-treated group. This study, for the first time, provides a method to produce the enzyme and shows the potential applicability of the enzyme in the treatment of inflammatory bowel diseases.     

Dextran Sulfate Sodium-Induced Colitis in Immunodeficient Rats

To examine the morphology of colitis and study the role of the immune system in colitis, we compared colitis in immunocompetent Wistar-Kyoto rats with that in spontaneously hypertensive rats, known to have T-cell dysfunction. Rats were treated with 3% dextran sulfate in drinking water for periods ranging from 3 to 60 days. Diarrhea developed earlier and was associated with a more severe weight loss in Wistar-Kyoto rats than spontaneously hypertensive rats. The morphologic findings (flattening of the gland epithelium, gland dropout and ulceration) in spontaneously hypertensive rats were milder than in Wistar-Kyoto rats. Only spontaneously hypertensive rats survived 60 days of treatment; the findings included ulceration, crypt distortion, and inflammatory pseudopolyp formation. Immunostaining for B-cell, T-cell, and macrophage markers showed no difference in the distribution of these cells in the mucosa of Wistar-Kyoto rats and spontaneously hypertensive rats. Spontaneously hypertensive rats with T-cell dysfunction develop dextran sulfate sodium-induced colitis.     

Relation Between Colonic Inflammation Severity and Total Low-Molecular-Weight Antioxidant Profiles in Experimental Colitis

Tissue antioxidant status is altered as a response to oxidative stress. This oxidative stress, caused by reactive oxygen species, is associated with inflammatory bowel disease (IBD). Our aim was to examine the relationship between total tissue low-molecular-weight antioxidant (LMWA) profile and inflammation severity in dinitrobenzene sulfonic acid (DNBS) experimental colitis in the rat. Rats were treated with three doses of DNBS: 1, 10, and 20 mg. Inflammation severity was assessed by tissue colonic wet weight, macroscopic evaluation, and tissue myeloperoxidase (MPO) activity. The capacity of water-soluble LMWA was assessed by measuring the reducing power of the tissues with cyclic voltammetry (CV) and by measuring tissue levels of reduced glutathione. While typical markers of inflammation (MPO, macroscopic examination, and colonic wet weight) indicated DNBS dose dependency, such dependency could not be demonstrated for the tissue LMWA as measured by reduced glutathione levels and by the tissues' reducing power. Mild colonic inflammation (induced by ethanol or by 1 mg of DNBS) caused an increase in the overall capacity of water-soluble LMWA. However, severe inflammation (induced by 20 mg of DNBS) caused a reduction in the tissue LMWA capacity. An intermediate dose of DNBS (10 mg) caused moderate inflammation, but did not cause a significant change in the tissue LMWA compared with a saline control treatment. In conclusion, LMWA changed in a biphasic pattern reflective of the severity of mucosal colonic inflammation. It is suggested that: low dose of DNBS (1 mg) and topical alcohol (25% v/v) caused an adaptation effect to the mild oxidative stress associated with mild inflammation. This resulted in an increase in the LMWA. A higher dose of DNBS (20 mg) caused more severe inflammation with an overall reduction in LMWA. The increased efflux of reactive oxygen species, associated with severe inflammation, led to an overall consumption of the tissue LMWA, which masked the increase in LMWA caused by the mild oxidative stress.     

Binding of Hydrogen Sulfide by Bismuth Does Not Prevent Dextran Sulfate-Induced Colitis in Rats

Several lines of evidence suggest that ulcerative colitis could be caused by excessive bacterial production of H₂S in the colon. A rodent model of colitis involves the feeding of nonabsorbable, carbohydrate-bound sulfate in the form of dextran sulfate or carrageenan. The observation that metronidazole blocks the development of this colitis suggested that the injurious agent could be a sulfur-containing compound (such as H₂S) that is released during the bacterial metabolism of the nonabsorbed sulfate. We tested this possibility by feeding rats dextran sulfate, with or without bismuth subsalicylate, a compound that avidly binds H₂S. Bismuth subsalicylate reduced the fecal release of H₂S in dextran sulfate-treated rats to values well below that of controls. Nevertheless, all the animals developed colitis. We conclude that excessive H₂S production does not play a role in the dextran sulfate model of colitis.     

Intestinal 5-Hydroxytryptamine and Mast Cell Infiltration in Rat Experimental Colitis

The present study evaluated the extent of dysfunction of the 5-hydroxytryptaminergic system in inflamed (distal colon) and noninflamed segments (jejunum and ileum) after intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in the rat. Dexamethasone was administered to control rats and TNBS-treated animals before and for 7 days after TNBS treatment. Tissue levels of 5-hydroxytryptamine (5-HT) in the inflamed colon were higher than in controls. The densitmast cells was also markedly increased. Treatment with dexamethasone attenuated the inflammatory response but did not prevent the increase in colonic 5-HT. In the noninflamed jejunum and terminal ileum, 5-HT tissue levels were markedly increased, but treatment with dexamethasone prevented this increase. It is concluded that the increase in 5-HT levels in the inflamed colon in TNBS-induced colitis may result fmast cell infiltration. In the noninflamed intestine, 5-HT tissue levels were also increased, favoring the view of a generalized mast cell infiltration.     

炎症性肠病患者服用铁剂的耐受性及疗效

目的 回顾性地比较炎症性肠病（IBD）患者与非IBD患者服用铁剂的耐受性与疗效.方法 对2000年1月至2005年3月期间住院病历中符合IBD的217例患者及26例非炎症性原因引起缺铁的患者进行回顾性分析.结果 217例IBD患者中有42例（19.4%）,非IBD组有15例（57.7%）患者接受过口服铁剂治疗,IBD组有7例（16.7%）,非IBD组有3例（11.5%）不能耐受口服铁剂治疗（P＞0.05）.依据检查结果,IBD组有11例（31.4%）,非IBD组有8例（38.1%）治疗有效.结论 IBD患者对口服铁剂的耐受性和治疗效果与非IBD患者相比,没有明显差异.     

Iron Absorption in Relation to Iron Status

The absorption from a 3 mg dose of ferrous iron was measured in 250 male subjects. The absorption was related to the log concentration of serum ferritin in 186 subjects of whom 99 were regular blood donors (r = —0.76), and to bone marrow haemosiderin grading in 52 subjects with varying iron status. The purpose was to try and establish a percentage absorption from such a dose that is representative of subjects who are borderline iron deficient. This information is necessary for food iron absorption studies in order (1) to calculate the absorption of iron from the diet at a given iron status and (2) compare the absorption of iron from different meals studied in different groups of subjects by different investigators. The results suggest that an absorption of about 40 % of a 3 mg reference dose of ferrous iron is given in a fasting state, roughly corresponds to the absorption in borderline-iron-deficient subjects. The results indicate that this 40% absorption value corresponds to a serum ferritin level of 30 μg/1 and that food iron absorption in a group of subjects should be expressed preferably as the absorption corresponding to a reference-dose absorption of 40 %, or possibly a serum ferritin level of 30 μg/1.