Fatty acid specificity for the esterification of vitamin A and cholesterol by intestinal and pancreatic enzymes in rats

VITAMIN A and cholesterol esters have been shown to undergo extensive hydrolysis in the lumen of the small intestine during the process of absorption; they are re-esterified to appear in the lymph mostly as esters1,2. However, the vitamin A esters of the lymph, blood and liver of the rat are formed by long-chain fatty acids3 and in the normal rat liver, probably as palmitates4. On the other hand, cholesterol esters are usually made up of poly-unsaturated fatty acids in the lymph and blood of rats5. For the absorption of the two lipid materials, the enzymes of the pancreas have been largely implicated, while not much attention has been paid to the possible role of the mucosal enzymes. From the behaviour of the mucosal enzymes, as presented here, it appears that probably these enzymes play a more important part in the re-esterification of the two lipid materials during their absorption.

High cholesterol diet and esterification of cholesterol by the intestinal mucosa of rats

Young male rats maintained on a diet containing 1% cholesterol were sacrificed at the end of 1st, 2nd, 3rd, 5th, and 7th week. Acetone powders prepared from their intestinal mucosa and pancreas were tested for the synthetic and hydrolytic activities for Vitamin A and cholesterol esters. The esterifying activity of the mucosal enzymes for both Vitamin A and cholesterol increased progressively up to the end of the 5th week; the increase in esterification of cholesterol was more marked with respect to saturated fatty acids, as compared to the unsaturated ones. The pancreatic enzymes remained unaffected. It is suggested that one of the reasons for the accumulation of cholesterol esters in animal tissues may be the increased esterification of the sterol in the mucosa induced by dietary cholesterol.

Real-Time PCR : A Molecular Approach to Investigate the Role of Intestinal Microbiota in the Pathophysiology of Irritable Bowel Syndrome

Irritable bowel syndrome (IBS) is a common multifactorial functional intestinal disorder, the pathogenesis of which is not completely understood. Increasing scientific evidence suggests that microbes are involved in the onset and maintenance of IBS symptoms. The microbiota of the human gastrointestinal (GI) tract constitutes a massive and complex ecosystem consisting mainly of obligate anaerobic microorganisms making the use of culture-based methods demanding and prone to misinterpretation. To overcome these drawbacks, an extensive panel of species- and group-specific assays for an accurate quantification of bacteria from fecal samples with real-time PCR was developed, optimized, and validated. As a result, the target bacteria were detectable at a minimum concentration range of approximately 10 000 bacterial genomes per gram of fecal sample, which corresponds to the sensitivity to detect 0.000001% subpopulations of the total fecal microbiota. The real-time PCR panel covering both commensal and pathogenic microorganisms was assessed to compare the intestinal microbiota of patients suffering from IBS with a healthy control group devoid of GI symptoms. Both the IBS and control groups showed considerable individual variation in gut microbiota composition. Sorting of the IBS patients according to the symptom subtypes (diarrhea, constipation, and alternating predominant type) revealed that lower amounts of Lactobacillus spp. were present in the samples of diarrhea predominant IBS patients, whereas constipation predominant IBS patients carried increased amounts of Veillonella spp. In the screening of intestinal pathogens, 17% of IBS samples tested positive for Staphylococcus aureus, whereas no positive cases were discovered among healthy controls. Furthermore, the methodology was applied to monitor the effects of a multispecies probiotic supplementation on GI microbiota of IBS sufferers. In the placebo-controlled double-blind probiotic intervention trial of IBS patients, each supplemented probiotic strain was detected in fecal samples. Intestinal microbiota remained stable during the trial, except for Bifidobacterium spp., which increased in the placebo group and decreased in the probiotic group. The combination of assays developed and applied in this thesis has an overall coverage of 300-400 known bacterial species, along with the number of yet unknown phylotypes. Hence, it provides good means for studying the intestinal microbiota, irrespective of the intestinal condition and health status. In particular, it allows screening and identification of microbes putatively associated with IBS. The alterations in the gut microbiota discovered here support the hypothesis that microbes are likely to contribute to the pathophysiology of IBS. The central question is whether the microbiota changes described represent the cause for, rather than the effect of, disturbed gut physiology. Therefore, more studies are needed to determine the role and importance of individual microbial species or groups in IBS. In addition, it is essential that the microbial alterations observed in this study will be confirmed using a larger set of IBS samples of different subtypes, preferably from various geographical locations.

DNA damage recognition in the normal epithelium of human prostate and seminal vesicles

Prostate cancer is one of the most prevalent cancer types in men. The development of prostate tumors is known to require androgen exposure, and several pathways governing cell growth are deregulated in prostate tumorigenesis. Recent genetic studies have revealed that complex gene fusions and copy - number alterations are frequent in prostate cancer, a unique feature among solid tumors. These chromosomal aberrations are though to arise as a consequence of faulty repair of DNA double strand breaks (DSB). Most repair mechanisms have been studied in detail in cancer cell lines, but how DNA damage is detected and repaired in normal differentiated human cells has not been widely addressed. The events leading to the gene fusions in prostate cancer are under rigorous studies, as they not only shed light on the basic pathobiologic mechanisms but may also produce molecular targets for prostate cancer treatment and prevention. Prostate and seminal vesicles are part of the male reproductive system. They share similar structure and function but differ dramatically in their cancer incidence. Approximately fifty primary seminal vesicle carcinomas have been reported worldwide. Surprisingly, only little is known on why seminal vesicles are resistant to neoplastic changes. As both tissues are androgen dependent, it is a mystery that androgen signaling would only lead to tumors in prostate tissue. In this work, we set up novel ex vivo human tissue culture models of prostate and seminal vesicles, and used them to study how DNA damage is recognized in normal epithelium. One of the major DNA - damage inducible pathways, mediated by the ATM kinase, was robustly activated in all main cell types of both tissues. Interestingly, we discovered that secretory epithelial cells had less histone variant H2A.X and after DNA damage lower levels of H2AX were phosphorylated on serine 139 (γH2AX) than in basal or stromal cells. γH2AX has been considered essential for efficient DSB repair, but as there were no significant differences in the γH2AX levels between the two tissues, it seems more likely that the role of γH2AX is less important in postmitotic cells. We also gained insight into the regulation of p53, an important transcription factor that protects genomic integrity via multiple mechanisms, in human tissues. DSBs did not lead to a pronounced activation of p53, but treatments causing transcriptional stress, on the other hand, were able to launch a notable p53 response in both tissue types. In general, ex vivo culturing of human tissues provided unique means to study differentiated cells in their relevant tissue context, and is suited for testing novel therapeutic drugs before clinical trials. In order to study how prostate and seminal vesicle epithelial cells are able to activate DNA damage induced cell cycle checkpoints, we used primary cultures of prostate and seminal vesicle epithelial cells. To our knowledge, we are the first to report isolation of human primary seminal vesicle cells. Surprisingly, human prostate epithelial cells did not activate cell cycle checkpoints after DSBs in part due to low levels of Wee1A, a kinase regulating CDK activity, while primary seminal vesicle epithelial cells possessed proficient cell cycle checkpoints and expressed high levels of Wee1A. Similarly, seminal vesicle cells showed a distinct activation of the p53 - pathway after DSBs that did not occur in prostate epithelial cells. This indicates that p53 protein function is under different control mechanisms in the two cell types, which together with proficient cell cycle checkpoints may be crucial in protecting seminal vesicles from endogenous and exogenous DNA damaging factors and, as a consequence, from carcinogenesis. These data indicate that two very similar organs of male reproductive system do not respond to DNA damage similarly. The differentiated, non - replicating cells of both tissues were able to recognize DSBs, but under proliferation human prostate epithelial cells had deficient activation of the DNA damage response. This suggests that prostate epithelium is most vulnerable to accumulating genomic aberrations under conditions where it needs to proliferate, for example after inflammatory cellular damage.

Determination of intestinal permeability in healthy horses using the contrast medium iohexol

Tämä lisensiaatin tutkielma koostuu kolmesta osasta; kirjallisuuskatsauksesta, kokeellisesta osasta ja liitteistä. Iohexol on ionisoitumaton, trijodattu ja vesiliukoinen röntgenvarjoaine. Iohexolia on hyödynnetty lääketieteessä useita vuosia. Iohexolia on käytetty muun muassa angio- ja myelografiassa, lisäksi iohexolia on hyödynnetty arvioitaessa munuaiskerästen suodattumisnopeutta sekä suoliston läpäisevyyden muutoksia. Hevosen tulehduksellisessa suolistosairaudessa (Inflammatory bowel disease, IBD) suoliston rakenne ja sen läpäisevyys muuttuu; tyypillistä on tulehdussolujen kertyminen suoliston seinämään ja myös sidekudosmuodostusta saattaa esiintyä. Suolisto muutoksia saatetaan havaita sekä ohut- että paksusuolessa. IBD aiheuttaa hevoselle laihtumista, johtuen ravintoaineiden puutteellisesta imeytymisestä ja proteiinien menetyksestä suoleen suoliston häiriötilan yhteydessä. Tällä hetkellä IBD:n diagnostiikka perustuu tyypillisiin oireisiin, kliiniseen tutkimukseen, verinäytteisiin, glukoosin imeytymistestiin ja peräsuolesta otettuun koepalaan. IBD:n diagnostiikka on kuitenkin erittäin haastavaa ja tutkimusmenetelmiin liittyy lukuisia ongelmia, jotka vähentävät niiden luotettavuutta IBD:n diagnostiikassa. Tutkimuksemme tarkoituksena on kehittää hevosen IBD:n diagnostiikkaa entistä helpompaan, luotettavampaan ja turvallisempaan suuntaan. Tämän alustavan tutkimuksen tavoitteet olivat: (1) tutkia voidaanko iohexol havaita hevosen seerumissa oraalisen annostelun jälkeen ja (2) muodostaa iohexolin pitoisuuskuvaaja ajan funktiona terveillä hevosilla. Materiaalimme koostui kymmenestä terveestä hevosesta, joilla ei ollut havaittu laihtumista tai ripulia. Ennen iohexolin annostelua hevosille suoritettiin kliininen tutkimus ja verinäytteet otettiin maha-suolikanavan sairauden poissulkemiseksi. Hevosille suoritettiin myös mahalaukun tähystys. 16 tunnin paaston jälkeen 1 ml/kg Iohexolia annosteltiin 10 % -liuoksena nenämahaletkulla suoraan mahaan ja verinäytteet otettiin 0, 30, 60, 120, 180, 240, 300 ja 360 minuuttia annostelun jälkeen. Iohexolin pitoisuus määritettiin käyttämällä korkean erotuskyvyn nestekromatografiaa. Iohexolin pitoisuuksista tietyillä ajanhetkillä muodostettiin kuvaaja. Hevosilla ei havaittu maha-suolikanavan sairauksia. Kaikki hevoset olivat hyvässä kuntoluokassa ja mahalaukun tähystyksessä ei havaittu merkittäviä muutoksia. Verinäytteiden tulokset olivat viiterajoissa. Kaikki hevoset sietivät iohexolia hyvin ja haittavaikutuksia ei havaittu. Iohexol oli havaittavissa seerumissa 60 minuutin kuluttua annostelusta. Kuvaajassa voitiin havaita kaksi huippua. Statistiset menetelmät tukivat löydöksiä. Iohexol testi oli yksinkertainen suorittaa ja siihen ei liittynyt haittavaikutuksia. Annos 1ml/kg oli havaittavissa seerumissa. Iohexolin pitoisuuskuvaaja muodosti kaksi huippua, ja tämänkaltainen ilmiö on kuvattu kirjallisuudessa aikaisemmin useiden lääkkeiden tapauksessa. Hevosella ilmiö liittyy todennäköisesti maha-suolikanavan rakenteellisiin ja fysiologisiin eroavaisuuksiin ja lisätutkimuksia ilmiön varmistamiseksi tarvitaan. Iohexol näyttää olevan potentiaalinen merkkiaine suoliston läpäisevyyden arviointiin ja lisätutkimuksia IBD:tä sairastavien hevosten seerumin iohexolin pitoisuuksista verrattuna terveiden hevosten seerumin iohexolin pitoisuuksiin on suunnitteilla.

Expression of the receptor guanylyl cyclase C and its ligands in reproductive tissues of the rat: A potential role for a novel signaling pathway in the epididymis

Guanylyl cyclase C (GC-C) is a membrane-associated form of guanylyl cyclase and serves as the receptor for the heat-stable enterotoxin (ST) peptide and endogenous ligands guanylin, uroguanylin, and lymphoguanylin. The major site of expression of GC-C is the intestinal epithelial cell, although GC-C is also expressed in extraintestinal tissue such as the kidney, airway epithelium, perinatal liver, stomach, brain, and adrenal glands. Binding of ligands to GC-C leads to accumulation of intracellular cGMP, the activation of protein kinases G and A, and phosphorylation of the cystic fibrosis transmembrane conductance regulator (CFTR), a chloride channel that regulates salt and water secretion. We examined the expression of GC-C and its ligands in various tissues of the reproductive tract of the rat. Using reverse transcriptase and the polymerase chain reaction, we demonstrated the presence of GC-C, uroguanylin, and guanylin mRNA in both male and female reproductive organs. Western blot analysis using a monoclonal antibody to GC-C revealed the presence of differentially glycosylated forms of GC-C in the caput and cauda epididymis. Exogenous addition of uroguanylin to minced epididymal tissue resulted in cGMP accumulation, suggesting an autocrine or endocrine activation of GC-C in this tissue. Immunohistochemical analyses demonstrated expression of GC-C in the tubular epithelial cells of both the caput epididymis and cauda epididymis. Our results suggest that the GC-C signaling pathway could converge on CFTR in the epididymis and perhaps control fluid and ion balance for optimal sperm maturation and storage in this tissue.

The multiple and enigmatic roles of guanylyl cyclase C in intestinal homeostasis

Guanylyl cyclase C (GC-C) is predominantly expressed in intestinal epithelial cells and serves as the receptor for the gastrointestinal hormones guanylin and uroguanylin, and the heat-stable enterotoxin, the causative agent for Travellers' Diarrhea. Activation of GC-C results in an increase in intracellular levels of cGMP, which can regulate fluid and ion secretion, colon cell proliferation, and the gut immune system. This review highlights recent findings arising from studies in the GC-C knockout mouse, along with enigmatic results obtained from the first descriptions of human disease caused by mutations in the GC-C gene. We provide some insight into these new findings and comment on areas of future study, which may enhance our knowledge of this evolutionarily conserved receptor and signaling system. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

Cyclic nucleotide signaling in intestinal epithelia: getting to the gut of the matter

The intestine is the primary site of nutrient absorption, fluid-ion secretion, and home to trillions of symbiotic microbiota. The high turnover of the intestinal epithelia also renders it susceptible to neoplastic growth. These diverse processes are carefully regulated by an intricate signaling network. Among the myriad molecules involved in intestinal epithelial cell homeostasis are the second messengers, cyclic AMP (cAMP) and cyclic GMP (cGMP). These cyclic nucleotides are synthesized by nucleotidyl cyclases whose activities are regulated by extrinsic and intrinsic cues. Downstream effectors of cAMP and cGMP include protein kinases, cyclic nucleotide gated ion channels, and transcription factors, which modulate key processes such as ion-balance, immune response, and cell proliferation. The web of interaction involving the major signaling pathways of cAMP and cGMP in the intestinal epithelial cell, and possible cross-talk among the pathways, are highlighted in this review. Deregulation of these pathways occurs during infection by pathogens, intestinal inflammation, and cancer. Thus, an appreciation of the importance of cyclic nucleotide signaling in the intestine furthers our understanding of bowel disease, thereby aiding in the development of therapeutic approaches.

Intestinal Cell Proliferation and Senescence Are Regulated by Receptor Guanylyl Cyclase C and p21

Guanylyl cyclase C (GC-C) is expressed in intestinal epithelial cells and serves as the receptor for bacterial heat-stable enterotoxin (ST) peptides and the guanylin family of gastrointestinal hormones. Activation of GC-C elevates intracellular cGMP, which modulates intestinal fluid-ion homeostasis and differentiation of enterocytes along the crypt-villus axis. GC-C activity can regulate colonic cell proliferation by inducing cell cycle arrest, and mice lacking GC-C display increased cell proliferation in colonic crypts. Activation of GC-C by administration of ST to wild type, but not Gucy2c(-/-), mice resulted in a reduction in carcinogen-induced aberrant crypt foci formation. In p53-deficient human colorectal carcinoma cells, ST led to a transcriptional up-regulation of p21, the cell cycle inhibitor, via activation of the cGMP-responsive kinase PKGII and p38 MAPK. Prolonged treatment of human colonic carcinoma cells with ST led to nuclear accumulation of p21, resulting in cellular senescence and reduced tumorigenic potential. Our results, therefore, identify downstream effectors for GC-C that contribute to regulating intestinal cell proliferation. Thus, genomic responses to a bacterial toxin can influence intestinal neoplasia and senescence.

Development of an ex vivo organ culture model using human gastro-intestinal tissue and Campylobacter jejuni.

Campylobacter jejuni is an important food-borne pathogen. However, relatively little is understood regarding its pathogenesis, and research is hampered by the lack of a suitable model. Recently, a number of groups have developed assays to study the pathogenic mechanisms of C. jejuni using cell culture models. Here, we report the development of an ex vivo organ culture model, allowing for the maintenance of intestinal mucosal tissue, to permit more complex host-bacterium interactions to be studied. Ex vivo organ culture highlights the propensity for C. jejuni to adhere to mucosal tissue via the flagellum, either as discrete colonies or as multicellular units.

Mechanism of transport of saquinavir-loaded nanostructured lipid carriers across the intestinal barrier

[EN] The aims of this work were (i) to evaluate the potential of nanostructured lipid carriers (NLCs) as a tool to 24 enhance the oral bioavailability of poorly soluble compounds using saquinavir (SQV), a BCS class IV drug 25 and P-gp substrate as a model drug, and (ii) to study NLC transport mechanisms across the intestinal barrier. 26 Three different NLC formulations were evaluated. SQV transport across Caco-2 monolayers was enhanced up 27 to 3.5-fold by NLCs compared to SQV suspension. M cells did not enhance the transport of NLCs loaded with 28 SQV. The size and amount of surfactant in the NLCs influenced SQV's permeability, the transcytosis pathway 29 and the efflux of SQV by P-gp. An NLC of size 247 nm and 1.5% (w/v) surfactant content circumvented P-gp 30 efflux and used both caveolae- and clathrin-mediated transcytosis, in contrast to the other NLC formulations, 31 which used only caveolae-mediated transcytosis. By modifying critical physicochemical parameters of the 32 NLC formulation, we were thus able to overcome the P-gp drug efflux and alter the transcytosis mechanism 33 of the nanoparticles. These findings support the use of NLCs approaches for oral delivery of poorly 34 water-soluble P-gp substrates.

Intestinal absorption by Sarotherodon galilaeus (syn Tilapia galilaea ) of Lake Kainji, Nigeria

Carbohydrates, protein, lipid and crude fibre were found to reduce in amount from the anterior to posterior regions along the gut of Sarotherodon galilaeus collected from Lake Kainji. Different regions of the gut exhibited different absorptive powers and all the compounds were differently absorbed in amount. Different sizes of fish showed different absorptive capacity

Avaliação do estado nutricional de pacientes com doença inflamatória intestinal

A doença Inflamatória Intestinal (DII) é uma desordem caracterizada pela inflamação crônica do trato gastrointestinal. Os dois principais tipos de DII são a Retocolite Ulcerativa (RCU) e a Doença de Crohn (DC) e ambas cursam com importantes alterações no estado nutricional (EN). O objetivo deste estudo foi identificar as diferenças na composição corporal entre pacientes com DC, RCU e indivíduos saudáveis, além de comparar o estado nutricional dos três grupos de pacientes, ajustando para fatores que podem interferir no EN, como o uso atual de corticosteróides, a atividade física, a atividade de doença, a idade e o sexo. Foi realizado um estudo transversal que incluiu 101 pacientes com DII (50 com DC e 51 com RCU) e 35 indivíduos saudáveis, selecionados no Ambulatório do Hospital Universitário Pedro Ernesto (HUPE) da Universidade do Estado do Rio de Janeiro (UERJ). Foram colhidas informações sócio-demográficas e pessoais, tais como: prática de atividade física, tabagismo, doenças pregressas e procedimentos cirúrgicos prévios. Outras informações necessárias à pesquisa foram coletadas em prontuário médico. A avaliação antropométrica foi realizada por meio das seguintes medidas: peso corporal; altura; circunferências do braço, da cintura (CC) e do quadril; dobras cutâneas do tríceps, subescápula, supra-ilíaca e da coxa; e circunferência muscular do braço (CMB). A análise da composição corporal foi realizada por meio da bioimpedância elétrica (BIA), utilizando-se o aparelho Biodynamics modelo 450. As variáveis laboratoriais analisadas foram: glicose, hemograma completo, perfil lipídico, proteínas totais, albumina, globulina, velocidade de hemossedimentação e proteína C reativa. O peso, o índice de massa corporal, a CC e o percentual de gordura corporal calculado a partir da aferição das dobras cutâneas, foram menores nos pacientes com DC, quando comparados aos indivíduos saudáveis e/ou aos pacientes com RCU. A CMB foi menor nos pacientes com DC e RCU quando comparados aos indivíduos saudáveis, porém sem apresentar diferenças entre os dois grupos de pacientes. Por BIA, verificou-se que os pacientes com DC apresentaram valores de massa magra, massa celular corpórea, massa extracelular, água corporal total e água extracelular menores quando comparados aos indivíduos saudáveis. Os níveis séricos de colesterol total, proteínas totais e albumina, e a contagem total de hemácias foram menores nos indivíduos com DC quando comparados aos indivíduos do grupo controle e/ou aos indivíduos do grupo da RCU. Os pacientes com RCU exibem composição corporal semelhante à da população saudável. Em contraposição, os pacientes com DC apresentam EN amplamente comprometido com depleção de gordura corporal e massa magra em relação aos demais indivíduos

Condição oral em pacientes com doença inflamatória intestinal

O objetivo deste estudo foi avaliar a prevalência de periodontite e a presença de lesões cariosas, restauradas e elementos perdidos por cárie em pacientes com Doença de Crohn (DC) e Retocolite Ulcerativa (RCUI), comparado-os a pacientes saudáveis sistemicamente. Como objetivo secundário, avaliamos a condição clínica da mucosa oral nos três grupos. Foram examinados 99 pacientes com DC (39.0 DP 12.9 anos), 80 com RCUI (43.3 13.2 anos) e 74 no grupo C (40.3 12.9 anos). A condição periodontal foi avaliada através do índice de placa visível, do sangramento gengival à sondagem, da profundidade de bolsa à sondagem (PBS) e do nível de inserção à sondagem (NIS). Indivíduos que apresentavam pelo menos quatro sítios com NIS ≥3 forma considerados como portadores de periodontite. As condições dentárias foram avaliadas pelo índice de dentes com lesões cariosas, restaurados e perdidos por cárie (CPOD). A condição clínica da mucosa oral foi investigada através da presença de lesões no tecido mole. A porcentagem de placa foi significativamente menor no grupo DC (44.0 30.5) que no C (54.1 26.4), p= 0.017. O sangramento gengival a sondagem era significativamente menor nos pacientes com DC (22.5 18.0) comparado ao grupo C (29.2 22.1), p= 0.038. A quantidade total de sítios com PBS ≥ 4mm foi significativamente menor no grupo DC (5.4 6.6), comparado ao grupo C (12.9 17.7), p= 0.02. A porcentagem de pacientes portadores de periodontite foi significativamente maior nos grupos RCUI (92.6%, p= 0.004) e DC (91.9%, p=0.019), comparado ao grupo C (79.7%). O índice de CPOD foi significativamente maior nos grupos RCUI (16.4 6.6; p< 0.0001) e no DC (15.1 7.3; p= 0.016) quando comparados ao C (12.5 6.8). Foram observadas significativamente mais lesões bucais nos grupos DC (17.2%; p= 0.0041) e RCUI (28.7%; p < 0.0001) quando comparadas ao grupo C (6.7%). Assim, conclui-se que os pacientes com Doença de Crohn e Retocolite Ulcerativa apresentam maior prevalência de periodontite, e maior índice de CPOD quando comparados aos indivíduos do grupo controle. A perda de inserção foi significativamente maior no grupo da Retocolite Ulcerativa quando comparado a Doença de Crohn. Além disso, os pacientes com comprometimento intestinal apresentam significativamente mais lesões bucais que os pacientes do grupo controle.

Efeito da L-Arginina e Glicina na parede do cólon irradiado Estudo experimental em ratos

A radioterapia é amplamente utilizada no tratamento de tumores pélvicos, incluindo os de bexiga, intestino e reto. Ela apresenta efeitos danosos, notadamente em tecidos que apresentam intensa renovação celular, sendo a mucosa intestinal altamente susceptível. Nesse contexto, a suplementação dietética com aminoácidos tem se mostrado uma terapia promissora para minimizar este dano. O objetivo desse estudo foi determinar o efeito da suplementação dietética com os aminoácidos L-arginina e glicina na estrutura da parede do cólon de ratos submetidos a irradiação abdominal. Quarenta ratos Wistar machos adultos foram distribuídos aleatoriamente em quatro grupos, cada um com dez animais: I controle não irradiado e sem suplementação de aminoácidos; II controle irradiado e sem suplementação de aminoácidos; III irradiado e suplementado com L-arginina; IV irradiado e suplementado com glicina. O período de suplementação dietética foi de 14 dias, com a irradiação ocorrendo no 8. dia do experimento. A análise estereológica mostrou que a irradiação provocou diminuição do volume total da parede colônica dos animais dos grupos II e III em relação aos animais saudáveis, mas não dos ratos que receberam suplementação de glicina. A camada mucosa dos animais irradiados de todos os grupos diminuiu quando comparada com os ratos saudáveis não irradiados. Os animais irradiados que não receberam suplementação de aminoácido apresentaram diminuição da camada muscular da mucosa, quando comparados com os grupos I e IV, e o grupo de ratos suplementados com glicina apresentou aumento significativo da camada submucosa em relação aos grupos I e II. Os animais do grupo III mostraram diminuição da camada muscular própria em comparação aos grupos I e IV. A suplementação com L-arginina foi eficaz na manutenção do volume parcial do epitélio da camada mucosa. Nossos resultados sugerem que a suplementação de glicina apresentou efeitos superiores ao da suplementação com L-arginina na estrutura da parede colônica, haja vista que foi capaz de manter a espessura da parede e a superfície epitelial da mucosa, enquanto a Larginina foi capaz de manter o volume parcial do epitélio e a superfície epitelial, mas não o volume total da parede intestinal.