Unsymmetrical DMH – An isomer of 1,2 DMH – Is it potent to induce gastrointestinal carcinoma in rats?

Very few animal studies have used 1,1-dimethyl hydrazine (unsymmetrical dimethyl hydrazine – UDMH) as a carcinogen. This study was designed to investigate the carcinogenicity of UDMH in the gastrointestinal tract in a rat model. We wanted to observe if there were any changes in tissue zinc levels and tissue copper zinc superoxide dismutase (CuZnSOD) enzyme activity during the carcinogenic process, and to compare these values with those of control rats in the medium- and long-term. Six-week-old Wistar rats were given a subcutaneous injection of UDMH (30 mg/kg body wt) twice a week for 20 weeks, and sacrificed after 5 and 9 months of treatment. Tissue zinc levels showed a significant decrease (p<0.05) in the large intestine at 9 months, whereas in the stomach and small intestine there were no significant changes at 5 and 9 months. Tissue CuZnSOD enzyme activity in the stomach, small intestine and large intestine showed no significant decrease at 5 and 9 months as compared to controls. Histologically, the large intestine was normal at 9 months.

This study suggests that UDMH administered at the above dosage was not carcinogenic in this model.     

Intestinal Mechanomorphological Remodeling Induced by Long-Term Low-Fiber Diet in Rabbits

Short-term feeding with low-fiber diet remodels the mechanomorphological properties in the rabbit small intestine. The aims were to study the effect of feeding low-fiber diet for 5 months on mechanomorphological properties including the collagen fraction in the rabbit intestines. Fifteen rabbits were divided into an Intervention group (IG, n = 10) fed a low-fiber diet and a Control group (CG, n = 5) fed a normal diet for 5 months. Five months later, four 10-cm-long segments obtained from the duodenum, jejunum, ileum and large intestine were used for histological and mechanical analysis, respectively. The wall thickness, wall area, mucosa and muscle layer thickness decreased whereas the submucosa layer thickness increased in the IG (p < 0.05). The collagen fraction decreased in all layers and segments in the IG (p < 0.05). The opening angle increased in the large intestine and decreased in the ileum in the IG (p < 0.05). The intestinal stress–strain curves for IG shifted to the right, indicating softening. The creep did not change in the four segments. The wall stiffness was associated with wall thickness and collagen fraction in the submucosa layer. Long-term low-fiber diet in rabbits induced histomorphometric and biomechanical remodelling of the intestines.     

The intestinal zinc transport in aged rats

To determine if there are any age-related alterations in the intestinal zinc absorption that may contribute to zinc deficiency, we studied the zinc transport across the jejunal segments of 3-, 12- and 24-month-old Fisher 344 male rats using the Ussing chamber technique. We also evaluated the effect of 5 microM arachidonic acid in tissue bathing media. The zinc transport from mucosa to serosa in 24-month-old rats (55.0 +/- 3.5 nmol/h/cm2) was significantly greater than the transport in 12-month-old (30.1 +/- 6.3 nmol/h/cm2) and 3-month-old rats (41.0 +/- 5.2 nmol/h/cm2). There was no age-dependent differences in the zinc transport from the serosa to the mucosa. The addition of 5 microM arachidonic acid to the serosal side only resulted in a significant decrease in zinc transport rate from serosa to mucosa. The magnitude of change in the 24-month-old rats (36.0 +/- 3.9 vs. 26.5 +/- 3.2 nmol/h/cm2) was similar to the change seen in 12-month-old rats (34.5 +/- 4.6 vs. 20.1 +/- 3.5 nmol/h/cm2) and 3-month-old rats (34.5 +/- 4.6 vs. 26.1 +/- 3.9 nmol/h/cm2). The results indicate that intestinal zinc transport is increased in the aged rats, and that arachidonic acid or one of its metabolites may be important regulators of net zinc absorption through their effect on intestinal zinc secretion rates.     

Expression of carcinoembryonic antigen, T-antigen, and oncogene products as markers of neoplastic and preneoplastic colonic mucosa

Several crypt abnormalities have been demonstrated in the mucosa of neoplastic and preneoplastic lesions of the large intestine. In addition, certain tumor markers are expressed in large intestinal carcinoma but not in normal mucosa. To determine whether any correlation exists between tumor marker expression and crypt abnormalities and at what stage markers are expressed, we studied specimens of large intestinal mucosa from 13 patients with preneoplastic conditions (adenomatous polyp, familial polyposis, Crohn's disease, and ulcerative colitis). The tumor markers examined include carcinoembryonic antigen (CEA), the ras gene products p21 and p21ser (mutated form), and beta-D-galactosyl-(1----3)-alpha-N-acetyl-D-galactosamine (gal--gal NAc, also known as T-antigen). Results were compared to those of five cases of adenocarcinoma of colon and three control cases of colonic mucosa obtained at immediate autopsy. All four markers were expressed in three of the five cases of adenocarcinoma, but none were expressed in the control cases. Variable expression of each marker was demonstrated in the dilated, distorted crypts of preneoplastic lesions. CEA and gal--gal NAc appeared to be expressed most frequently, suggesting that these are common markers or are expressed at an earlier stage in the neoplastic process than p21 or p21ser. Demonstration of such markers in preneoplastic conditions may be of use in determining the malignant potential and in monitoring these lesions.     

Ulcerative colitis--contemporary morphological criteria

Regular bioptical examinations of patients with ulcerative colitis (UC) performed in recent years show that the inflammatory changes of the mucosa of the large intestine are not necessarily diffuse, and that their extent may vary in the course of the disease. To establish the diagnosis of UC and to assess the treatment efficacy it is important to examine histologically multiple mucosal specimens from different levels of the large intestine. In our series of 27 patients with ulcerative colitis (18 men and 9 women at the age of 17 to 76 years), active or active and inactive pancolitis was diagnosed in 25 cases (93%). In 11 of these, the whole of the large intestine was affected. Two patients showed diffuse pancolitis without caecal involvement, in 5 cases there was inactive inflammation in the rectum or in the sigmoid colon. Seven patients had active colitis of the rectum and sigmoid. In another 2 patients (7%), the inflammation was limited to several segments of the large intestine only (the descending colon, and the descending and transverse colon). On bioptical examination of 6 patients repeated after 2-29 months (mean 14 months), there were changes in the distribution and appearance of the inflammation. Thus our findings correspond with the results of previous studies: UC does not always affect the mucosa of the large intestine diffusely. Further, the extent and distribution of inflammatory changes vary in the course of the disease.     

Effect of estrogens on the blood serum level of carcino-embryonic antigen in rats with neoplasms of the intestine and nonspecific injuries of its mucosa

Carcino-embryonic antigen (CEA) was detected in the blood serum of 70% of rats with tumors of the large intestine induced by 1,2-dimethylhydrazine and with posttraumatic regeneration of the mucosa of the large intestine. After injection of estrogen (diethylstilbestrol proionate, 0.57 g daily for 6 days) the frequency of appearance of CEA in such animals increased, as also did the CEA level in the blood serum. In rats with injury to the mucosa of the large intestine, injection of estrogen prevented the natural decrease in the CEA concentration as the intensity of the regenerative process diminished.Laboratories of Experimental Tumors and Endocrinology, N. N. Petrov Scientific-Research Institute of Oncology, Ministry of Health of the USSR, Leningrad. (Presented by Academician of the Academy of Medical Sciences of the USSR V. I. Ioffe.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 83, No. 5, pp. 582–583, May, 1977.     

Tissue engineering of the small intestine by acellular collagen sponge scaffold grafting

Tissue engineering of the small intestine will prove a great benefit to patients suffering from short bowel disease. However cell seeding in tissue engineering, such as fetal cell use, is accompanied by problems of ethical issues, rejection, and short supply. To overcome these problems, we carried out an experimental study on tissue engineering of the small intestine by acellular collagen sponge scaffold grafting. We resected the 5 cm long jejunum from beagle dogs and reconstructed it by acellular collagen sponge grafting with a silicon tube stent. The graft was covered with the omentum. At 1 month after operation, the silicon stent was removed endoscopically. Animals were sacrificed 1 and 4 months after operation, and were examined microscopically. Neo-intestinal regeneration was observed and the intestinal mucosa covered the luminal side of the regenerated intestine across the anastomosis. Thus, the small intestine was regenerated by tissue engineering technology using an acellular collagen sponge scaffold.     

A strategy for the ubiquitous overexpression of human catalase and CuZn superoxide dismutase genes in transgenic mice

In the present study, we generated transgenic mice that overexpress catalase or CuZn superoxide dismutase (CuZnSOD) in all tissues using large genomic DNA fragments. An 80 kb human genomic DNA, containing the 33 kb human CAT gene as well as the 41 kb of 5' and the 6 kb of 3' flanking regions, was obtained by screening a human P1 library and was used to produce transgenic mice Tg(CAT). Transgenic mice Tg(SOD1) were produced by a similar strategy using a 64 kb human genomic DNA containing the 10 kb human SOD1 gene and the 27 kb of both 5' and 3' flanking regions. Catalase mRNA levels were 2-6- fold higher and catalase activity levels were 2-4- fold higher in the various tissues of the hemizygous Tg(CAT) mice compared with wild type mice. The mRNA levels for CuZnSOD were 2-12- fold higher and the CuZnSOD activity levels were 2-5- fold higher in the hemizygous Tg(SOD1) mice compared with wild type mice. In summary, our study demonstrates that a strategy of using large genomic DNA containing either the entire human CAT or SOD1 gene with large flanking regions gives ubiquitous increased expression of CuZnSOD and catalase. In addition, the expression of catalase closely reflects the tissue specific pattern found in the endogenous gene. These transgenic mice will be useful in studying the role of oxidative stress/damage in aging and age-related pathologies.     

Age-related changes in antioxidant enzymes and lipid peroxidation in brains of control and transgenic mice overexpressing copper-zinc superoxide dismutase

The aim of our study was first to obtain a comprehensive profile of the brain antioxidant defense potential and peroxidative damage during aging. We investigated copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), seleno-dependent glutathione peroxidase (GSH-PX), glutathione reductase (GSSG-R) activities, endogenous and in vitro stimulated lipid perxidation in 40 brains of control mice divided into 3 age groups: 2 months (young), 12 months (middle-aged) and 28 months (old). We found a positive correlation between age and activities of CuZnSOD (r = 0.47); P < 0.01) and GSH-PX (r = 0.72; P < 0.0001). CuZnSOD and GSH-PX activities are independently regulated during brain aging since temporal changes of these two enzymes do not correlate. No modification in MnSOD activity and basal lipid peroxidation was observed as a function of age. Nevertheless, stimulated lipid peroxidation was significantly higher at 12 months (6.53 ± 0.71 μmole MDA/g tissue) thatn at 2 months (5.69 ± 0.90) and significantly lower than 28 months (5.13 ± 0.33) than at 12 months.Second, we used genetic manipulations to construct transgenic mice that specifically overexpress CuZnSOD to understand the role of CuZnSOD in neuronal aging. The human CuZnSOD transgene expression was stable during aging. The increased CuZnSOD activity in the brain (1.9-fold) of transgenic mice resulted in an enhanced rate of basal lipid peroxidation and in increased MnSOD activity in the 3 age groups. Other antioxidant enzymes did not exhibit modifications indicating the independence of the regulation between CuZnSOD and glutathione-related enzymes probably due to their different cellular localization in the brain.     

Potassium deposition during and after hypokinesia in potassium supplemented and unsupplemented rats

The aim of this study was to determine that hypokinesia (restricted motor activity) could increase potassium (K+) losses with decreased tissue K+ content showing decreased K+ deposition. To this end, measurements were made of K+absorption, tissue K+ content, plasma K+ levels, fecal and urinary K+ excretion during and after hypokinesia (HK) with and without K+ supplementation. Studies conducted on male Wistar rats during a pre-hypokinetic period, a hypokinetic period and a post-hypokinetic period. Rats were equally divided into four groups: unsupplemented vivarium control rats (UVCR), unsupplemented hypokinetic rats (UHKR), supplemented vivarium control rats (SVCR) and supplemented hypokinetic rats (SHKR). SHKR and UHKR were kept in small individual cages which restricted their movements in all directions without hindering food and water consumption. SVCR and UVCR were housed in individual cages under vivarium control conditions. SVCR and SHKR consume daily 3.96 mEq potassium chloride (KCl) per day. Absorption of K+, and K+ levels in bone, muscle, plasma, urine and feces and PA levels did not change in SVCR and UVCR compared with their pre-HK levels. During HK, plasma, fecal and urinary K+ levels and plasma aldosterone (PA) levels increased significantly (p<0.05) with time, while K+ absorption, muscle and bone K+ content decreased significantly (p<0.05) with time in SHKR and UHKR compared with their pre-HK values and the values in their respective vivarium controls (SVCR and UVCR). During the initial 9-days of post-HK, K+ absorption increased significantly (p<0.05) and plasma K+ levels, fecal and urinary K+ losses and PA levels decreased significantly (p<0.05) and muscle and bone K+ content remained significantly (p<0.05) depressed in SHKR and UHKR compared with their pre-HK and their respective vivarium control values. During HK and post-HK periods, K+ absorption, bone and muscle K+ content, and K+ levels in plasma, urine and feces and PA levels were affected significantly (p<0.05) more in SHKR than in UHKR. By the 15th day of post-HK the values in SHKR and UHKR approach the control values. The higher K+ losses during HK with decreased tissue K+ levels shows decreased K+ deposition. The higher K+ loss with lower tissue K+ levels in SHKR than in UHKR shows that K+ deposition decreases more with K+ supplementation than without. Because SHKR had shown lower tissue K+ content and lost higher K+ amounts than UHKR it was concluded that the risk of decreased K+ deposition and tissue K+ depletion is inversely related to K+ intake, i.e., the higher K+ intake, the greater the risk for decreased K+ deposition, and the higher K+ losses and the greater the risk for tissue K+ depletion. The dissociation between tissue K+ depletion and K+ excretion indicates decreased K+ deposition as the principal mechanism of tissue K+ depletion during prolonged HK.     

Villous tissue osmolality,water and electrolyte transport in the cat small intestine at varying luminal osmolalities

Villous tissue osmolality and net transport for water, sodium, potassium and chloride were determined in the feline small intestine when exposing the mucosa to solutions with different mannitol concentrations (0, 100, 315 and 600 mmol/l). Tissue osmolality at the villous tip varied with luminal osmolality. At the villous base, on the other hand, tissue osmolality remained around the plasma osmolality regardless of the osniolality of the luminal fluid. Transport rates for water were affected in the way predicted from the lumen to tissue osmolality difference. A net flux from tissue to lumen was always recorded for the studied electrolytes. The hydraulic conductivity (L_p) of the intestinal epithelium with dilated intercellular spaces was estimated from the present results to be around 30times10–¹² cm xs^-1xPa^-1. When the intercellular spaces were collapsed L_p was estimated to be 15times10–¹² cmxs^-1xPa^-l.     

间充质干细胞移植修复炎性肠组织过程中的主导基因筛选

背景：前期研究已证明间充质干细胞可定植于炎症性肠黏膜修复炎症性肠组织。 目的：应用表达谱芯片技术研究间充质干细胞移植修复前后大鼠炎症性大肠组织的差异基因表达情况,初步揭示与间充质干细胞定植、分化、修复炎症性肠组织过程相关的主导基因。 方法：健康SD大鼠随机分为2组：移植实验组用三硝基苯磺酸灌肠制作炎症性肠病模型,造模后24 h经尾静脉注入绿色荧光蛋白标记的间充质干细胞;对照组以生理盐水代替三硝基苯磺酸同法灌肠处理。于移植后28 d取移植实验组和对照组大肠组织,利用基因芯片技术筛选移植实验组和对照组的差异表达基因。 结果与结论：对照组和移植实验组大肠组织全基因组表达谱芯片结果有差异性表达的基因共388个(P < 0.05,FC>2),其中表达上调基因191个、表达下调基因197个,主要与炎症反应、免疫反应和细胞分化3个方面有关。前10位显著上调和下调的差异基因(共20条)中,与炎症反应相关的有3个,与免疫反应相关的有3个,与干细胞分化相关的有2个。388个差异基因主要涉及33条信号通路(P < 0.05),其中与炎症反应相关的有6条,与免疫反应相关的有8条,与干细胞分化相关的有5条。结果可见利用全基因组表达谱基因芯片的方法初步筛选了间充质干细胞修复炎症性肠组织的主要相关基因。中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程全文链接：     

利用组织芯片技术研究CA19-9在直肠癌组织中表达

目的探讨CA19-9在直肠癌中的表达,为临床直肠癌的病理诊断和鉴别诊断提供参考。方法应用组织芯片技术和免疫组化染色SP法,检测50例直肠癌直肠粘膜中CA19-9的表达情况,对照组为39例正常直肠粘膜中CA19-9的表达。结果CA19-9在50例的直肠癌组织芯片中阳性率62%,在39例正常直肠粘膜的阳性率为15.4%。两者结果比较相差显著(P<0.05)。结论CA19-9对直肠癌的病理诊断有重要的参考价值。组织芯片技术的信息容量大,实验操作简便,可供临床参考使用。     

The effects of development of a food-related operant reflex on the receptor binding of glutamate in the rat brain

Receptor binding of glutamate was studied in the striatum, hippocampus, and cerebral cortex of rats with different abilities to acquire an operant food-related reflex in a Skinner box. The striatum of rapidly-learning rats and rats unable to learn showed significantly higher levels of glutamate binding than controls were not trained in the Skinner box (p<0.05). Striatal receptor binding of glutamate in slow-learning rats was lower than that in rapidly-learning rats and rats which were unable to learn (p<0.05). In the hippocampus, all groups of rats (rapidly-learning, slow-learning, and those unable to learn) showed increased receptor binding of glutamate as compared with controls (p<0.05), in the cerebral cortex, there was a significant decrease in glutamate binding as compared with controls in all groups of animals subjected to training (p<0.05). Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 84, No. 9, pp. 913–919, September, 1998.     

肠血管活性多肽对多器官功能障碍综合征大鼠肠淋巴细胞归巢的影响

为观察肠血管活性多肽 (VIP )对大鼠肠缺血再灌注致多器官功能障碍综合征 (MODS )时 ,肠淋巴细胞归巢至肠相关淋巴细胞 (GALT )的调节以及对MODS转归的影响。本研究用微型无创动脉夹夹住大鼠肠系膜动脉根部 4 5min ,松夹后再灌注6h ,制备MODS模型。将VIP分别从股静脉输入和从腹腔注入大鼠体内。收集肠淋巴液 ,计数淋巴细胞总数及T、B淋巴细胞比例 ,了解淋巴细胞进入血循环状况。体外用51Cr标记肠淋巴细胞 ,回输入大鼠体内 ,用γ计数器检测各器官组织内的51Cr 肠淋巴细胞 ,了解肠淋巴细胞归巢。检测血及肠淋巴TNF α、内毒素 ;测定血D 乳酸、谷丙转氨酶 (ALT )、肌肝 (Cr)、血氧分压 ;观察重要器官组织学改变 ,评价VIP对MODS时各脏器形态及功能改变。结果显示 ,VIP使MODS大鼠肠粘膜迁移至血循环肠淋巴细胞总数 [(0 4 2± 0 18)× 10 7/h]较未予处理的MODS组 [(0 2 8± 0 15 )× 10 7/h]显著增加 (P <0 0 5 ) ,以T细胞数上升明显。VIP减少了MODS大鼠归巢至肠粘膜的肠淋巴细胞 ,Peyer淋巴结及小肠分布的51Cr 细胞量分别占总51Cr量的 2 14 %± 1 4 9%、 1 5 8%± 0 4 2 % ,显著低于未予处理的MODS组 (5 0 4 %± 1 2 3%和 3 2 3%± 1 6 9% ,P <0 0 1及P <0 0 5 )。外源性给予MODS大鼠VIP后 ,肠淋巴     

Expression of alpha-smooth muscle actin as special and morphometric assessment in the small intestine during the postnatal development in hamster

Immunoreactivity of alpha-smooth muscle actin (ASMA), along, with morphometric values in the hamster small intestine, was examined during postnatal development. Twelve healthy hamsters were divided into three age groups of 2·5 months (group 1), 3 months (group 2), and 4 months (group 3). For morphometrical study, routine tissue processing was carried out by autotechnicon tissue processor, the processed tissues were embedded and sectioned serially into 5-μm thick sections. The sections were stained with hematoxylin and eosin (H&E). Immunohistochemistry (IHC) was performed by primary antibodies against alpha-smooth muscle actin (ASMA). All samples showed ASMA expression in the muscularis mucosa and circular and longitudinal layers of muscularis propria. The small intestine samples in group 1 showed minimal ASMA expression in total muscular layers. Alpha-smooth muscle actin labeling was increased in groups 2 and 3 in the muscularis mucosa and both layers of inner and outer circular muscle as compared to group 1. A more intense ASMA expression was observed in the longitudinal layers in both groups 2 and 3. The morphometrical results showed that there was a smaller increase in thickness of the mucosa, submucosa, and muscular layers from group 1 to group 2 that was followed by a larger increase between groups 2 and 3. There were significant increases in thickness of all morphometrical parameters (mucosa, submucosa, and muscularis) in groups 2 and 3 in comparison with group 1, and also group 3 compared with group 2. In groups 2 and 3, thickness of the submucosa and muscular layers were significantly higher in the jejunum compared with the ileum.     

CuZn-SOD suppresses the bovine papillomavirus-induced proliferation of fibroblasts

Eukaryotic cells continuously produce reactive oxygen species (ROS) and have mechanisms to control ROS levels. ROS have been shown to mediate cell proliferation and transformation. We studied the effect of CuZn-superoxide dismutase (CuZnSOD) on the focus-forming ability of bovine papillomavirus (BPV-1) wtDNA and hypertransforming mutant of its major oncoprotein E5, E5-17S. We found that CuZnSOD suppresses the focus-forming ability of BPV-1 wtDNA and E5 oncoprotein. Significantly fewer foci were detected in pCGCuZnSOD- and BPV-1 DNA-cotransfected cell culture compare to BPV-1 DNA-transfected cell culture (p<0.001). CuZnSOD decreases the rate of cell proliferation in both non-transformed C127 and BPV-1- and E5-transformed cell lines. CuZnSOD decelerates cell entry into the S phase of the cell cycle and has a suppressing effect on the actively dividing cells. As the transformed cells proliferate faster than normal cells when confluent, CuZnSOD inhibits the growth of foci. These results indicate that superoxide radicals may be involved in signaling for cell proliferation and that SOD suppresses cell proliferation.     

Differential expression of superoxide dismutases in lung cancer

Oxidant-antioxidant balance is known to regulate growth factors and invasion of tumor cells. Manganese superoxide dismutase (MnSOD), copper zinc SOD (CuZnSOD), and extracellular SOD (ECSOD), the first-line antioxidant defenses, were studied in lung carcinomas by immunohistochemical analysis (n = 139, 56, and 37, respectively) and in 8 lung tumor specimens by Western blot analysis and SOD activity measurement. Altogether, 49% of squamous cell carcinomas and 43% of the adenocarcinomas were positive for MnSOD by immunohistochemical analysis; corresponding values for CuZnSOD were 79% and 93%, respectively. MnSOD and CuZnSOD by Western blot analysis were 27% and 22% higher, and CuZnSOD activity was 93% higher (P = .06) in carcinomas than in nonmalignant lung tissue samples. ECSOD, a mainly extracellular enzyme, showed weak positivity only in 4 of 37 carcinomas, and by Western blot analysis showed 70% lower immunoreactivity (P < .0001) than in nonmalignant lung tissue samples. It is highly likely that low expression of ECSOD might have fundamental effects on the extracellular redox state of lung tumors with potential consequences on tumor behavior.     

Increased expression of matrix metalloproteinase-9 in nasal polyps

To investigate the role of gelatinases in nasal polyposis, a common and disabling airway disease characterized by chronic inflammation and tissue remodelling, matrix metalloproteinase-2 (MMP-2) and MMP-9 expression was investigated in the nasal polyps (NP) of 24 patients undergoing ethmoidectomy and compared with 15 control nasal mucosal (CM) samples obtained from snorers during turbinectomy. Tissue samples were either frozen for enzymatic analysis or paraffin wax-embedded for immunohistochemistry. Zymography and quantitative image analysis showed that MMP-9 active forms were significantly increased (p<0.05) in NPs compared to CM (44 +/- 40 versus 13 +/- 19x10(3) AU/10 microg protein), while MMP-2 expression was similar in both tissues. Concomitant studies of gelatinase immunoexpression showed that MMP-9 expression was enhanced (4- to 16-fold) in surface epithelium, glands (p<0.05), and submucosal inflammatory cells (p<0.05). In addition, MMP-9 positivity was markedly increased in endothelial cells (p<0.01). In situ zymography demonstrated marked gelatinolytic activity, consistent with the immunolocalization of MMP-2 and MMP-9. These results suggest up-regulation of active MMP-9 in the glands and vessels characteristic of NPs. It is concluded that MMP-9 may play a role in the upper airway remodelling observed during nasal polyposis.     

Matrix metalloproteinase-9 (MMP-9) in allergic nasal polyps

Matrix metalloproteinases (MMPs) are known to play important roles in the invasion of nasal mucosa by inflammatory cells through degradation of extracellular matrix. Matrix metalloproteinase-9 (MMP-9) is considered to play a role in the pathogenesis of nasal polyp. The aim of the present study was to compare plasma MMP-9 levels of patients with nasal polyp of different etiologic origins, those with allergic nasal polyp (ANP) and non-allergic nasal polyp (NANP). In all, 29 patients (20 NANP and 9 ANP) and 20 healthy subjects were included in this study. Plasma MMP-9 levels were measured using ELISA. Plasma MMP-9 levels were higher (p<0.05) in ANP patients than in NANP patients and controls. In the group with ANP, plasma MMP-9 levels showed a positive correlation (p<0.05) with eosinophil counts. Plasma MMP-9 levels of NANP patients and control groups were similar (p>0.05). Moreover, that the highest levels of MMP-9 were in ANP patients may indicate the usefulness of this parameter in differentiating between the different etiologic origins of nasal polyp. Further studies are required to elaborate on the relationship between MMP-9 levels and allergic reactions.