In vivo experimental study to investigate cytogenotoxicity of a contaminated estuary from Southeastern Brazilian Coast.

The aim of this study was to evaluate cytogenotoxicity in mammalian cells induced by ingestion of superficial water from SESS. For this purpose, surface water was collected from two points of SESS: São Vicente Channel (SVC) and Piaçaguera Channel (PIC). Four groups (n = 5) of adult male Wistar (8 weeks old) received for 5 days: (a) filtered tap water (water control), (b) tap water with 2.4% of NaCl (saline control), (c) estuarine water from PIC and (d) estuarine water from SVC. Results demonstrated that Ki67 immunoexpression was higher in hepatocytes exposed to both sampling site, while caspase-3 demonstrated downregulation in rat liver exposed to estuarine water. There was also significant increase in micronuclei frequency in bone marrow cells and hepatocytes, and DNA damage in blood and liver of rats exposed to estuarine water from SVC and PIC. In summary, studies with complex mixtures, such as contaminated estuarine water are important since this work confirmed by experiments using in vivo mammalian cells of rats that SESS water are genotoxic, mutagenic and cytotoxic, denoting concern for environmental health.

Paradoxical sleep deprivation induces differential biological response in rat masticatory muscles: Inflammation, autophagy and myogenesis.

BACKGROUND: The aim of this study was to evaluate whether sleep deprivation (SD) induces inflammation, autophagy and myogenesis in the following masticatory muscles: masseter and temporal. METHODS: In this study, 18 animals were randomly distributed into three groups: control group (CTL, n = 6), SD for 96 hours (SD96, n = 6), and SD for 96 hours and more 96 hours of sleep recovery (SD96 + R, n = 6). RESULTS: In the histopathological analysis, SD 96 was able to induce inflammation in masseter and temporal. Nevertheless, the lack of inflammatory process was evidenced to the masseter in the group SD96 + R. Upregulation of TNF-alpha production was detected in the SD96 group, while SD96 + R decreased TNF immunoexpression for both skeletal muscles evaluated. MyoD and myogenin increased in rats submitted to SD96. By contrast, the levels of MyoD decreased in the group SD96 + R. Myogenin pointed out high immunoexpression in SD96 + R groups. In temporal, pAkt decreased in animals submitted to SD96, but it increased in the group SD96 + R. The levels of LC3 protein increased in both skeletal muscles studied, and masseter decreased LC3 protein expression in the SD96 + R. CONCLUSION: In summary, our results demonstrate that SD is able to induce inflammation, atrophy and myogenesis in rat masticatory muscles, being more intense in temporal when compared to masseter.

Association of expression of inflammatory response genes and DNA repair genes in colorectal carcinoma.

Inflammation is an important etiological factor of colorectal carcinoma and may be related to colorectal carcinoma growth and proliferation. This study aimed to verify whether the presence of chronic inflammation represented by tumor necrosis factor-α, interleukin-2, interleukin-6, and interleukin-10 gene expression is related to hMLH1, hMSH2, hMSH6, and PMS2 gene expression and the corresponding protein levels of these genes from the DNA repair system. A total of 83 patients were operated on for curative or palliative colorectal carcinoma. Expression of the inflammatory response genes tumor necrosis factor-α, interleukin-2, interleukin-6, and interleukin-10 as well as expression of the hMLH1, hMSH2, hMSH6, and PMS2 genes of the DNA repair system (mismatch repair) and the expression levels of the corresponding mismatch repair proteins were measured in neoplastic tissue by reverse transcription polymerase chain reaction and immunohistochemistry, respectively. Associations were observed between hMSH6 mRNA expression and interleukin-2 mRNA expression (p = 0.026) as well as between hMLH1 and hMSH2 gene expression and tumor necrosis factor-α gene expression (p = 0.042). Higher tissue levels of interleukin-2 and tumor necrosis factor-α gene expression were associated with lower hMSH6, hMLH1, and hMSH2 gene expression.

Genotoxicity and mutagenicity induced by acute crack cocaine exposure in mice.

CONTEXT: Crack cocaine is an illicit drug derived from cocaine, in which use and abuse have increased around the world, especially in developing countries. OBJECTIVES: The aim of this study was to evaluate genomic damage in multiple organs of mice following acute exposure to crack cocaine. For this purpose, single cell gel (comet) assay in peripheral blood, liver, kidney, and brain cells was performed and micronucleus test for bone narrow and liver cells was also made in this setting. MATERIAL AND METHODS: A total of 20 C57BL/10 male mice were distributed into four groups, as follows: 0, 4.5, 9, and 18 mg/kg b.w. of crack cocaine dissolved to 1% dimethyl sulfoxide by intraperitoneal (i.p.) route. All animals were sacrificed 24 h after i.p. injection. RESULTS: The results showed that crack cocaine induced DNA damage in peripheral blood, and brain cells for higher doses used as depicted by single cell gel (comet) assay data. Analysis of kidney cells showed no genetic damage for all groups tested. The number of micronucleated cells did not increase after crack cocaine exposure in bone narrow or liver cells. CONCLUSION: In summary, crack cocaine is a genotoxic agent in peripheral blood, liver, and brain cells but not mutagenic in multiple organs of mice.

Antioxidant activity of apple extract protects against rat tongue carcinogenesis induced by 4-nitroquinoline 1-oxide.

Several studies have shown that apple (Malus sp.) has many components able to exert chemopreventive activity. The aim of this study was to evaluate the chemopreventive potential of apple extract following medium-term oral carcinogenesis assay induced by 4-nitroquinoline 1-oxide (4NQO) by means of histopathological analysis and gene expression of antioxidant enzymes, such as CuZnSOD, MnSOD and catalase. A total of 30 male Wistar rats were distributed into five groups, as follows (n = 6 per group): Group 1 - negative control group (non-treated group); Group 2 - received 4NQO during 8 weeks in drinking water and treated with apple extract by gavage between the 1st and 4th weeks daily (initiation phase); Group 3 - received 4NQO for 8 weeks in drinking water and treated with apple extract by gavage between the 5th and 8th weeks daily (promotion phase); Group 4 - received apple extract by gavage for eight consecutive weeks only; and Group 5 - received 4NQO for 8 weeks in drinking water daily. Histopathological analysis revealed that apple extract protect oral lesions induced by 4NQO at initiation or promotion phase. Higher gene expression of CuZnSOD and MnSOD enzymes were noticed in groups treated with apple extract as well. Taken together, our results demonstrate that the apple extract is able to modulate medium-term oral carcinogenesis assay as a result of antioxidant activity.

Grape juice concentrate (G8000™) modulates apoptosis but not oxidative stress following rat colon carcinogenesis induced by azoxymethane.

OBJECTIVES: The aim of this study was to evaluate if grape juice concentrate is able to protect against experimental colon carcinogenesis. MATERIAL AND METHODS: For this purpose, a total of 35 male Wistar rats were randomly distributed into seven groups: G1: SHAM animals receiving only saline; G2: animals receiving 15 mg/kg azoxymethane (AOM); G3: animals receiving 1% grape juice concentrate 2 weeks before the administration of AOM; G4: animals receiving 2% grape juice concentrate 2 weeks before the administration of AOM; G5: animals receiving 1% grape juice concentrate 4 weeks after the last administration of AOM; G6: animals receiving 2% grape juice concentrate 4 weeks after the last administration of AOM; G7: animals receiving only 2% grape juice concentrate. RESULTS: The group that received 2% grape juice concentrate before induction with AOM showed the decreased expression of Bcl-2 compared to those animals that were induced by AOM (positive control). Regarding Bax, animals that received grape juice at 2% decreased Bax immunoexpression when compared to AOM group. Furthermore, animals that intake grape juice at 1% after induced by AOM decreased Bax immunoexpression as well. 8-OHdGLI did not show significant statistically differences (p > 0.05) among groups. CONCLUSION: In summary, our results demonstrate that grape juice is able to modulate rat colon carcinogenesis as a result of induction of apoptosis.

Expression of galectin-3 in gastric adenocarcinoma.

BACKGROUND & OBJECTIVES: Galectin-3 a member of the galectin family is an endogenous ß-galactoside binding lectin. It has been found to be associated with cell adhesion, recognition, proliferation, differentiation, immunomodulation, angiogenesis, apoptosis and can be a reliable marker for cancer aggressiveness. The aim of this study was to verify protein expression in gastric adenocarcinoma tissues and correlate the results with the clinical aspects in the study population. METHODS: Galectin-3 expression was examined by immunohistochemistry in 57 samples of gastric adenocarcinomas tissues. Galectin-3 protein expression was observed in the cytoplasm and the nucleus of examined tissues. RESULTS: Thirty one (54.4%) samples had strong or moderate staining and 26 (45.6%) tumours had negative or weak staining. The galectin-3 did not show association with the sex (p=0.347), age (p=0.999), Lauren's classification (p=0.731) and TNM stage (p=0.222). Regarding the TNM stage, 66.7 per cent of stage I tumours had strong or moderate staining; with tumours stage IV this percentage was 33.3 per cent. INTERPRETATION & CONCLUSION: Our results suggest that gal-3 is not a reliable biomarker for prognosis of the gastric adenocarcinoma by immunohistochemistry. Further studies need to be done on a large sample of tumour tissues in different clinical staging.

Anti-tumor activity of grape juice concentrate in the rat tongue two-stage initiation-promotion protocol induced by 4-nitroquinoline 1-oxide.

The aim of this study was to evaluate the anti-tumor activity of grape juice concentrate following medium-term oral carcinogenesis assay induced by 4-nitroquinoline 1-oxide (4NQO). A total of 30 male Wistar rats were distributed into five groups, as follows (n = 6 per group): Group 1 - negative control group (non-treated group); Group 2 - received grape juice concentrate at 1% dose by gavage for eight consecutive weeks; Group 3 - received 4NQO for 8 weeks at 20 ppm dose in drinking water daily; Group 4 - received 4NQO at 20 ppm dose during 8 weeks in drinking water and treated with grape juice concentrate at 1% dose orally by gavage for first 4 weeks after 4-NQO administration; Group 5 - received 4NQO at 20 ppm dose for 8 weeks in drinking water and treated with grape juice concentrate at 1% dose orally by gavage between the 5th and 8th weeks daily. Histopathological analysis revealed a decrease in hyperplasic and dysplastic lesions in Group 4. Groups 4 and 5 showed decreased COX-2 and TNF-alpha and eNOS gene expression. Grape juice concentrate also increased SOD Cu/Zn and catalase expression. However, Ki-67 immunoexpression was reduced at the promotion step of oral carcinogenesis (G5). Taken together, our results demonstrate that grape juice concentrate modulates rat tongue carcinogenesis as a result of anti-inflammatory activity, antioxidant activity and down-regulation of oral cells proliferation.

IMMUNOEXPRESSION OF DEK AND PHOSPHO-P38 PROTEINS IN RECTAL CANCER BEFORE CHEMORADIATION THERAPY.

BACKGROUND: Colorectal cancer is the third cause of cancer worldwide and a quarter of them are in the rectum. DEK oncogene is involved in several nuclear processes and can accelerate tumorigenesis. OBJECTIVE: This study aims to evaluate the immunoexpression of DEK and Phospho-P38 proteins before neoadjuvant therapy in patients with rectum adenocarcinoma and correlate it with a clinical response and survival. METHODS: Patients with adenocarcinoma of the middle and low rectum who underwent chemotherapy and radiotherapy followed by surgical tumor resection were included. The expression and quantification were studied by immunohistochemistry in the tumor biopsy tissues using a HScore system. Score ≥4 were considered positive and those with <4 negative. RESULTS: 22 patients were included with a mean age of 63.55 years (SD: ±13.49). The clinical-stage before treatment was T3 on 72.7%, T4 on 18.2%, 31.8% were N1, 50% N0 and all M0. After chemo and radiotherapy, 54.6% were T3; 22.7% were classified as T2; 9.1% as T1, and 13.6% were T0. Among the tumors, 22.7% were positive for DEK and 63.6% positive for Phospho-P38. There was a positive correlation between DEK protein before treatment and pTNM stage (P=0.011). Phospho-P38 protein showed no correlation with these parameters. Patients with a negative HScore had a mean survival of 141.33 months (95%CI: 112.41-170.25) and those with a positive HSscore had a mean survival of 25.10 months (95%CI: 17.36-32.84; P<0.001). CONCLUSION: A higher expression of DEK was observed in advanced stages. Patients who presented DEK expression <4 had a higher survival, being a factor of worst prognosis.

Dimethoate induces genotoxicity as a result of oxidative stress: in vivo and in vitro studies.

Dimethoate ([O,O-dimethyl S-(N-methylcarbamoylmethyl) phosphorodithioate]) is an organophosphate insecticide and acaricide widely used for agricultural purposes. Genotoxicity refers to the ability of a chemical agent interact directly to DNA or act indirectly leading to DNA damage by affecting spindle apparatus or enzymes involved in DNA replication, thereby causing mutations. Taking into consideration the importance of genotoxicity induced by dimethoate, the purpose of this manuscript was to provide a mini review regarding genotoxicity induced by dimethoate as a result of oxidative stress. The present study was conducted on studies available in MEDLINE, PUBMED, EMBASE, and Google scholar for all kind of articles (all publications published until May, 2020) using the following key words: dimethoate, omethoate, DNA damage, genetic damage, oxidative stress, genotoxicity, mutation, and mutagenicity. The results showed that many studies were published in the scientific literature; the approach was clearly demonstrated in multiple tissues and organs, but few papers were designed in humans. In summary, new studies within the field are important for better understanding the pathobiological events of genotoxicity on human cells, particularly to explain what cells and/or tissues are more sensitive to genotoxic insult induced by dimethoate.

Biomonitoring of oral epithelial cells in smokers and non-smokers submitted to panoramic X-ray: comparison between buccal mucosa and lateral border of the tongue.

The aim of the present study was to comparatively evaluate DNA damage (micronucleus) and cellular death (pyknosis, karyolysis, and karyorrhexis) in exfoliated oral mucosa cells from smokers and non-smokers submitted to dental X-ray using two anatomic sites: buccal mucosa and lateral border of the tongue. A total of 15 heavy smokers and 17 non-smokers were submitted to panoramic dental radiography for orthodontic reasons. Individuals had epithelial cells from cheek and lateral border of the tongue mechanically exfoliated, placed in fixative, and dropped in clean slides which were checked for the above nuclear phenotypes. The results pointed out no significant statistically differences (p > 0.05) of micronucleated oral mucosa cells before versus after X-ray exposure for both oral sites evaluated either to smokers or to non-smokers. X-ray exposure was able to increase other nuclear alterations closely related to cytotoxicity such as karrhyorexis, pyknosis, and karyolysis for two groups evaluated. Nevertheless, the most pronunciated effects were found to lateral border of the tongue of smokers. In summary, these data indicate that panoramic X-ray is able to induce cellular death in oral mucosa cells. It seems that lateral border of the tongue is more sensitive site to cytotoxic insult induced by ionizing radiation combined with continuous cigarette smoke exposure.

The relationship between the commensal microbiota levels and Crohn's disease activity.

BACKGROUND AND AIM: Human gut microbiota play an important role in metabolism and host physiology. Perturbations of the gut microbial communities lead to the development of various diseases such as inflammatory bowel disease, celiac disease, allergic diseases, and metabolic diseases. Crohn's disease is a chronic inflammatory bowel disease characterized by periods of remission and relapse. Several studies suggest that intestinal inflammation arises due to an abnormal response of the intestinal immune system to the fecal microbiota. The goal of the study was to evaluate the relative amount of four bacterial groups in fecal samples of Crohn's disease patients and their relation to the inflammatory activity. METHODS: We studied stool samples of 105 individuals, 54 with Crohn's disease and 51 as a control group. The DNA extracted from the stool samples was subjected to real-time polymerase chain reaction (qPCR) for quantification of the Bacteroidetes phylum, class Bacilli, and Bifidobacteriaceae and Enterobacteriaceae families. RESULTS: We found a significant increase in Bacteroidetes in Crohn's disease samples when compared to the control group (14 650 and 2060 CFU/ng DNA, respectively) (P = 0.014). On the other hand, we observed a significant reduction in Bacilli and Bifidobacteriaceae (13 and 58 CFU/ng DNA, respectively) (P < 0.0001). In contrast, patients without any drug treatment presented an increase of Bacilli and Bifidobacteriaceae (102 521 and 6235 CFU/ng DNA, respectively) (P < 0.0001). CONCLUSION: The commensal bacteria were decreased in fecal samples of participants with Crohn's disease when compared to the control group. There was no relation between the disease location and/or disease activity with the microbiota.

p53, Cyclin-D1, ß-catenin, APC and c-myc in Tumor Tissue from Colorectal and Gastric Cancer Patients with Suspected Lynch Syndrome by the Bethesda Criteria.

Colorectal cancer (CRC) is one of the most frequent neoplasms worldwide, and up to 15% have a family history. Lynch syndrome (LS) is a hereditary cause of CRC and gastric (GC). Individuals with LS have mutations in mismatch genes repair. p53, cyclin D1, ß-catenin, APC and c-myc proteins are involved in the cell cycle and carcinogenesis. OBJECTIVE: To study the expression of p53, Cyclin D1, ß-catenin, APC and c-myc proteins in patients with CRC and GC with at least one of the Bethesda positive criteria. Compare the expression of these proteins with the presence or absence of expression of the DNA repair proteins. PATIENTS AND METHODS: We included 70 individuals with CRC or GC with at least one of the Bethesda positive criteria. Protein expression of MLH1, MSH2, MSH6, PMS2, p53, cyclin D1, ß-catenin, APC and c-myc were analized by immunohistochemistry tumours tissues. RESULTS: Deficient expression of MLH1, MSH2, MSH6 and PMS2 were respectively 38.7%; 17.7%; 26.22% and 48.38%. We found a negative association between deficiency of PMS2 and age, and positive association between PMS2 deficiency and APC positive. The positive imunoexpression of APC increases by 4 times the chance of having deficiency of PMS2. CONCLUSIONS: Patients with loss of expression of PMS2 had a higher risk of mutation or deletion of APC and tumours with positive immunoexpression of cyclin D1 had an increased risk of loss of expression of MSH2. These results suggest that tumours with loss of expression of DNA repair proteins had a higher loss of cell control cycle.
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Canonical and noncanonical Wnt pathway: a comparison among normal ovary, benign ovarian tumor and ovarian cancer.

The Wnt family is involved in tumorigenesis of several tissues. In ovarian cancer, the role played by Wnts and its pathways is not clearly defined. In order to analyze the canonical and noncanonical Wnt pathway in normal ovary, benign ovarian tumor and ovarian cancer, we evaluated the immunohistochemical expression of Wnt1, Frizzled-1 (FZD1), Wnt5a, Frizzled-5 (FZD5) and beta-catenin. Ovarian specimens were obtained from surgeries performed between 1993 and 2004. The patients were divided in three groups: group A, epithelial ovarian cancer (n=38); group B, benign epithelial neoplasia (n=28); and group C, normal ovaries (n=26). Immunoreactivity for Wnt1, FZD1, Wnt5a, FZD5 and beta-catenin was scored for each group. The proportion of Wnt1 positive women in group A (29.4%) was significantly higher than in group B (4.3%) and C (9.1%) (p=0.020). The proportion of FZD1 positive patients in group C (54.5%) was significantly lower than in group A (97.1%) and B (90.0%) (p<0.001). The proportion of Wnt5a positive women was significantly higher for group A (80.0%) compared to group B (25.0%) and C (27.3%) (p<0.001). The proportion of beta-catenin positive patients in group C (95.8%) was significantly higher than group B (52.4%) (p=0.004). Comparison of the survival curves in group A according to Wnt5a expression showed a significant difference between positive and negative patients, whereas the Wnt5a positive women showed worse results (p=0.050). Our findings suggest that the pathways related to Wnt5a have an important role in ovarian malignant neoplasia. Furthermore, Wnt5a was found to be a predictor of poor prognosis for ovarian cancer.

Imbalance of tumor suppression genes expression following rat tongue carcinogenesis induced by 4-nitroquinoline 1-oxide.

This study was undertaken to investigate, by immunohistochemistry, the expression of some tumor suppressor genes such as p16, p21 and Retinoblastoma (Rb) during 4-Nitroquinoline 1-oxide induced rat tongue carcinogenesis. Male Wistar rats were distributed into three groups of 10 animals each and treated with 50 ppm 4NQO solution through their drinking water for 4, 12 or 20 weeks. Ten animals were used as negative control. Neither histopathological abnormalities were induced in the epithelium after 4 weeks of carcinogen exposure, nor statistically significant differences (p>0.05) in expression of all the tumor suppressor genes were found when compared to the negative control. However, the levels of Rb were increased (p<0.05) in pre-neoplastic lesions at 12 weeks following carcinogen exposure. In well-differentiated squamous cell carcinoma induced after 20 weeks of treatment with 4NQO, p16 and Rb were expressed in some tumor cells. Taken together, the results support the belief that the expression of Rb is closely event-related to malignant transformation and conversion of the oral mucosa, being a reliable biomarker linked to oral cancer pathogenesis.

The Role of Dimethoate and UV-B on Skin of Wistar Rats.

BACKGROUND/AIM: The pesticide dimethoate (O-dimethyl-S- Nmethylcarbamoylmethyl phosphorodithioate) is able to induce severe acute toxicity in living organisms. The aim of this study was to evaluate the effects of ultraviolet radiation, alone or combined with exposure to dimethoate, on the rat skin. MATERIALS AND METHODS: A total of 38 Wistar female rats (Rattus norvegicus albinus), were distributed into four groups: A (n=9) control group, B (n=10) exposed to ultraviolet-B radiation (UV-B), C (n=10) exposed to UV-B followed by application of dimethoate (UV-B+AGRO) and group D (n=9) exposed to dimethoate (AGRO). Histological examination of the tissues, as well as immunohistochemistry for cleaved caspase 3, Ki-67 and COX-2 expression were performed to all groups. RESULTS: Animals submitted to UV-B exhibited hyperkeratosis with moderate cell atypia. Regarding exposure to UV-B+AGRO, the animals presented hyperkeratosis and atrophy, whereas in animals exposed to AGRO, only atrophy was noticed. The immunohistochemical results on skin revealed that UVB, AGRO and UVB+AGRO decreased cleaved caspase 3 and Ki-67 expression when compared to the control group (p<0.05). COX-2 expression decreased to UVB or AGRO groups compared to controls (p<0.05). CONCLUSION: UV-B or AGRO exposure is able to induce histopathological changes and altered expression of cleaved caspase-3 and Ki-67 in rat skin, thus being categorized as a risk condition for skin carcinogenesis.

THE CANONICAL WNT PATHWAY IN GASTRIC CARCINOMA.

BACKGROUND: It is believed that the Wnt pathway is one of the most important signaling involved in gastric carcinogenesis. AIM: To analyze the protein expression of canonical and non-canonical Wnt pathways in gastric carcinoma. METHOD: The immunohistochemistry was performed in 72 specimens of gastric carcinomas for evaluating the expression of Wnt-5a, FZD5, GSK3ß, axin, CK1, ubiquitin, cyclin D1 and c-myc. RESULTS: There were significant differences for cytoplasm and nucleus ubiquitin for moderately and well differentiated tumors (p=0.03) and for those of the intestinal type of the Lauren classification (p=0.03). The absence of c-myc was related to Lauren's intestinal tumors (p=0.03). Expression of CK1 in the cytoplasm was related to compromised margin (p=0.03). Expression of cyclin D1 protein was more intense in male patients (p=0.03) There was no relation of the positive or negative expression of the Wnt-5a, FZD5, GSK3 and Axin with any clinicopathological variables. CONCLUSION: The canonical WNT pathway is involved in gastric carcinoma.

[Weight, educational achievement, basic sanitation, alcoholism, smoking and eating habit in patients with gastric cancer]. / Variação de peso, grau de escolaridade, saneamento básico, etilismo, tabagismo e hábito alimentar pregresso em pacientes com cancêr de estômago.

BACKGROUND: About 35% of the cancer patients are involved in factors coming from the diet and others like alcohol, smoking, sunlight, chemical agents and infections caused by virus. The stomach cancer is the second cause of cancer in the world with 9.9 % of all diagnosis and about 12.1 % of death cases. AIMS: Evaluate the body weight, educational achievement, basic sanitation, smoking, alcoholism and eating habit among patients with gastric cancer and a control group. METHODS: Seventy patients with gastric cancer were paired with 70 subjects without cancer. Data on the weight and height, educational attainment, basic sanitation, smoking, alcoholism and eating habits of the patients were collected from the clinical records and from interviews. RESULTS: Forty two patients were men, the mean age were 60 years old. The actual weight and body mass index of the patients were smaller when compared to the controls. Within the group of patients with gastric cancer, 21 never attended school, and for those who attended, 55% did not finish the elementary school. Among the patient group, 32.9% of them lived in housing with basic sanitation and 37.1% with electricity, against 68.6% of the controls, and 58.6% of the patients lived in rural area, against only 7.1% of the controls. Among the test group, 65.7% of the patients were smokers, whereas in the control group, 44.3% were smokers. In addition, there was also difference in the duration of smoking habit. Alcoholism was also more frequent in the cancer group (44% vs 19%). Food rich in salt, condiments, nitrates, saturated fat, complex carbohydrates, refined sugar and fried salted food had been more used by gastric cancer patients. CONCLUSION: The patients with gastric cancer presented with: less weight, low quality of life as indicated by lower or no access to basic sanitation, electricity and schooling, lived predominantly in rural area, high incidence of alcohol intake and higher intake of high fat foods and industrialized foods.

Effect of different periods of hyperbaric oxygen on ischemia-reperfusion injury of rat small bowel.

PURPOSE: To determine whether hyperbaric oxygen (HBO) could effectively protect the small intestine mucosa against an ischemic insult, according to different periods of application. METHODS: The gut of 32 male rats was subjected to 60-min ischemia (clamping the mesenteric artery and vein); After they were further reperfused upon clamp opening during 60 min. Animal groups were as follows. GII = placed on HBO during the ischemia period; GIII = placed on HBO during reperfusion; GIV = treated with HBO throughout the ischemia-reperfusion period. Some animals (GI) did not receive HBO treatment at all and served as reference of ischemia-reperfusion injury (IR). HBO was carried out in a cylindrical acrylic chamber (2.0 ATA). Samples of small bowel were prepared for H.E staining for histological evaluations. RESULTS: The histological injury of mucosa was significantly less when HBO was administered during the ischemia period (17.6 +/- 0.6) as compared with the IR (21.3 +/- 1.8). HBO was not effective when applied during reperfusion (23.1 +/- 2.1) or during the ischemia plus reperfusion period (18.7 +/- 1.9). The thickness of the mucosa was preserved by HBO in ischemia (327.50 +/- 30.23 microm) in comparison with the IR (172.79 +/- 5.95 microm). In the periods of reperfusion (162.50 +/- 6.05 microm) and ischemia plus reperfusion (296.49 +/- 20.01 microm) the mucosa revealed a structural injury. CONCLUSION: Hyperbaric oxygen affects the ischemic insult of small bowel, being the favorable effect obtained when hyperbaric oxygen was administered early in the ischemic period.

The effects of pentoxifylline into the kidneys of rats in a model of unilateral hindlimb ischemia/reperfusion injury.

PURPOSE: To study the role of pentoxifylline (PTX) on remote kidney injury caused by muscle ischemia of left hindlimb of rats. METHODS: After xylazine and ketamine anesthesia, the left hindlimb of rats (n=66) were submitted to 6 hours ischemia (clamping the left common iliac artery). Three groups were used: sham group (SG, n=6), early group (EG, n=30) with reperfusion after 4 hours and late group (LG, n=30) with reperfusion after 24 hours. The saline solution (EG1, n=10 and LG1, n=10) or PTX (40 mg.Kg-1) was administered in the reperfusion beginning (EG2, n=10/LG2, n=10) or divided in two doses in the ischemia beginning and reperfusion beginning (EG3, n=10/LG3, n=10). The plasmatic creatinokinase, urea, creatinine, sodium and potassium values were measure and histological samples from left kidney were prepared and H&E stained for scored cellular necrosis and degeneration of kidney tubules and thickness glomerulus determination. The apoptosis index was determined by immunohistochemical expression of the caspase-3. The tests of Mann-Whitney and Kruskal-Wallis (p